WISP tissue networks integrate 174 genome-scale datasets, encompassing ~56,179 measurements from ~7,978 publications and include both expression and interaction measurements.
| Dataset Name | Title | Description |
| biogrid | biogrid | biogrid |
| GSM1008087 | N2_1 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008088 | N2_2 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008089 | N2_3 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008090 | N2_4 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008091 | N2_inf_1 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008092 | N2_inf_2 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008093 | N2_inf_3 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008094 | N2_inf_4 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008095 | JU1580_1 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008096 | JU1580_2 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008097 | JU1580_3 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008098 | JU1580_inf_1 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008099 | JU1580_inf_2 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008100 | JU1580_inf_3 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008101 | RDE_1_1 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008102 | RDE_1_2 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008103 | RDE_1_3 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008104 | RDE_1_inf_1 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008105 | RDE_1_inf_2 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1008106 | RDE_1_inf_3 (GSE41058: Competition between viral-derived and endogenous small RNA pathways regulates gene expression in response to viral infection in C.elegans.) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1015556 | control-continuous_expose-2h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015557 | low_DDVP-continuous_expose-2h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015558 | high_DDVP-continuous_expose-2h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015559 | control-2h_expose-8h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015560 | low_DDVP-2h_expose-8h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015561 | high_DDVP-2h_expose-8h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015562 | control-2h_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015563 | low_DDVP-2h_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015564 | high_DDVP-2h_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015565 | control-2h_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015566 | low_DDVP-2h_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015567 | high_DDVP-2h_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015568 | control-2h_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015569 | low_DDVP-2h_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015570 | high_DDVP-2h_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015571 | control-continuous_expose-8h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015572 | low_DDVP-continuous_expose-8h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015573 | high_DDVP-continuous_expose-8h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015574 | control-8h_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015575 | low_DDVP-8h_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015576 | high_DDVP-8h_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015577 | control-8h_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015578 | low_DDVP-8h_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015579 | high_DDVP-8h_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015580 | control-8h_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015581 | low_DDVP-8h_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015582 | high_DDVP-8h_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015583 | control-continuous_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015584 | low_DDVP-continuous_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015585 | high_DDVP-continuous_expose-14h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015586 | control-continuous_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015587 | low_DDVP-continuous_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015588 | high_DDVP-continuous_expose-20h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015589 | control-continuous_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015590 | low_DDVP-continuous_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015591 | high_DDVP-continuous_expose-26h_harvest-rep1 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015592 | control-continuous_expose-0h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015593 | control-continuous_expose-2h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015594 | low_DDVP-continuous_expose-2h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015595 | high_DDVP-continuous_expose-2h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015596 | control-2h_expose-8h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015597 | low_DDVP-2h_expose-8h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015598 | high_DDVP-2h_expose-8h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015599 | control-2h_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015600 | low_DDVP-2h_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015601 | high_DDVP-2h_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015602 | control-2h_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015603 | low_DDVP-2h_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015604 | high_DDVP-2h_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015605 | control-2h_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015606 | low_DDVP-2h_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015607 | high_DDVP-2h_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015608 | control-continuous_expose-8h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015609 | low_DDVP-continuous_expose-8h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015610 | high_DDVP-continuous_expose-8h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015611 | control-8h_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015612 | low_DDVP-8h_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015613 | high_DDVP-8h_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015614 | control-8h_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015615 | low_DDVP-8h_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015616 | high_DDVP-8h_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015617 | control-8h_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015618 | low_DDVP-8h_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015619 | high_DDVP-8h_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015620 | control-continuous_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015621 | low_DDVP-continuous_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015622 | high_DDVP-continuous_expose-14h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015623 | control-continuous_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015624 | low_DDVP-continuous_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015625 | high_DDVP-continuous_expose-20h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015626 | control-continuous_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015627 | low_DDVP-continuous_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015628 | high_DDVP-continuous_expose-26h_harvest-rep2 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015629 | control-continuous_expose-0h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015630 | control-continuous_expose-2h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015631 | low_DDVP-continuous_expose-2h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015632 | high_DDVP-continuous_expose-2h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015633 | control-2h_expose-8h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015634 | low_DDVP-2h_expose-8h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015635 | high_DDVP-2h_expose-8h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015636 | control-2h_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015637 | low_DDVP-2h_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015638 | high_DDVP-2h_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015639 | control-2h_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015640 | low_DDVP-2h_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015641 | high_DDVP-2h_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015642 | control-2h_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015643 | low_DDVP-2h_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015644 | high_DDVP-2h_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015645 | control-continuous_expose-8h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015646 | low_DDVP-continuous_expose-8h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015647 | control-8h_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015648 | low_DDVP-8h_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015649 | high_DDVP-8h_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015650 | control-8h_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015651 | low_DDVP-8h_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015652 | high_DDVP-8h_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015653 | control-8h_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015654 | low_DDVP-8h_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015655 | high_DDVP-8h_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015656 | control-continuous_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015657 | low_DDVP-continuous_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015658 | high_DDVP-continuous_expose-14h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015659 | control-continuous_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015660 | low_DDVP-continuous_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015661 | high_DDVP-continuous_expose-20h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015662 | control-continuous_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015663 | low_DDVP-continuous_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015664 | high_DDVP-continuous_expose-26h_harvest-rep3 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015665 | control-continuous_expose-0h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015666 | control-continuous_expose-2h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015667 | low_DDVP-continuous_expose-2h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015668 | high_DDVP-continuous_expose-2h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015669 | control-2h_expose-8h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015670 | low_DDVP-2h_expose-8h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015671 | high_DDVP-2h_expose-8h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015672 | control-2h_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015673 | low_DDVP-2h_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015674 | high_DDVP-2h_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015675 | control-2h_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015676 | low_DDVP-2h_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015677 | high_DDVP-2h_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015678 | control-2h_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015679 | low_DDVP-2h_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015680 | high_DDVP-2h_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015681 | control-continuous_expose-8h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015682 | low_DDVP-continuous_expose-8h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015683 | high_DDVP-continuous_expose-8h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015684 | control-8h_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015685 | low_DDVP-8h_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015686 | high_DDVP-8h_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015687 | control-8h_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015688 | low_DDVP-8h_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015689 | high_DDVP-8h_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015690 | control-8h_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015691 | low_DDVP-8h_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015692 | high_DDVP-8h_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015693 | control-continuous_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015694 | low_DDVP-continuous_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015695 | high_DDVP-continuous_expose-14h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015696 | control-continuous_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015697 | low_DDVP-continuous_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015698 | high_DDVP-continuous_expose-20h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015699 | control-continuous_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015700 | low_DDVP-continuous_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1015701 | high_DDVP-continuous_expose-26h_harvest-rep4 (GSE41366: Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery) | The principal toxicity of acute organophosphate (OP) pesticides poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms. We exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA sampled at multiple time points throughout the exposure. The worms showed a time-dependent response that progressively worsened. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively, rapidly return to steady-state levels. The changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption. |
| GSM1034592_C | C.elegans fed with E.coli OP50 3 days rep1 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034593_C | C.elegans fed with E.coli OP50 3 days rep2 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034594_C | C.elegans fed with E.coli OP50 3 days rep3 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034595_C | C.elegans fed with CNCM I-3690 3 days rep1 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034596_C | C.elegans fed with CNCM I-3690 3 days rep2 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034597_C | C.elegans fed with CNCM I-3690 3 days rep3 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034598_C | C.elegans fed with CNCM I-4317 3 days rep1 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034599_C | C.elegans fed with CNCM I-4317 3 days rep2 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034600_C | C.elegans fed with CNCM I-4317 3 days rep3 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034601_C | C.elegans fed with E.coli OP50 10 days rep1 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034602_C | C.elegans fed with E.coli OP50 10 days rep2 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034603_C | C.elegans fed with E.coli OP50 10 days rep3 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034604_C | C.elegans fed with CNCM I-3690 10 days rep1 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034605_C | C.elegans fed with CNCM I-3690 10 days rep2 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034606_C | C.elegans fed with CNCM I-3690 10 days rep3 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034607_C | C.elegans fed with CNCM I-4317 10 days rep1 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034608_C | C.elegans fed with CNCM I-4317 10 days rep2 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1034609_C | C.elegans fed with CNCM I-4317 10 days rep3 (GSE42192: Gene expression data from C.elegans) | Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans. |
| GSM1045580_CE_551_005_001 | acrylamide_control_expose-0h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045581_CE_551_005_002 | acrylamide_control_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045582_CE_551_005_003 | acrylamide_low_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045583_CE_551_005_004 | acrylamide_mid_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045584_CE_551_005_005 | acrylamide_high_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045585_CE_551_005_006 | acrylamide_control_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045586_CE_551_005_007 | acrylamide_low_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045587_CE_551_005_008 | acrylamide_mid_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045588_CE_551_005_009 | acrylamide_high_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045589_CE_551_006_001 | acrylamide_control_expose-0h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045590_CE_551_006_002 | acrylamide_control_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045591_CE_551_006_003 | acrylamide_low_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045592_CE_551_006_004 | acrylamide_mid_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045593_CE_551_006_005 | acrylamide_high_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045594_CE_551_006_006 | acrylamide_control_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045595_CE_551_006_007 | acrylamide_low_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045596_CE_551_006_008 | acrylamide_mid_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045597_CE_551_006_009 | acrylamide_high_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045598_CE_551_007_001 | acrylamide_control_expose-0h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045599_CE_551_007_002 | acrylamide_control_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045600_CE_551_007_003 | acrylamide_low_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045601_CE_551_007_004 | acrylamide_mid_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045602_CE_551_007_005 | acrylamide_high_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045603_CE_551_007_006 | acrylamide_control_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045604_CE_551_007_007 | acrylamide_low_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045605_CE_551_007_008 | acrylamide_mid_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045606_CE_551_007_009 | acrylamide_high_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045607_CE_552_004_011 | cadmium_control_expose-0h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045608_CE_552_004_002 | cadmium_control_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045609_CE_552_004_003 | cadmium_low_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045610_CE_552_004_012 | cadmium_mid_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045611_CE_552_004_005 | cadmium_high_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045612_CE_552_004_010 | cadmium_control_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045613_CE_552_004_007 | cadmium_low_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045614_CE_552_004_008 | cadmium_mid_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045615_CE_552_004_009 | cadmium_high_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045616_CE_552_005_001 | cadmium_control_expose-0h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045617_CE_552_005_002 | cadmium_control_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045618_CE_552_005_003 | cadmium_low_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045619_CE_552_005_004 | cadmium_mid_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045620_CE_552_005_005 | cadmium_high_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045621_CE_552_005_006 | cadmium_control_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045622_CE_552_005_007 | cadmium_low_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045623_CE_552_005_008 | cadmium_mid_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045624_CE_552_005_009 | cadmium_high_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045625_CE_552_006_001 | cadmium_control_expose-0h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045626_CE_552_006_002 | cadmium_control_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045627_CE_552_006_003 | cadmium_low_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045628_CE_552_006_005 | cadmium_high_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045629_CE_552_006_006 | cadmium_control_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045630_CE_552_006_007 | cadmium_low_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045631_CE_552_006_008 | cadmium_mid_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045632_CE_552_006_009 | cadmium_high_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045633_CE_556_007_001 | mercury_control_expose-0h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045634_CE_556_007_002 | mercury_control_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045635_CE_556_007_003 | mercury_low_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045636_CE_556_007_004 | mercury_mid_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045637_CE_556_007_005 | mercury_high_expose-4h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045638_CE_556_007_006r | mercury_control_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045639_CE_556_007_007 | mercury_low_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045640_CE_556_007_008 | mercury_mid_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045641_CE_556_007_009 | mercury_high_expose-8h_rep1 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045642_CE_556_008_001 | mercury_control_expose-0h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045643_CE_556_008_002 | mercury_control_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045644_CE_556_008_003 | mercury_low_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045645_CE_556_008_004 | mercury_mid_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045646_CE_556_008_005 | mercury_high_expose-4h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045647_CE_556_008_006r | mercury_control_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045648_CE_556_008_007 | mercury_low_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045649_CE_556_008_008 | mercury_mid_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045650_CE_556_008_009 | mercury_high_expose-8h_rep2 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045651_CE_556_009_001 | mercury_control_expose-0h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045652_CE_556_009_002 | mercury_control_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045653_CE_556_009_003 | mercury_low_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045654_CE_556_009_004 | mercury_mid_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045655_CE_556_009_005 | mercury_high_expose-4h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045656_CE_556_009_006 | mercury_control_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045657_CE_556_009_007 | mercury_low_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045658_CE_556_009_008 | mercury_mid_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1045659_CE_556_009_009 | mercury_high_expose-8h_rep3 (GSE42592: Alterations in gene expression in Caenorhabditis elegans associated with exposure to several classes of toxic industrial chemicals/materials.) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. The objective of this research is to determine genomic and proteomic responses in the model nematode C. elegans to exposures to representatives of several classes of toxic industrial chemicals/materials (TICs/TIMs). A total of 3 chemicals (acrylamide, cadmium chloride, and mercuric chloride) were used in these experiments. Affymetrix GeneChip for C. elegans was used to examine genome-wide responses in the 19,000+ genes of this model organism. |
| GSM1047999 | mek-1 fed 1 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048000 | mek-1 fed 2 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048001 | mek-1 fed 3 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048002 | mek-1 fasted 1 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048003 | mek-1 fasted 2 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048004 | mek-1 fasted 3 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048005 | mlk-1 fed 1 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048006 | mlk-1 fed 2 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048007 | mlk-1 fasted 1 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048008 | mlk-1 fasted 2 (GSE42689: mek-1 and mlk-1 in fed or fasted condition) | Intermittent fasting is one of the most effective dietary restriction regimens that extend life-span in C. elegans and mammals. Fasting-stimulus responses are key to the longevity response; however, the mechanisms that sense and transduce fasting-stimulus have remained largely unknown. Through a comprehensive transcriptome analysis in C. elegans, we have found that along with the FOXO transcription factor DAF-16, AP-1 (JUN-1/FOS-1) plays a central role in fasting-induced transcriptional changes. KGB-1, one of the C. elegans JNKs, acted as an activator of AP-1, and was activated in response to fasting. KGB-1 and AP-1 were involved in intermittent fasting-induced longevity. Fasting-induced upregulation of the components of the SCF E3 ubiquitin ligase complex via AP-1 and DAF-16 enhanced protein ubiquitination, and reduced protein carbonylation. Our results have thus identified a fasting-responsive KGB-1/AP-1 signaling pathway, which, together with DAF-16, causes transcriptional changes that mediate longevity partly through regulating proteostasis. |
| GSM1048197_C | WT incubated with H2O, biological rep1 (GSE42703: Expression data from C. elegans in the presence or absence of copper sulfate) | MAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized. To understand how the KGB-1 pathway modulates gene activity and to define the physiological processes in which the heavy metal stress response may be involved, we used microarray to examine gene expression changes in wild-type and kgb-1 mutant animals subjected to heavy metal stress. |
| GSM1048198_C | WT incubated with 1mM copper sulfate, biological rep1 (GSE42703: Expression data from C. elegans in the presence or absence of copper sulfate) | MAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized. To understand how the KGB-1 pathway modulates gene activity and to define the physiological processes in which the heavy metal stress response may be involved, we used microarray to examine gene expression changes in wild-type and kgb-1 mutant animals subjected to heavy metal stress. |
| GSM1048199_C | kgb-1 incubated with H2O, biological rep1 (GSE42703: Expression data from C. elegans in the presence or absence of copper sulfate) | MAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized. To understand how the KGB-1 pathway modulates gene activity and to define the physiological processes in which the heavy metal stress response may be involved, we used microarray to examine gene expression changes in wild-type and kgb-1 mutant animals subjected to heavy metal stress. |
| GSM1048200_C | kgb-1 incubated with 1mM copper sulfate, biological rep1 (GSE42703: Expression data from C. elegans in the presence or absence of copper sulfate) | MAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized. To understand how the KGB-1 pathway modulates gene activity and to define the physiological processes in which the heavy metal stress response may be involved, we used microarray to examine gene expression changes in wild-type and kgb-1 mutant animals subjected to heavy metal stress. |
| GSM106344 | Pooled glp-1 C elegans embryos_bleach NaOH prep_rep1 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106345 | Pooled glp-1 C elegans embryos_bleach NaOH prep_rep2 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106346 | Pooled glp-1 C elegans embryos_bleach NaOH prep_rep3 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106347 | Pooled glp-1 C elegans young adults_rep1 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106348 | Pooled glp-1 C elegans young adults_rep2 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106349 | Pooled glp-1 C elegans young adults_rep3 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106350 | Pooled glp-1 C elegans old adults_rep1 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM106351 | Pooled glp-1 C elegans old adults_rep2 (GSE4766: Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans) | We used gene expression profiling to address several specific questions that arose in a study of repair of ultraviolet C radiation in C elegans, as well as to generate hypotheses regarding the possible mechanism(s) of decreased DNA repair observed in old adults in that study. This analysis was performed in order to analyze gene expression in the strain (JK1107) and experimental conditions that we used for our DNA repair studies. The supplementary file GSE4766_Resolver_all_data.txt includes Resolver generated fold-changes and p values based on ratios built in Rosetta Resolver as described in the Rosetta Biosoftware Technical Note (Lee Weng, 2004), Data processing and analysis methods in the Rosetta Resolver system (http://www.rosettabio.com/tech/default.htm). Keywords: C elegans, glp-1, age, nucleotide excision repair, ultraviolet radiation, DNA damage |
| GSM1074920_DA1 | N2 gravid adult fed Comamonas DA1877 rep 1 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074921_DA2 | N2 gravid adult fed Comamonas DA1877 rep 2 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074922_DA3 | N2 gravid adult fed Comamonas DA1877 rep 3 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074923_METR1_1 | metr-1(ok521) fed Comamonas DA1877 rep 1 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074924_METR1_2 | metr-1(ok521) fed Comamonas DA1877 rep 2 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074925_METR1_3 | metr-1(ok521) fed Comamonas DA1877 rep 3 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074926_PCCA1_1 | pcca-1(ok2282) fed Comamonas DA1877 rep1 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074927_PCCA1_2 | pcca-1(ok2282) fed Comamonas DA1877 rep2 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074928_PCCA1_3 | pcca-1(ok2282) fed Comamonas DA1877 rep3 (GSE43952: Integration of Metabolic and Gene Regulatory Networks Modulates The C. elegans Dietary Response) | Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877 Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. Expression profiles are tailored according to dietary input. However, the networks that control dietary responses remain largely uncharacterized. Here, we combine forward and reverse genetic screens to delineate a network of 184 genes that affect the C. elegans dietary response to Comamonas DA1877 bacteria. We find that perturbation of a mitochondrial network comprised of enzymes involved in amino acid metabolism and the TCA cycle affects the dietary response. In humans, mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which are treated by dietary intervention. We identify several TFs that mediate the changes in gene expression upon metabolic network perturbations. Altogether, our findings unveil a transcriptional response system that is poised to sense dietary cues and metabolic imbalances, illustrating extensive communication between metabolic networks in the mitochondria and gene regulatory networks in the nucleus. |
| GSM1074929_DA1877GA_1 | N2 gravid adult on Comamonas DA1877 rep 1 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074930_DA1877GA_2 | N2 gravid adult on Comamonas DA1877 rep 2 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074931_DA1877GA_3 | N2 gravid adult on Comamonas DA1877 rep 3 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074932_DIL1877GA_1 | N2 gravid adult on 1:1000 Comamonas DA1877 rep 1 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074933_DIL1877GA_2 | N2 gravid adult on 1:1000 Comamonas DA1877 rep 2 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074934_DIL1877GA_3 | N2 gravid adult on 1:1000 Comamonas DA1877 rep 3 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074935_OP50GA_1 | N2 gravid adult on E. coli OP50 rep 1 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074936_OP50GA_2 | N2 gravid adult on E. coli OP50 rep 2 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074937_OP50GA_3 | N2 gravid adult on E. coli OP50 rep 3 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074938_OP50_1 | N2 young adult on E. coli OP50 rep 1 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074939_OP50_2 | N2 young adult on E. coli OP50 rep 2 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074940_OP50_3 | N2 young adult on E. coli OP50 rep 3 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074941_HT115_1 | N2 young adult on E. coli HT115 rep 1 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074942_HT115_2 | N2 young adult on E. coli HT115 rep 2 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074943_HT115_3 | N2 young adult on E. coli HT115 rep 3 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074944_DA1877_1 | N2 young adult on Comamonas DA1877 rep 1 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074945_DA1877_2 | N2 young adult on Comamonas DA1877 rep 2 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1074946_DA1877_3 | N2 young adult on Comamonas DA1877 rep 3 (GSE43959: Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans) | This SuperSeries is composed of the SubSeries listed below. |
| GSM1089129 | C. elegans N2, germline-ablated versus un-ablated intact animals; Biological Replicate 1 (GSE44702: C. elegans germline-ablated (Z2-, Z3-) animals versus intact animals, N2 strain) | Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain |
| GSM1089130 | C. elegans N2, germline-ablated versus un-ablated intact animals; Biological Replicate 2 (Dye-swap) (GSE44702: C. elegans germline-ablated (Z2-, Z3-) animals versus intact animals, N2 strain) | Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain |
| GSM1089131 | C. elegans N2, germline-ablated versus un-ablated intact animals; Biological Replicate 3 (Dye-swap) (GSE44702: C. elegans germline-ablated (Z2-, Z3-) animals versus intact animals, N2 strain) | Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain |
| GSM1089132 | C. elegans N2, gonad-ablated versus un-ablated intact animals; Biological Replicate 1 (GSE44703: C. elegans gonad-ablated (Z1-,Z4-) animals versus intact animals, N2 strain) | Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain |
| GSM1089133 | C. elegans N2, gonad-ablated versus un-ablated intact animals; Biological Replicate 2 (Dye-swap) (GSE44703: C. elegans gonad-ablated (Z1-,Z4-) animals versus intact animals, N2 strain) | Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain |
| GSM1089134 | C. elegans N2, gonad-ablated versus un-ablated intact animals; Biological Replicate 3 (GSE44703: C. elegans gonad-ablated (Z1-,Z4-) animals versus intact animals, N2 strain) | Transcriptional profiling of C. elegans germline-ablated worms versus unablated intact animals, N2 strain |
| GSM11044 | VREI_SL098_2-22-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11045 | VREI_SJ053_2-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11046 | VREI_SJ088_2-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11047 | VREI_SG041_2-10-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11048 | VREI_SI032_2-15-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11049 | VREI_SJ059_2-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11050 | VREI_SJ090_2-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11051 | VREI_SI009_2-12-01 (GSE715: glp-4 adults) | glp-4 adults vs mixed stage reference Keywords: other |
| GSM11052 | VREI_SI041_2-15-01 (GSE715: glp-4 adults) | glp-4 adults vs mixed stage reference Keywords: other |
| GSM11053 | VREI_SJ064_2-19-01 (GSE715: glp-4 adults) | glp-4 adults vs mixed stage reference Keywords: other |
| GSM11054 | VREI_SL021_2-19-01 (GSE715: glp-4 adults) | glp-4 adults vs mixed stage reference Keywords: other |
| GSM11055 | VREI_SJ070_3-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11056 | VREI_SL019_3-20-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11057 | VREI_SL048_2-20-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11058 | VREI_SG069_2-22-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11059 | VREI_SJ098_3-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11060 | VREI_SJ033_3-18-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11061 | VREI_SI064_2-18-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11062 | VREI_SL066_2-22-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11063 | VREI_SJ102_3-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11064 | VREI_SI099_3-17-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11065 | VREI_SH132_3-07-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11066 | VREI_SJ042_2-18-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11067 | VREI_SJ106_3-19-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11068 | VREI_SL020_3-20-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11069 | VREI_SJ020_2-18-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11070 | VREI_SJ048_2-18-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11071 | VREI_A047_4-22-02 (GSE723: adult males vs reference) | wild type adult males vs mixed stage reference Keywords: other |
| GSM11072 | VREI_A044_4-24-02 (GSE723: adult males vs reference) | wild type adult males vs mixed stage reference Keywords: other |
| GSM11073 | VREI_A042_6-05-02 (GSE723: adult males vs reference) | wild type adult males vs mixed stage reference Keywords: other |
| GSM11074 | VREI_A043_6-03-02 (GSE723: adult males vs reference) | wild type adult males vs mixed stage reference Keywords: other |
| GSM11075 | VREI_A048_4-19-02 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11076 | VREI_A046_4-22-02 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11077 | VREI_A041_6-05-02 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11082 | VREI_A001_7-21-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11083 | VREI_A015_7-25-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11084 | VREI_A027_7-29-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11085 | VREI_A002_7-22-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11086 | VREI_A016_7-25-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11087 | VREI_A028_7-29-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11089 | VREI_A003_7-22-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11090 | VREI_A017_7-25-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11091 | VREI_A029_7-29-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11092 | VREI_A005_7-22-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11093 | VREI_A018_7-25-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11094 | VREI_A030_7-29-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11095 | VREI_A006_7-24-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11096 | VREI_A019_7-25-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11097 | VREI_A032_7-29-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11098 | VREI_A009_7-24-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11099 | VREI_A020_7-25-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11100 | VREI_A033_7-29-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11101 | VREI_A007_7-21-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11102 | VREI_A021_7-26-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11103 | VREI_A040_8-21-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11112 | VREI_A008_7_21_01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11113 | VREI_A022_7-26-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11114 | VREI_A035_7-31-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11116 | VREI_A011_7-24-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11117 | VREI_A023_7-26-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11118 | VREI_A036_7-31-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11119 | VREI_A012_7-24-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11120 | VREI_A024_7-26-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11121 | VREI_A037_7-31-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11122 | VREI_A013_7-24-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11123 | VREI_A025_7-26-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11124 | VREI_A038_7-31-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11125 | VREI_A014_7-24-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11126 | VREI_A026_7-26-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM11127 | VREI_A039_7-31-01 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM113611 | WCHI_D012_01-28-04 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113612 | WCHI_D013_01-28-04 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113613 | WCHI_D041_01-09-04 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113614 | WCHI_D042_01-09-04 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113664 | WCHI_D030_10-28-03 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113665 | WCHI_D031_10-28-03 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113666 | WCHI_D032_10-28-03 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113726 | WCHI_D026_10-02-03 (GSE5071: Promotion of oogenesis and embryogenesis in the C. elegans gonad by EFL-1/DPL-1(E2F)does not require LIN-35(pRB)) | Microarray-based expression profiling of dissected gonads from efl-1, dpl-1 and lin-35 mutants reveals that EFL-1 and DPL-1 promote expression of an extensively overlapping set of target genes, consistent with the expectation that these two proteins function as a heterodimer. Regulatory regions upstream of many of these target genes have a canonical E2F binding site, suggesting that their regulation by EFL-1/DPL-1 is direct. Many EFL-1/DPL-1 responsive genes encode proteins required for oogenesis and early embryogenesis, rather than cell cycle components. By contrast, LIN-35 appears to function primarily as a repressor of gene expression in the germ line, and the genes that it acts on are for the most part distinct from those regulated by EFL-1 and/or DPL-1 Keywords: Mutant analysis of dpl-1, efl-1, and lin-35 in dissected C. elegans gonads |
| GSM113894 | SWES_C037_03-27-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM113895 | SWES_C050_04-15-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM113896 | SWES_C013_04-27-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114115 | SWES_C027_03-26-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114116 | SWES_C024_04-04-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114117 | SWES_C015_06-20-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114118 | SWES_C048_03-26-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114119 | SWES_C040_04-04-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114120 | SWES_C009_06-20-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114121 | SWES_C047_03-26-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114122 | SWES_C023_04-04-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114123 | SWES_C011_06-20-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114124 | SWES_C028_03-21-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114125 | SWES_C062_04-24-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114126 | SWES_C044_03-25-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114127 | SWES_C021_04-15-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114128 | SWES_C017_04-15-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114129 | SWES_C036_03-27-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114130 | SWES_C020_04-14-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114131 | SWES_C012_04-27-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114132 | SWES_C038_03-27-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114133 | SWES_C065_04-15-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114134 | SWES_C014_04-27-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM114135 | SWES_C022_04-04-03 (GSE5069: Expression Profiling of MAP Kinase-Mediated Meiotic Progression in C. elegans) | A unique allele of MAP kinase, mpk-1(ga111), displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I. We performed gene expression profiling on mpk-1(ga111) animals at multiple times after shift to permissive temperature to identify candidate downstream effectors of MPK-1 signaling in the germline. This analysis delineated a cohort of genes whose expression requires MPK-1 (MAP kinase) signaling in germ cells in the pachytene stage of meiosis I. Keywords: Timecourse of C. elegans mpk-1 mutants |
| GSM1175369 | WT_embryo_rep1 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175370 | WT_embryo_rep2 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175371 | WT_embryo_rep3 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175372 | smo1_embryo_rep1 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175373 | smo1_embryo_rep2 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175374 | smo1_embryo_rep3 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175375 | sdc2_embryo_rep1 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175376 | sdc2_embryo_rep2 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1175377 | sdc2_embryo_rep3 (GSE48347: C. elegans mixed stage embryo total RNA levels by microarray: L4440 RNAi, smo-1 RNAi and sdc-2 (y93)+RNAi) | The essential process of dosage compensation equalizes X-chromosome gene expression between C. elegans XO males and XX hermaphrodites through a dosage compensation complex (DCC) that resembles condensin. The DCC binds to both X chromosomes of hermaphrodites to repress transcription by half. Here we show that post-translational modification by the SUMO conjugation pathway is essential for sex-specific assembly of the DCC onto X. Depletion of the SUMO peptide in vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene expression similar to those caused by disrupting genes encoding DCC subunits. Three DCC subunits are themselves SUMOylated, and depletion of SUMO preferentially reduces their binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X. DCC SUMOylation is triggered by the signal that initiates DCC assembly onto X. The initial step of assembly--binding of X-targeting factors to recruitment sites on X (rex sites)--is independent of SUMOylation, but robust binding of the complete complex requires SUMOylation. SUMOylated DCC subunits are enriched at rex sites, and SUMOylation enhances interactions between X-targeting factors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOylation. DCC subunits also participate in condensin complexes essential for chromosome segregation, but their SUMOylation occurs only in the context of the DCC. Our results reinforce a newly emerging theme in which multiple proteins of a complex are SUMOylated in response to a specific stimulus, leading to accelerated complex formation and enhanced function. |
| GSM1197083 | ad609 Replicate 1 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197084 | kyIR9 Replicate 1 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197085 | ky13 Replicate 1 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197086 | CB4856 Replicate 1 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197087 | CB4856 Replicate 2 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197088 | qgIR1 Replicate 1 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197089 | ky13 Replicate 2 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197090 | N2 Replicate 1 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197091 | ad609 Replicate 2 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197092 | qgIR1 Replicate 2 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197093 | kyIR9 Replicate 2 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197094 | kyIR9 Replicate 3 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197095 | ky13 Replicate 3 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197096 | qgIR1 Replicate 3 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1197097 | N2 Replicate 2 (GSE49307: A variant in the neuropeptide receptor npr-1 is a major determinant of Caenorhabditis elegans growth and physiology) | The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in C. elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsive for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food. |
| GSM1220540 | L4440 OP50 - rep 1 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220541 | L4440 PA14 - rep 1 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220542 | zip-2 OP50 - rep 1 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220543 | zip-2 PA14 - rep 1 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220544 | L4440 OP50 - rep 2 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220545 | L4440 PA14 - rep 2 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220546 | zip-2 OP50 - rep 2 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220547 | zip-2 PA14 - rep 2 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220548 | L4440 OP50 - rep 3 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220549 | L4440 PA14 - rep 3 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220550 | zip-2 OP50 - rep 3 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM1220551 | zip-2 PA14 - rep 3 (GSE50513: Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h) | Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. |
| GSM124976 | VREI_F049_10-07-04 (GSE5454: MES-4, an autosome-associated HMT that participates in silencing the X chromosomes in the C. elegans germ line) | Microarray-based expression profiling of dissected gonads from mes-4 mutants reveals that MES-4 is required to repress expression of a set of X-linked genes. Keywords: Mutant analysis of mes-4 in dissected C. elegans gonads |
| GSM124977 | VREI_F049_10-03-04 (GSE5454: MES-4, an autosome-associated HMT that participates in silencing the X chromosomes in the C. elegans germ line) | Microarray-based expression profiling of dissected gonads from mes-4 mutants reveals that MES-4 is required to repress expression of a set of X-linked genes. Keywords: Mutant analysis of mes-4 in dissected C. elegans gonads |
| GSM124978 | VREI_F045_10-31-04 (GSE5454: MES-4, an autosome-associated HMT that participates in silencing the X chromosomes in the C. elegans germ line) | Microarray-based expression profiling of dissected gonads from mes-4 mutants reveals that MES-4 is required to repress expression of a set of X-linked genes. Keywords: Mutant analysis of mes-4 in dissected C. elegans gonads |
| GSM124979 | VREI_F041_11-02-04 (GSE5454: MES-4, an autosome-associated HMT that participates in silencing the X chromosomes in the C. elegans germ line) | Microarray-based expression profiling of dissected gonads from mes-4 mutants reveals that MES-4 is required to repress expression of a set of X-linked genes. Keywords: Mutant analysis of mes-4 in dissected C. elegans gonads |
| GSM1250580 | day8 hermaphrodite -males rep 1 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250581 | day8 hermaphrodite -males rep 2 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250582 | day8 hermaphrodite -males rep 3 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250583 | day8 hermaphrodite +males rep 1 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250584 | day8 hermaphrodite +males rep 2 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250585 | day8 hermaphrodite +males rep 3 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250586 | day8 hermaphrodite utx-1 RNAi -males rep 1 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250587 | day8 hermaphrodite utx-1 RNAi -males rep 2 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250588 | day8 hermaphrodite utx-1 RNAi -males rep 3 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250589 | day8 hermaphrodite utx-1 RNAi +males rep 1 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1250590 | day8 hermaphrodite utx-1 RNAi +males rep 3 (GSE51691: Expression data from glp-1(e2141) hermaphrodites maintained with or without males for 8 days) | Males induce dramatic physiological changes to hermaphrodites, including a significant shortening of lifespan. We have termed this effect as male-induced demise (MID) of hermaphrodites. This experiment was performed to analyse changes in gene expression due to the presence of males. We have shown that Knock down of utx-1 ameliorates the MID. In this experiment we also examine male-induce gene expression that may be altered when knocking down expression of utx-1 via RNAi. We used microarrays to detail the global program of gene expression andidentified distinct classes of up-regulated and down-regulated genes upon the addition of males. |
| GSM1258141 | wildtype_1 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258142 | wildtype_2 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258143 | wildtype_3 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258144 | lin-54_1 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258145 | lin-54_2 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258146 | lin-54_3 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258147 | mes-4_1 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258148 | mes-4_2 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258149 | mes-4_3 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258150 | lin-54;mes-4_1 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258151 | lin-54;mes-4_2 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM1258152 | lin-54;mes-4_3 (GSE52064: DRM complex mutant lin-54 vs. H3K36 methyltransferase mutant mes-4 vs. lin-54; mes-4 double mutant vs. wild type C.elegans germline) | Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, “yin-yang” regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. |
| GSM135322 | Celegans_OP50_4hours_RepA (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135323 | Celegans_OP50_4hours_RepB (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135324 | Celegans_OP50_4hours_RepC (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135325 | Celegans_OP50_8hours_RepA (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135326 | Celegans_OP50_8hours_RepB (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135327 | Celegans_OP50_8hours_RepC (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135328 | Celegans_gacA_4hours_RepA (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135329 | Celegans_gacA_4hours_RepB (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135330 | Celegans_gacA_4hours_RepC (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135340 | Celegans_gacA_8hours_RepA (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135355 | Celegans_gacA_8hours_RepB (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135365 | Celegans_gacA_8hours_RepC (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135382 | Celegans_PA14_4hours_RepA (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135383 | Celegans_PA14_4hours_RepB (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135384 | Celegans_PA14_4hours_RepC (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135385 | Celegans_PA14_8hours_RepA (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135386 | Celegans_PA14_8hours_RepB (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135387 | Celegans_PA14_8hours_RepC (GSE5793: C. elegans gene expression in response to the pathogenic P. aeruginosa strain PA14.) | Analysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: Time course, response to pathogen infection |
| GSM135395 | daf2_RepA (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135467 | daf2_RepB (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135468 | daf2_RepC (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135469 | daf2daf16_RepA (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135476 | daf2daf16_RepB (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135477 | daf2daf16_RepC (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135478 | daf2pmk1_RepA (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135479 | daf2pmk1_RepB (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM135480 | daf2pmk1_RepC (GSE5801: Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.) | Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification |
| GSM146422 | N2 (wt) worms at L1 stage, first replicate (GSE9246: Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger) | Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, >; 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays) Keywords: analysis of staged mutant worms |
| GSM146423 | N2 (wt) worms at L1 stage, second replicate (GSE9246: Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger) | Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, >; 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays) Keywords: analysis of staged mutant worms |
| GSM147330 | N2 (wt) worms at L1 stage, third replicate (GSE9246: Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger) | Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, >; 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays) Keywords: analysis of staged mutant worms |
| GSM147331 | lin-35(n745) worms at L1 stage, first replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147332 | lin-35(n745) worms at L1 stage, second replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147333 | lin-35(n745) worms at L1 stage, third replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147334 | N2 (wt) worms at L4 stage, first replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147335 | N2 (wt) worms at L4 stage, second replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147336 | N2 (wt) worms at L4 stage, third replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147337 | lin-35(n745) worms at L4 stage, first replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147338 | lin-35(n745) worms at L4 stage, second replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147339 | lin-35(n745) worms at L4 stage, third replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147340 | N2 (wt) worms at embryonic stage, first replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147341 | N2 (wt) worms at embryonic stage, second replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147342 | N2 (wt) worms at embryonic stage, third replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147344 | lin-35(n745) worms at embryonic stage, first replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147345 | lin-35(n745) worms at embryonic stage, second replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM147346 | lin-35(n745) worms at embryonic stage, third replicate (GSE6547: Developmental transcriptome profiling of the C. elegans pocket protein ortholog, lin-35) | LIN-35 is the single C. elegans ortholog of the mammalian pocket protein family members, pRb, p107, and p130. To gain insight into the roles of pocket proteins during development, a microarray analysis was performed with lin-35 mutants. Stage-specific regulation patterns were revealed, indicating that LIN-35 plays diverse roles at distinct developmental stages. LIN-35 was found to repress the expression of many genes involved in cell proliferation in larvae, an activity that is carried out in conjunction with E2F. In addition, LIN-35 was found to regulate neuronal genes during embryogenesis and targets of the intestinal-specific GATA transcription factor, ELT-2, at multiple developmental stages. Additional findings suggest that LIN-35 functions in cell cycle regulation in embryos in a manner that is independent of E2F. A comparison of LIN-35-regulated genes with known fly and mammalian pocket-protein targets revealed a high degree of overlap, indicating strong conservation of pocket protein functions in diverse phyla. Based on microarray results and our refinement of the C. elegans E2F consensus sequence, we were able to generate a comprehensive list of putative E2F-regulated genes in C. elegans. These results implicate a large number of genes previously unconnected to cell cycle control as having potential roles in this process. Keywords: time course |
| GSM151745 | daf19(m86)_daf12(sa204) replicate 1 (GSE6563: Analysis of expression of genes regulated by DAF-19) | By screening for genes possessing canonical X-box sequences in promoters of three Caenorhabditis species, namely C. elegans, C. briggsae and C. remanei, we identified 93 genes (including known X-box regulated genes) that encode putative components of ciliated neurons in C. elegans and are subject to the same regulatory control. For many of these genes, restricted anatomical expression in ciliated cells was confirmed, and control of transcription by the ciliogenic DAF-19 RFX transcription factor was demonstrated by comparative transcriptional profiling of daf-19(+) and daf-19(-) animals. Keywords: Microarry analysis; DAF-19; X-box motif; C. elegans; transcription; comparative genomics |
| GSM151746 | daf19(m86)_daf12(sa204) replicate 2 (GSE6563: Analysis of expression of genes regulated by DAF-19) | By screening for genes possessing canonical X-box sequences in promoters of three Caenorhabditis species, namely C. elegans, C. briggsae and C. remanei, we identified 93 genes (including known X-box regulated genes) that encode putative components of ciliated neurons in C. elegans and are subject to the same regulatory control. For many of these genes, restricted anatomical expression in ciliated cells was confirmed, and control of transcription by the ciliogenic DAF-19 RFX transcription factor was demonstrated by comparative transcriptional profiling of daf-19(+) and daf-19(-) animals. Keywords: Microarry analysis; DAF-19; X-box motif; C. elegans; transcription; comparative genomics |
| GSM151747 | daf19(WT)_daf12(sa204) replicate 1 (GSE6563: Analysis of expression of genes regulated by DAF-19) | By screening for genes possessing canonical X-box sequences in promoters of three Caenorhabditis species, namely C. elegans, C. briggsae and C. remanei, we identified 93 genes (including known X-box regulated genes) that encode putative components of ciliated neurons in C. elegans and are subject to the same regulatory control. For many of these genes, restricted anatomical expression in ciliated cells was confirmed, and control of transcription by the ciliogenic DAF-19 RFX transcription factor was demonstrated by comparative transcriptional profiling of daf-19(+) and daf-19(-) animals. Keywords: Microarry analysis; DAF-19; X-box motif; C. elegans; transcription; comparative genomics |
| GSM151748 | daf19(WT)_daf12(sa204) replicate 2 (GSE6563: Analysis of expression of genes regulated by DAF-19) | By screening for genes possessing canonical X-box sequences in promoters of three Caenorhabditis species, namely C. elegans, C. briggsae and C. remanei, we identified 93 genes (including known X-box regulated genes) that encode putative components of ciliated neurons in C. elegans and are subject to the same regulatory control. For many of these genes, restricted anatomical expression in ciliated cells was confirmed, and control of transcription by the ciliogenic DAF-19 RFX transcription factor was demonstrated by comparative transcriptional profiling of daf-19(+) and daf-19(-) animals. Keywords: Microarry analysis; DAF-19; X-box motif; C. elegans; transcription; comparative genomics |
| GSM177131 | whole animal, nucleus accumbens: Extract1_le1 (GSE7354: Regulation of presenilin genes (rogae-affy-c.ele-431660)) | Regulation of presenilin genes. Presenilins are intramembrane aspartic proteases. These proteases are critical proteins in pathogenesis of Alzheimer's disease. The function of recently identified presenilin-homologous proteases (IMPAS or SPP)s is unknown. Our preliminary data in C.elegans model suggested the role of these proteins in early-development and , perhaps, in pathway related- to cholesterol -regulated signalling (Grigorenko et al, 2004, PNAS). The overall goal is to determine pattern of gene expression alterations in cells with knock-out or knock-down presenilin related proteins (IMPAS). The cultured cells, C.elegans and mouse models are planned to be used in this study. Here , we will determine gene expression patterns in C.elegans strain NL2099, fed with bacteria HT115, producing dsRNA for Ce-imp-2 gene (knock-down of imp-2 gene by RNAi )or GFP gene as a control. We hypothesize that novel family of presenilin-related proteases is important for cholesterol-regulated intracellular signalling and early development (including CNS/neuronal development and function). C.elegans (strain NL2099) on L1 stage were placed on agarose plates with bacteria HT115, producing dsRNA for: 1) Ce-imp-2 gene; 2) GFP as a control gene. After 48 hours at 20C , worms were washed in M9 buffer and total RNA was isolated by TRIzol method. Keywords: dose response |
| GSM177132 | whole animal, nucleus accumbens: Extract-Control_le1 (GSE7354: Regulation of presenilin genes (rogae-affy-c.ele-431660)) | Regulation of presenilin genes. Presenilins are intramembrane aspartic proteases. These proteases are critical proteins in pathogenesis of Alzheimer's disease. The function of recently identified presenilin-homologous proteases (IMPAS or SPP)s is unknown. Our preliminary data in C.elegans model suggested the role of these proteins in early-development and , perhaps, in pathway related- to cholesterol -regulated signalling (Grigorenko et al, 2004, PNAS). The overall goal is to determine pattern of gene expression alterations in cells with knock-out or knock-down presenilin related proteins (IMPAS). The cultured cells, C.elegans and mouse models are planned to be used in this study. Here , we will determine gene expression patterns in C.elegans strain NL2099, fed with bacteria HT115, producing dsRNA for Ce-imp-2 gene (knock-down of imp-2 gene by RNAi )or GFP gene as a control. We hypothesize that novel family of presenilin-related proteases is important for cholesterol-regulated intracellular signalling and early development (including CNS/neuronal development and function). C.elegans (strain NL2099) on L1 stage were placed on agarose plates with bacteria HT115, producing dsRNA for: 1) Ce-imp-2 gene; 2) GFP as a control gene. After 48 hours at 20C , worms were washed in M9 buffer and total RNA was isolated by TRIzol method. Keywords: dose response |
| GSM197716 | Embryonic Reference, biological rep 1 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197717 | Embryonic Reference, biological rep 2 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197718 | Embryonic Reference, biological rep 3 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197719 | Embryonic Reference, biological rep 4 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197720 | Embryonic Pan-neural, biological rep 1 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197721 | Embryonic Pan-neural, biological rep 2 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197722 | Embryonic Pan-neural, biological rep 3 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197723 | Larval Reference, biological rep 1 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197724 | Larval Reference, biological rep 2 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197725 | Larval Reference, biological rep 3 of set 1 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197726 | Larval Reference, biological rep 4 of set 2 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197727 | Larval Reference, biological rep 5 of set 2 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197728 | Larval Pan-neural, biological rep 1 of set 2 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197729 | Larval Pan-neural, biological rep 2 of set 2 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197730 | Larval Pan-neural, biological rep 3 of set 2 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197731 | Larval A-class, biological rep 1 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197732 | Larval A-class, biological rep 2 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197733 | Larval A-class, biological rep 3 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197734 | Larval A-class, biological rep 4 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197735 | Larval Reference, biological rep 1 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197736 | Larval Reference, biological rep 2 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197737 | Larval Reference, biological rep 3 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197738 | Larval Reference, biological rep 4 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM197739 | Larval Reference, biological rep 5 of set 3 (GSE8004: Cell-specific microarray profiling of the C. elegans nervous system.) | Background: With its fully sequenced genome and simple, well-defined nervous system, the nematode C. elegans offers a unique opportunity to correlate gene expression with neuronal differentiation. The lineal origin, cellular morphology and synaptic connectivity of each of the 302 neurons are known. In many instances, specific behaviors can be attributed to particular neurons or circuits. Here we describe microarray-based methods that monitor gene expression in C. elegans neurons and thereby link comprehensive profiles of neuronal transcription to key developmental and functional attributes of the nervous system. Results: We employed complementary microarray-based strategies to profile gene expression in the embryonic and larval nervous systems. In the MAPCeL (Micro-Array Profiling C. elegans Cells) method, we used Fluorescence Activated Cell Sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis. To profile the larval nervous system, we used the mRNA-tagging technique in which an epitope-labeled mRNA binding protein (FLAG-PAB-1) was transgenically expressed in neurons for immunoprecipitation of cell-specific transcripts. These combined approaches identified approximately 2,500 mRNAs that are highly enriched in either the embryonic or larval C. elegans nervous system. These data are validated in part by the detection of gene classes (e.g. transcription factors, ion channels, synaptic vesicle components) with established roles in neuronal development or function. In addition to utilizing these profiling approaches to define stage specific gene expression, we also applied the mRNA-tagging method to fingerprint a specific neuron type, the A-class group of cholinergic motor neurons, during early larval development. A comparison of these data to a MAPCeL profile of embryonic A-class motor neurons identified genes with common functions in both types of A-class motor neurons as well as transcripts with roles specific to each motor neuron type. Conclusion: We describe microarray-based strategies for generating expression profiles of embryonic and larval C. elegans neurons. These methods can be applied to particular neurons at specific developmental stages and therefore provide an unprecedented opportunity to obtain spatially and temporally defined snapshots of gene expression in a simple model nervous system. Keywords: nervous system, development |
| GSM201989 | Embryonic Reference, biological rep 1 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM201990 | Embryonic Reference, biological rep 2 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM201991 | Embryonic Reference, biological rep 3 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM201992 | Embryonic Reference, biological rep 4 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM201993 | Embryonic A-class, biological rep 1 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM201994 | Embryonic A-class, biological rep 2 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM201995 | Embryonic A-class, biological rep 3 (GSE8159: A gene expression fingerprint of C. elegans embryonic motor neurons.) | Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Keywords: expression profile |
| GSM203610 | HLH-1 induction 0 hour replicate A (11-16-04_Krause_Celegans_H0A) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203611 | HLH-1 induction 0 hour replicate B (11-16-04_Krause_Celegans_H0B) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203612 | HLH-1 induction 0 hour replicate C (11-16-04_Krause_Celegans_H0C) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203613 | HLH-1 induction 2 hour replicate A (11-16-04_Krause_Celegans_H2A) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203614 | HLH-1 induction 2 hour replicate B (11-16-04_Krause_Celegans_H2B) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203615 | HLH-1 induction 2 hour replicate C (11-16-04_Krause_Celegans_H2C) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203616 | HLH-1 induction 4 hour replicate A (11-16-04_Krause_Celegans_H4A) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203617 | HLH-1 induction 4 hour replicate B (11-16-04_Krause_Celegans_H4B) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203618 | HLH-1 induction 4 hour replicate C (11-16-04_Krause_Celegans_H4C) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203619 | HLH-1 induction 6 hour replicate A (11-16-04_Krause_Celegans_H6A) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203620 | HLH-1 induction 6 hour replicate B (11-16-04_Krause_Celegans_H6B) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM203621 | HLH-1 induction 6 hour replicate C (11-16-04_Krause_Celegans_H6C) (GSE8231: The embryonic muscle transcriptome of C. elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of C. elegans (MAPCeL) to muscle cell populations extracted from developing C. elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early C. elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,324 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing C. elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in C. elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: time course, muscle cells, HLH-1 induction |
| GSM210107 | 0 hr Reference, biological rep 1 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210108 | 0 hr Reference, biological rep 2 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210109 | 0 hr Reference, biological rep 3 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210110 | 0 hr muscle, biological rep 1 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210111 | 0 hr muscle, biological rep 2 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210112 | 0 hr muscle, biological rep 3 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210113 | 24 hr Reference, biological rep 1 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210114 | 24 hr Reference, biological rep 2 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210115 | 24 hr Reference, biological rep 3 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210116 | 24 hr Reference, biological rep 4 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210117 | 24 hr muscle, biological rep 1 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210118 | 24 hr muscle, biological rep 2 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM210119 | 24 hr muscle, biological rep 3 (GSE8462: The embryonic muscle transcriptome of Caenorhabditis elegans) | Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP |
| GSM211534 | N2b (red, channel 2) vs. lin-4b (green, channel 1) (GSE8520: LIN-14 mutants) | A temporal gradient of the novel nuclear protein LIN-14 specifies the timing and sequence of stage-specific developmental events in Caenorhabditis elegans. The profound effects of lin-14 mutations on worm development suggest that LIN-14 directly or indirectly regulates stage-specific gene expression. We show that LIN-14 can associate with chromatin in vivo and has in vitro DNA binding activity. A bacterially expressed C-terminal domain of LIN-14 was used to select DNA sequences that contain a putative consensus binding site from a pool of randomized double-stranded oligonucleotides. To identify candidates for genes directly regulated by lin-14, we employed DNA microarray hybridization to compare the mRNA abundance of C. elegans genes in wild-type animals to that in mutants with reduced or elevated lin-14 activity. Five of the candidate LIN-14 target genes identified by microarrays, including the insulin/insulin-like growth factor family gene ins-33, contain putative LIN-14 consensus sites in their upstream DNA sequences. Genetic analysis indicates that the developmental regulation of ins-33 mRNA involves the stage-specific repression of ins-33 transcription by LIN-14 via sequence-specific DNA binding. These results reinforce the conclusion that lin-14 encodes a novel class of transcription factor. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM211535 | N2 (red, channel 2) vs. lin-14 (n179ts) (green, channel 1) (GSE8520: LIN-14 mutants) | A temporal gradient of the novel nuclear protein LIN-14 specifies the timing and sequence of stage-specific developmental events in Caenorhabditis elegans. The profound effects of lin-14 mutations on worm development suggest that LIN-14 directly or indirectly regulates stage-specific gene expression. We show that LIN-14 can associate with chromatin in vivo and has in vitro DNA binding activity. A bacterially expressed C-terminal domain of LIN-14 was used to select DNA sequences that contain a putative consensus binding site from a pool of randomized double-stranded oligonucleotides. To identify candidates for genes directly regulated by lin-14, we employed DNA microarray hybridization to compare the mRNA abundance of C. elegans genes in wild-type animals to that in mutants with reduced or elevated lin-14 activity. Five of the candidate LIN-14 target genes identified by microarrays, including the insulin/insulin-like growth factor family gene ins-33, contain putative LIN-14 consensus sites in their upstream DNA sequences. Genetic analysis indicates that the developmental regulation of ins-33 mRNA involves the stage-specific repression of ins-33 transcription by LIN-14 via sequence-specific DNA binding. These results reinforce the conclusion that lin-14 encodes a novel class of transcription factor. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM211536 | N2c (red, channel 2) vs. lin-4c (green, channel 1) (GSE8520: LIN-14 mutants) | A temporal gradient of the novel nuclear protein LIN-14 specifies the timing and sequence of stage-specific developmental events in Caenorhabditis elegans. The profound effects of lin-14 mutations on worm development suggest that LIN-14 directly or indirectly regulates stage-specific gene expression. We show that LIN-14 can associate with chromatin in vivo and has in vitro DNA binding activity. A bacterially expressed C-terminal domain of LIN-14 was used to select DNA sequences that contain a putative consensus binding site from a pool of randomized double-stranded oligonucleotides. To identify candidates for genes directly regulated by lin-14, we employed DNA microarray hybridization to compare the mRNA abundance of C. elegans genes in wild-type animals to that in mutants with reduced or elevated lin-14 activity. Five of the candidate LIN-14 target genes identified by microarrays, including the insulin/insulin-like growth factor family gene ins-33, contain putative LIN-14 consensus sites in their upstream DNA sequences. Genetic analysis indicates that the developmental regulation of ins-33 mRNA involves the stage-specific repression of ins-33 transcription by LIN-14 via sequence-specific DNA binding. These results reinforce the conclusion that lin-14 encodes a novel class of transcription factor. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM211537 | N2 (red, channel 2) vs. lin-14 (n179ts) (green, channel 1)- repeat #1 (GSE8520: LIN-14 mutants) | A temporal gradient of the novel nuclear protein LIN-14 specifies the timing and sequence of stage-specific developmental events in Caenorhabditis elegans. The profound effects of lin-14 mutations on worm development suggest that LIN-14 directly or indirectly regulates stage-specific gene expression. We show that LIN-14 can associate with chromatin in vivo and has in vitro DNA binding activity. A bacterially expressed C-terminal domain of LIN-14 was used to select DNA sequences that contain a putative consensus binding site from a pool of randomized double-stranded oligonucleotides. To identify candidates for genes directly regulated by lin-14, we employed DNA microarray hybridization to compare the mRNA abundance of C. elegans genes in wild-type animals to that in mutants with reduced or elevated lin-14 activity. Five of the candidate LIN-14 target genes identified by microarrays, including the insulin/insulin-like growth factor family gene ins-33, contain putative LIN-14 consensus sites in their upstream DNA sequences. Genetic analysis indicates that the developmental regulation of ins-33 mRNA involves the stage-specific repression of ins-33 transcription by LIN-14 via sequence-specific DNA binding. These results reinforce the conclusion that lin-14 encodes a novel class of transcription factor. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM211538 | N2 (red, channel 2) vs. lin-14 (n179ts) (green, channel 1)-repeat #2 (GSE8520: LIN-14 mutants) | A temporal gradient of the novel nuclear protein LIN-14 specifies the timing and sequence of stage-specific developmental events in Caenorhabditis elegans. The profound effects of lin-14 mutations on worm development suggest that LIN-14 directly or indirectly regulates stage-specific gene expression. We show that LIN-14 can associate with chromatin in vivo and has in vitro DNA binding activity. A bacterially expressed C-terminal domain of LIN-14 was used to select DNA sequences that contain a putative consensus binding site from a pool of randomized double-stranded oligonucleotides. To identify candidates for genes directly regulated by lin-14, we employed DNA microarray hybridization to compare the mRNA abundance of C. elegans genes in wild-type animals to that in mutants with reduced or elevated lin-14 activity. Five of the candidate LIN-14 target genes identified by microarrays, including the insulin/insulin-like growth factor family gene ins-33, contain putative LIN-14 consensus sites in their upstream DNA sequences. Genetic analysis indicates that the developmental regulation of ins-33 mRNA involves the stage-specific repression of ins-33 transcription by LIN-14 via sequence-specific DNA binding. These results reinforce the conclusion that lin-14 encodes a novel class of transcription factor. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM211539 | N2a (red, channel 2) vs. lin-4a (green, channel 1) (GSE8520: LIN-14 mutants) | A temporal gradient of the novel nuclear protein LIN-14 specifies the timing and sequence of stage-specific developmental events in Caenorhabditis elegans. The profound effects of lin-14 mutations on worm development suggest that LIN-14 directly or indirectly regulates stage-specific gene expression. We show that LIN-14 can associate with chromatin in vivo and has in vitro DNA binding activity. A bacterially expressed C-terminal domain of LIN-14 was used to select DNA sequences that contain a putative consensus binding site from a pool of randomized double-stranded oligonucleotides. To identify candidates for genes directly regulated by lin-14, we employed DNA microarray hybridization to compare the mRNA abundance of C. elegans genes in wild-type animals to that in mutants with reduced or elevated lin-14 activity. Five of the candidate LIN-14 target genes identified by microarrays, including the insulin/insulin-like growth factor family gene ins-33, contain putative LIN-14 consensus sites in their upstream DNA sequences. Genetic analysis indicates that the developmental regulation of ins-33 mRNA involves the stage-specific repression of ins-33 transcription by LIN-14 via sequence-specific DNA binding. These results reinforce the conclusion that lin-14 encodes a novel class of transcription factor. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM214716 | N2 replicate 1 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214725 | N2 replicate 2 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214727 | N2 replicate 3 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214728 | strain NL2099 replicate 1 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214729 | strain NL 2099 replicate 2 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214730 | strain NL2099 replicate 3 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214731 | strain GR1373 replicate 1 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214732 | strain GR1373 replicate 2 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM214733 | strain GR1373 replicate 3 (GSE8659: Whole genome microarray analysis of C. elegans rrf-3 and eri-1 mutants ) | RRF-3 and ERI-1 are first identified proteins required for accumulation of at least some endogenous secondary siRNAs in C.elegans. Genome wide gene expression analysis was performed on L4 stage rrf-3 and eri-1 mutant C. elegans to study effects caused by loss of these proteins. Mutant rrf-3 and eri-1 strains exhibited similar expression patterns when compared to N2 wild type, while 72 transcripts were found to be co-overexpressed and 4 transcripts co-underexpressed (>; 2-fold, p< 0.05). Ontology analysis indicated many of the gene products were associated with protein phosphorylation and sperm function. These results provide additional support for the hypothesis that RRF-3 and ERI-1 act together in a siRNA pathway and may indicate biological processes that are related to endo-siRNAs. Keywords: Mutant vs. wild type -comparison |
| GSM215547 | 4 uM hemin (4A) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215548 | 4 uM hemin (4B) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215549 | 4 uM hemin (4C) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215550 | 20 uM hemin (20A) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215551 | 20 uM hemin (20B) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215552 | 20 uM hemin (20C) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215553 | 500 uM hemin (500A) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215554 | 500 uM hemin (500B) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM215555 | 500 uM hemin (500C) (GSE8696: Heme homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins) | Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response |
| GSM230859 | AIN-1 IP replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230860 | AIN-1 IP replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230861 | AIN-1 IP replicate 3 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230862 | Preimmune IP replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230863 | Preimmune IP replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230864 | Preimmune IP replicate 3 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230865 | AIN-2::GFP IP replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230866 | AIN-2::GFP IP replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230867 | AIN-2::GFP IP replicate 3 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230868 | GFP IP replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230869 | GFP IP replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230870 | GFP IP replicate 3 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230871 | N2 total RNA replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230872 | N2 total RNA replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230873 | AIN-2::GFP total RNA replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230874 | AIN-2::GFP total RNA replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230875 | AIN-2::GFP total RNA replicate 3 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230876 | AIN-2 promoter GFP replicate 1 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230877 | AIN-2 promoter GFP replicate 2 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM230878 | AIN-2 promoter GFP replicate 3 (GSE9073: AIN-1 and AIN-2::GFP IP of C.elegans miRNA targets) | MicroRNAs (miRNAs) regulate gene expression for diverse functions, but only a limited number of mRNA targets have been experimentally identified. We show that GW182 family proteins AIN-1 and AIN-2 act redundantly to regulate the expression of miRNA targets, but not miRNA biogenesis. Immunoprecipitation (IP) and mass spectrometry indicate that AIN-1 and AIN-2 interact only with miRNA-specific Argonaute proteins ALG-1 and ALG-2 and with components of the core translational initiation complex. Known miRNA targets are enriched in AIN-2 complexes, correlating with the expression of corresponding miRNAs. Combining IP with pyrosequencing and microarray analysis of RNAs associated with AIN-1/AIN-2, we identified 106 previously annotated miRNAs plus 9 new candidate miRNAs, but nearly no siRNAs, and more than 3500 potential miRNA targets including nearly all known ones. Our results demonstrate an effective biochemical approach to systematically identify miRNA targets and provide valuable insights regarding the properties of miRNA effector complexes. Keywords: IP microarray of miRNA targets |
| GSM234788 | slr-2(ku297) worms at L1 stage, first replicate (GSE9246: Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger) | Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, >; 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays) Keywords: analysis of staged mutant worms |
| GSM234790 | slr-2(ku297) worms at L1 stage, second replicate (GSE9246: Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger) | Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, >; 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays) Keywords: analysis of staged mutant worms |
| GSM234791 | slr-2(ku297) worms at L1 stage, third replicate (GSE9246: Transcriptome profiling of slr-2, C.elegans C2H2 Zn-finger) | Our slr-2 dataset showed strong overrepresentation of genes previously identified in a serial analysis of gene expression (SAGE) intestinal library (McGhee et al., 2006) (p << 0.01); 812 genes were common to both data sets. Consistent with the deregulation of intestinal genes, we observed repression of several important metabolic pathways, including the TOR and insulin signaling networks, suggesting that slr-2(ku297) mutants experience metabolic stress. We also compared differentially regulated genes in slr-2 and lin-35 single mutants. Again, we saw a statistically significant overlap (p-value < 0.01); 261 genes were present in both data sets. Strikingly, >; 75% of genes common both datasets showed expression changes in the same direction, although the common dataset contained an approximately equal mixture of up and downregulated genes. Furthermore, more than fifty genes common to the lin-35 and slr-2 datasets are known to have intestinal-associated functions. That some of these common intestinal genes were absent from the gut SAGE library could be due to differences in the developmental stage of the animals assayed (adults versus L1s) as well as experimental approaches (SAGE versus microarrays) Keywords: analysis of staged mutant worms |
| GSM236987 | 3-day-old TJ1090 worms without any stress (C1) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM236988 | 3-day-old TJ1090 worms without any stress (C2) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237000 | 3-day-old TJ1090 worms without any stress (C3) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237005 | 3-day-old TJ1090 worms without any stress (C4) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237006 | 3-day-old TJ1090 worms with oxidative stress (O1) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237007 | 3-day-old TJ1090 worms with oxidative stress (O2) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237008 | 3-day-old TJ1090 worms with oxidative stress (O3) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237009 | 3-day-old TJ1090 worms with oxidative stress (O4) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237010 | 3-day-old TJ1090 worms with skn-1 RNAi & oxidative stress (SO1) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237011 | 3-day-old TJ1090 worms with skn-1 RNAi & oxidative stress (SO2) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM237012 | 3-day-old TJ1090 worms with skn-1 RNAi & oxidative stress (SO3) (GSE9301: SKN-1-dependent oxidative stress response in C. elegans) | Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response |
| GSM240705 | Larval Pan-neural, biological rep 1 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240706 | Larval Pan-neural, biological rep 2 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240707 | Larval Pan-neural, biological rep 3 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240708 | Larval Pan-neural, biological rep 4 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240709 | Larval Pan-neural, biological rep 5 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240710 | Larval Reference, biological rep 1 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240711 | Larval Reference, biological rep 2 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM240712 | Larval Reference, biological rep 3 (GSE9485: cRNA amplification methods enhance microarray identification of transcripts expressed in the nervous system) | Background: DNA microarrays provide a powerful method for global analysis of gene expression. The application of this technology to specific cell types and tissues, however, is typically limited by small amounts of available mRNA, thereby necessitating amplification. Here we compare microarray results obtained with two different methods of RNA amplification to profile gene expression in the C. elegans larval nervous system. Results: We used the mRNA-tagging strategy to isolate transcripts specifically from C. elegans larval neurons. The WT-Ovation Pico System (WT-Pico) was used to amplify 2 ng of Pan-neural RNA to produce labeled cDNA for microarray analysis. These WT-Pico-derived data were compared to microarray results obtained with a labeled aRNA target generated by two rounds of In Vitro Transcription (IVT) of 25 ng of Pan-neural RNA. WT-Pico results in a higher fraction of Present calls than IVT, a finding consistent with the proposal that DNA-DNA hybridization results in lower mismatch signals than the RNA-DNA heteroduplexes produced by IVT amplification. Microarray data sets from these samples were compared to a Reference profile of all larval cells to identify transcripts with elevated expression in neurons. These results were validated by the high proportion of known neuron-expressed genes detected in these profiles and by promoter-GFP constructs for previously uncharacterized genes in these data sets. Together, the IVT and WT-Pico methods identified 2,173 unique neuron-enriched transcripts. Only about half of these transcripts (1,044), however, are detected as enriched by both IVT and WT-Pico amplification. Conclusion: We show that two different methods of RNA amplification, IVT and WT-Pico, produce valid microarray profiles of gene expression in the C. elegans larval nervous system with a low rate of false positives. However, our results also show that each method of RNA amplification detects a unique subset of bona fide neural-enriched transcripts and thus a wider array of authentic neural genes are identified by the combination of these data sets than by the microarray profiles obtained with either method of RNA amplification alone. With its relative ease of implementation and greater sensitivity, WT-Pico is the preferred method of amplification for cases in which sample RNA is limiting. Keywords: expression profile |
| GSM243909 | mex-3 143 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM243910 | mex-3 143 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244167 | mex-3 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244169 | mex-3 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244173 | mex-3 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244176 | mex-3 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244177 | mex-3 scrt-1 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244180 | mex-3 tbx-8,9 143 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244181 | mex-3 tbx-8,9 143 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244182 | mex-3 tbx-8,9 143 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244183 | mex-3 tbx-8,9 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244184 | mex-3 elt-1 143 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244186 | mex-3 elt-1 143 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244187 | mex-3 elt-1 143 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244189 | mex-3 elt-1 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244190 | mex-3 elt-1 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244192 | mex-3 elt-1 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244193 | mex-3 vab-7 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244195 | mex-3 vab-7 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244196 | mex-3 vab-7 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244198 | mex-3 vab-7 230 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244199 | mex-3 hlh-1 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244200 | mex-3 hlh-1 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244201 | mex-3 hlh-1 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244202 | mex-3 nhr-25 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244203 | mex-3 nhr-25 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244204 | mex-3 nhr-25 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244205 | mex-3 nhr-25 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244206 | mex-3 nhr-25 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244207 | mex-3 elt-3 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244208 | mex-3 elt-3 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244209 | mex-3 elt-3 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244210 | mex-3 elt-3 230 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244211 | mex-3 nob-1 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244212 | mex-3 nob-1 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244213 | mex-3 nob-1 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244214 | mex-3 nob-1 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244215 | mex-3 nob-1 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244216 | mex-3 nob-1 230 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244217 | mex-3 unc-120 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244218 | mex-3 unc-120 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244219 | mex-3 unc-120 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244221 | mex-3 unc-120 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244222 | mex-3 unc-120 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244223 | mex-3 unc-120 230 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244225 | mex-3 hnd-1 143 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244226 | mex-3 hnd-1 143 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244227 | mex-3 hnd-1 143 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244229 | mex-3 hnd-1 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244230 | mex-3 hnd-1 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244231 | mex-3 lin-26 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244233 | mex-3 lin-26 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244234 | mex-3 lin-26 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244236 | mex-3 lin-26 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244238 | mex-3 scrt-1 143 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244245 | mex-3 scrt-1 143 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244247 | mex-3 scrt-1 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244250 | mex-3 pal-1 143 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244252 | mex-3 scrt-1 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244255 | mex-3 vab-7 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244257 | mex-3 vab-7 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244258 | mex-3 hlh-1 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244260 | mex-3 nhr-25 230 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244261 | mex-3 elt-3 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244262 | mex-3 elt-3 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244264 | mex-3 hnd-1 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244265 | mex-3 pal-1 101 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244266 | mex-3 pal-1 143 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244267 | mex-3 pal-1 143 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244268 | mex-3 pal-1 186 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244269 | mex-3 pal-1 186 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244270 | mex-3 pal-1 186 C (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244271 | mex-3 pal-1 230 A (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM244272 | mex-3 pal-1 230 B (GSE9665: Pairing competitive and topologically distinct regulatory modules enhances patterned gene expression) | Biological networks are inherently modular, yet little is known about how modules are assembled to enable coordinated and complex functions. We used RNAi and time-series, whole-genome microarray analyses to systematically perturb and characterize components of a C. elegans lineage-specific transcriptional regulatory network. These data are supported by select reporter gene analyses and comprehensive yeast-one-hybrid and promoter sequence analyses. Based on these results we define and characterize two modules composed of muscle- and epidermal-specifying transcription factors that function together within a single cell lineage to robustly specify multiple cell types. The expression of these two modules, although positively regulated by a common factor, is reliably segregated among daughter cells. Our analyses indicate that these modules repress each other, and we propose that this cross-inhibition coupled with their relative time of induction function to enhance the initial asymmetry in their expression patterns, thus leading to the observed invariant gene expression patterns and cell lineage. The coupling of asynchronous and topologically distinct modules may be a general principle of module assembly that functions to potentiate genetic switches. Keywords: Gene expression response of RNAi knockdowns |
| GSM245276 | Microarrays N2 L4 stage C. elegans control(RNAi) vs. mdt-15(RNAi) (40hr RNAi) (GSE9720: Microarray expression profiling of C. elegans N2 L4 control(RNAi) vs. mdt-15(RNAi)) | We previously showed that the C. elegans Mediator subunit MDT-15 impacts expression of select genes involved in fatty acid (FA) metabolism (Taubert et al, Genes & Dev, 2006). To comprehensively identify processes downstream of MDT-15 in an unbiased manner, we set out to globally discover new MDT-15-dependent genes. Keywords: Expression profiling, RNAi depletion |
| GSM245277 | Microarrays N2 L4 stage C. elegans control(RNAi) vs. mdt-15(RNAi) (40hr RNAi) Replicate #2 (GSE9720: Microarray expression profiling of C. elegans N2 L4 control(RNAi) vs. mdt-15(RNAi)) | We previously showed that the C. elegans Mediator subunit MDT-15 impacts expression of select genes involved in fatty acid (FA) metabolism (Taubert et al, Genes & Dev, 2006). To comprehensively identify processes downstream of MDT-15 in an unbiased manner, we set out to globally discover new MDT-15-dependent genes. Keywords: Expression profiling, RNAi depletion |
| GSM245278 | Microarrays N2 L4 stage C. elegans control(RNAi) vs. mdt-15(RNAi) (40hr RNAi) Replicate #3 (GSE9720: Microarray expression profiling of C. elegans N2 L4 control(RNAi) vs. mdt-15(RNAi)) | We previously showed that the C. elegans Mediator subunit MDT-15 impacts expression of select genes involved in fatty acid (FA) metabolism (Taubert et al, Genes & Dev, 2006). To comprehensively identify processes downstream of MDT-15 in an unbiased manner, we set out to globally discover new MDT-15-dependent genes. Keywords: Expression profiling, RNAi depletion |
| GSM245279 | Microarrays N2 L4 stage C. elegans control(RNAi) vs. mdt-15(RNAi) (40hr RNAi) Replicate #4 (GSE9720: Microarray expression profiling of C. elegans N2 L4 control(RNAi) vs. mdt-15(RNAi)) | We previously showed that the C. elegans Mediator subunit MDT-15 impacts expression of select genes involved in fatty acid (FA) metabolism (Taubert et al, Genes & Dev, 2006). To comprehensively identify processes downstream of MDT-15 in an unbiased manner, we set out to globally discover new MDT-15-dependent genes. Keywords: Expression profiling, RNAi depletion |
| GSM245280 | Microarrays N2 L4 stage C. elegans control(RNAi) vs. mdt-15(RNAi) (40hr RNAi) Replicate #5 (GSE9720: Microarray expression profiling of C. elegans N2 L4 control(RNAi) vs. mdt-15(RNAi)) | We previously showed that the C. elegans Mediator subunit MDT-15 impacts expression of select genes involved in fatty acid (FA) metabolism (Taubert et al, Genes & Dev, 2006). To comprehensively identify processes downstream of MDT-15 in an unbiased manner, we set out to globally discover new MDT-15-dependent genes. Keywords: Expression profiling, RNAi depletion |
| GSM250111 | Mutant, biological rep1 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250112 | Mutant, biological rep2 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250113 | Mutant, biological rep3 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250114 | Mutant, biological rep4 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250115 | Mutant, biological rep5 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250116 | Wildtype, biological rep1 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250117 | Wildtype, biological rep2 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250118 | Wildtype, biological rep3 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250119 | Wildtype, biological rep4 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM250120 | Wildtype, biological rep5 (GSE9896: Expression data from wildtype and gas-1 mitochondrial mutant C. elegans) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251550 | Wildtype (control for missense) (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251551 | Wildtype (control for RNAi) (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251552 | Complex I missense mutant (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251553 | Complex II missense mutant (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251554 | Complex III missense mutant (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251555 | Complex I RNAi Mutant 1 (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251556 | Complex I RNAi Mutant 2 (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251557 | Complex I RNAi Mutant 3 (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251558 | Complex I RNAi Mutant 4 (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM251559 | Complex I RNAi Mutant 5 (GSE9897: Expression data from 2 wildtype and 8 C. elegans ETC mutants) | Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Keywords: Wildtype vs mutant comparison as a method for studying contributors to disease processes |
| GSM272398 | Sham (de_Pomerai_1_S1_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272399 | Microwave (de_Pomerai_2_E1_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272400 | Sham (de_Pomerai_3_S2_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272401 | Microwave (de_Pomerai_4_E2_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272402 | Sham (de_Pomerai_5_S3_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272403 | Microwave (de_Pomerai_6_E3_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272404 | Sham (de_Pomerai_7_S4_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272405 | Microwave (de_Pomerai_8_E4_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272406 | Sham (de_Pomerai_9_S5_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM272407 | Microwave (de_Pomerai_10_E5_C.Elegans) (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM279203_N2_2____2hr | embryo 2 hr before hatching (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279203_N2_3____2hr | embryo 2 hr before hatching (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279203_N2_4____2hr | embryo 2 hr before hatching (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279204_N2_2___0hr | L1 larvae 0 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279204_N2_3___0hr | L1 larvae 0 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279204_N2_4___0hr | L1 larvae 0 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279205_N2_2___1hr | L1 larvae 1 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279205_N2_3___1hr | L1 larvae 1 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279205_N2_4___1hr | L1 larvae 1 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279206_N2_2___3hr | L1 larvae 3 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279206_N2_3___3hr | L1 larvae 3 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279206_N2_4___3hr | L1 larvae 3 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279207_N2_2___6hr | L1 larvae 6 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279207_N2_3___6hr | L1 larvae 6 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279207_N2_4___6hr | L1 larvae 6 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279208_N2_2___12hr | L1 larvae 12 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279208_N2_3___12hr | L1 larvae 12 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279208_N2_4___12hr | L1 larvae 12 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279209_N2_2___15hr | L1 larvae 15 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279209_N2_3___15hr | L1 larvae 15 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279209_N2_4___15hr | L1 larvae 15 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279210_N2_2___24hr | L1 larvae 24 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279210_N2_3___24hr | L1 larvae 24 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279210_N2_4___24hr | L1 larvae 24 hr after hatching in the absence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279211_N2_2___0hr | L1 larvae 0 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279211_N2_3___0hr | L1 larvae 0 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279211_N2_4___0hr | L1 larvae 0 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279212_N2_2___1hr | L1 larvae 1 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279212_N2_3___1hr | L1 larvae 1 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279212_N2_4___1hr | L1 larvae 1 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279213_N2_2___3hr | L1 larvae 3 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279213_N2_3___3hr | L1 larvae 3 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279213_N2_4___3hr | L1 larvae 3 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279214_N2_2___6hr | L1 larvae 6 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279214_N2_3___6hr | L1 larvae 6 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279214_N2_4___6hr | L1 larvae 6 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279215_N2_2___12hr | L1 larvae 12 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279215_N2_3___12hr | L1 larvae 12 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279215_N2_4___12hr | L1 larvae 12 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279216_N2_2___15hr | L1-L2 larvae 15 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279216_N2_3___15hr | L1-L2 larvae 15 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279216_N2_4___15hr | L1-L2 larvae 15 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279217_N2_2___24hr | L2 larvae 24 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279217_N2_3___24hr | L2 larvae 24 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279217_N2_4___24hr | L2 larvae 24 hr after hatching in the presence of food (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279218_N2_2___M9_3hr | L1 larvae 3 hr after hatching in the absence of food in the alternative starvation buffer M9 (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279218_N2_3___M9_3hr | L1 larvae 3 hr after hatching in the absence of food in the alternative starvation buffer M9 (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279218_N2_4___M9_3hr | L1 larvae 3 hr after hatching in the absence of food in the alternative starvation buffer M9 (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279219_N2_2____ | L1 larvae starved for 12 hr after hatching and then fed for 3 hr (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279219_N2_3____ | L1 larvae starved for 12 hr after hatching and then fed for 3 hr (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279219_N2_4____ | L1 larvae starved for 12 hr after hatching and then fed for 3 hr (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279220_N2_2____ | L1 larvae fed for 12 hr after hatching and then starved for 3 hr (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279220_N2_3____ | L1 larvae fed for 12 hr after hatching and then starved for 3 hr (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM279220_N2_4____ | L1 larvae fed for 12 hr after hatching and then starved for 3 hr (GSE14009: Nutritional control of gene expression during C. elegans L1 arrest and recovery) | This SuperSeries is composed of the SubSeries listed below. |
| GSM28389 | e1370 Sample 1 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28390 | e1370 Sample 2 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28391 | e1370 Sample 3 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28392 | e1370 Sample 4 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28393 | e1370 Sample 5 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28394 | m577 Sample 1 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28395 | m577 Sample 2 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28396 | m577 Sample 3 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28397 | m577 Sample 4 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28398 | m577 Sample 5 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28399 | e1370df50 Sample 1 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28400 | e1370df50 Sample 2 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28401 | e1370df50 Sample 3 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28402 | e1370df50 Sample 4 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28403 | e1370df50 Sample 5 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28404 | m577df50 Sample 1 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28405 | m577df50 Sample 2 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28406 | m577df50 Sample 3 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28407 | m577df50 Sample 4 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM28408 | m577df50 Sample 5 (GSE1762: C. elegans daf2 mutant adults) | Analysis of gene expression in long-lived daf-2 mutants for the insulin/IGF-1 receptor. daf-2(e1370) and daf-2(m577) alleles each examined as single and as double mutations with the daf-16(df50) allele. DAF-2 regulates DAF-16, a transcription factor. Results provide insight into longevity. Keywords: other |
| GSM306253 | age-1; fer-15 (M) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306254 | fer-15 (Tedesco #112E) vs. N2 ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306255 | fer-15 (A) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306256 | fer-15 (12/03/01) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306257 | age-1; fer-15 (10/26/01) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306258 | age-1; fer-15 (Tedesco #120E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306259 | age-1; fer-15 (Tedesco #114E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306260 | fer-15 (11/24/01) vs. Mixed Stage N2 Ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306261 | fer-15 (11/09/02) vs. N2 ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306262 | fer-15 (Tedesco #111E) vs. N2 ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306263 | age-1; fer-15 (Tedesco #115E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306264 | age-1; fer-15 (12/01/01) vs. Mixed Stage N2 Ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306265 | fer-15; age-1 (Tedesco #129E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306266 | fer-15 (Tedesco #127E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306267 | fer-15 (Tedesco #134E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306268 | fer-15 (Tedesco #124E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306269 | age-1; fer-15 (A) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306270 | fer-15 (Tedesco #125E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306271 | age-1; fer-15 (Tedesco #131E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306272 | age-1; fer-15 (Tedesco #128E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306273 | fer-15 (Tedesco #113E) vs. N2 ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306274 | fer-15 (M) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306275 | daf-16; fer-15 (Tedesco #121E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306276 | daf-16; fer-15 (11/16/01) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306277 | daf-16; fer-15 (10/18/01) vs. Mixed Stage N2 Ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306278 | daf-16; fer-15 (12/01/01) vs. Mixed Stage N2 Ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306279 | daf-16; fer-15 (Tedesco #122E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306280 | daf-16; fer-15 (Tedesco #132E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306281 | daf-16; fer-15 (M) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306282 | daf-16; fer-15 (Tedesco #130E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306283 | daf-16; fer-15 (Tedesco #133E) vs. N2 mixed stage ref (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306284 | Aging time course - Day 13 - 3 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306285 | Aging time course - Day 7 - 3 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306286 | Aging time course - Day 13 - 4 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306287 | Aging time course - Day 7 - 4 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306288 | Aging time course - Day 10 - 1 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306289 | Aging time course - Day 4 - 1 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306290 | Aging time course - Day 10 - 2 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306291 | Aging time course - Day 4 - 2 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306292 | Aging time course - Day 10 - 3 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306293 | Aging time course - Day 4 - 3 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306294 | Aging time course - Day 10 - 4 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306295 | Aging time course - Day 4 - 4 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306296 | Aging time course - Day 13 - 1 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306297 | Aging time course - Day 13 - 2 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306298 | Aging time course - Day 7 - 1 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM306299 | Aging time course - Day 7 - 2 (GSE12094: Aging study) | This SuperSeries is composed of the SubSeries listed below. |
| GSM309200 | mefloquine_control-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309201 | mefloquine_low_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309202 | mefloquine_mid_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309203 | mefloquine_high_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309204 | mefloquine_control-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309205 | mefloquine_low_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309206 | mefloquine_mid_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309207 | mefloquine_high_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309208 | mefloquine_control-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309209 | mefloquine_low_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309210 | mefloquine_mid_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309211 | mefloquine_high_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309212 | dichlorvos_control-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309213 | dichlorvos_low_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309214 | dichlorvos_mid_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309215 | dichlorvos_high_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309216 | dichlorvos_control-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309217 | dichlorvos_low_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309218 | dichlorvos_mid_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309219 | dichlorvos_high_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309220 | dichlorvos_control-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309221 | dichlorvos_low_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309222 | dichlorvos_mid_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309223 | dichlorvos_high_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309224 | fenamiphos_control-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309225 | fenamiphos_low_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309226 | fenamiphos_mid_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309227 | fenamiphos_high_dose-rep1 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309228 | fenamiphos_control-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309229 | fenamiphos_low_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309230 | fenamiphos_mid_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309231 | fenamiphos_high_dose-rep2 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309232 | fenamiphos_control-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309233 | fenamiphos_low_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309234 | fenamiphos_mid_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM309235 | fenamiphos_high_dose-rep3 (GSE12298: Caenorhabditis elegans as a Genomic Model for Toxicology) | Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide) |
| GSM311471 | N2-controlRNAi-fed-biological rep1 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311472 | N2-controlRNAi-fed-biological rep2 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311473 | N2-controlRNAi-fed-biological rep3 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311474 | N2-controlRNAi-fed-biological rep4 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311475 | N2-controlRNAi-fed-biological rep5 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311476 | N2-controlRNAi-fasting-biological rep1 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311477 | N2-controlRNAi-fasting-biological rep2 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311478 | N2-controlRNAi-fasting-biological rep3 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311479 | N2-controlRNAi-fasting-biological rep4 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311480 | N2-controlRNAi-fasting-biological rep5 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311481 | N2-Cel-RhebRNAi-fed-biological rep1 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311482 | N2-Cel-RhebRNAi-fed-biological rep2 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311483 | N2-Cel-RhebRNAi-fed-biological rep3 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311484 | N2-Cel-RhebRNAi-fed-biological rep4 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311485 | N2-Cel-RhebRNAi-fasting-biological rep1 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311486 | N2-Cel-RhebRNAi-fasting-biological rep2 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311487 | N2-Cel-RhebRNAi-fasting-biological rep3 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311488 | N2-Cel-RhebRNAi-fasting-biological rep4 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311489 | N2-Cel-TORRNAi-fed-biological rep1 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311490 | N2-Cel-TORRNAi-fed-biological rep2 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311491 | N2-Cel-TORRNAi-fed-biological rep3 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311492 | N2-Cel-TORRNAi-fasting-biological rep1 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311493 | N2-Cel-TORRNAi-fasting-biological rep2 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM311494 | N2-Cel-TORRNAi-fasting-biological rep3 (GSE9682: Dietary restriction in Caenorhabditis elegans) | Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. |
| GSM334303 | Depomerai_heat_control_1 (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM334304 | Depomerai_heat_control_2 (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM334305 | Depomerai_heat_shock_1 (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM334306 | Depomerai_heat_shock_2 (GSE10787: Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult C. elegans) | Reports that low-intensity microwave radiation can induce heat-shock reporter gene expression in the nematode, Caenorhabditis elegans, have recently been reinterpreted as a subtle thermal effect caused by very slight heating. This study used a microwave exposure system (1.0 GHz, 0.5 W power input; SAR 0.9-3 mW kg-1 for 6-well plates) that minimises the temperature differential between sham and exposed conditions to <= 0.1°C. Comparable measurement and simulation studies of SAR distribution within this exposure system are presented. We compared 5 Affymetrix gene-arrays of pooled triplicate RNA populations from sham-exposed L4/adult worms against 5 gene-arrays of pooled RNA from microwave-exposed worms (taken from the same source population in each run). Few genes showed consistent expression changes across all 5 comparisons, and all such expression changes appeared modest after applying standard normalisation procedures (<= 30% up- or down-regulated). The number of statistically significant differences in gene expression (846) was less than the false-positive rate expected by chance (1131). As one example, an apparent up-regulation of the vit-3 vitellogenin gene by microwave exposure was not mirrored by similar changes affecting the other co-regulated members of the same vit gene family. We conclude that the pattern of gene expression in L4/adult C elegans is not substantially perturbed by low-intensity microwave radiation, and that the minor changes observed in this study may well be explicable as false positives. As a check on the sensitivity of the Affymetrix gene-arrays used, we also compared RNA samples from N2 worms subjected to a sub-heat-shock treatment (28°C) against controls kept at 26 °C (but using only 2 gene arrays per condition). After similar normalisation, many more genes (3712) showed substantial expression changes (i.e. >; 2-fold at p < 0.05), including a group of six heat-shock genes which were strongly but unexpectedly down-regulated (by >; 10-fold). However, further replication and confirmation by real-time RT-PCR would be needed to establish how many of these changes might also be false positives. Experimenter name: Adam Dawe Experimenter phone: +27 21 959 2364 adam@sanbi.ac.za Experimenter institute: South African National Bioinformatics Institute Experimenter address: University of Western Cape, Old Chemistry Building, University of Western Cape, Modderdam Road, Bellville 7530, Capetown Experimenter zip/postal_code: 7530 Experimenter country: South Africa Keywords: Microwave radiation, gene expression, gene arrays, Caenorhabditis elegans |
| GSM334715 | wild-type, biological rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334716 | wild-type, biological rep 2 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334717 | wild-type, biological rep 3 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334718 | alg-1 mutant, biological rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334719 | alg-1 mutant, biological rep 2 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334720 | alg-1 mutant, biological rep 3 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334721 | zfp-1 mutant, biological rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334722 | zfp-1 mutant, biological rep 2, technical rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334723 | zfp-1 mutant, biological rep 2, technical rep 2 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334724 | rde-4 mutant, biological rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334725 | rde-4 mutant, biological rep 2 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334726 | rde-4 mutant, biological rep 3 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334727 | lin-35 mutant, biological rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334728 | lin-35 mutant, biological rep 2, technical rep 1 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM334729 | lin-35 mutant, biological rep 2, technical rep 2 (GSE13258: RNA interference and retinoblastoma related genes are required for repression of endogenous siRNA targets in C. elegans) | Expession data from L1-L2 stage nematodes (C. elegans), wild type and four mutants (alg-1, zfp-1, rde-4, lin-35). In C. elegans, a vast number of endogenous short RNAs corresponding to thousands of genes have been discovered recently. This finding suggests that these short interfering RNAs may contribute to regulation of many developmental and other signaling pathways in addition to silencing viruses and transposons. Based on this microarray analysis of gene expression in RNA interference (RNAi)-related mutants rde-4, zfp-1 and alg-1 and the Retinoblastoma (Rb) mutant lin-35, we found that a component of Dicer complex RDE-4 and a chromatin-related zinc finger protein ZFP-1, not implicated previously in endogenous RNAi, regulate overlapping sets of genes. Notably, genes a) upregulated in the rde-4 and zfp-1 mutants and b) upregulated in the lin-35(Rb) mutant, but not the downregulated genes are highly represented in the set of genes with corresponding endogenous short interfering RNAs (endo-siRNAs). Keywords: wildtype-mutant comparison, RNAi, Rb, endo-siRNA |
| GSM339690 | op50 4/21 n2 24hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339691 | daf-2_OP50_1 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339692 | op50 5/29 new N2 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339693 | pa14 4/21 n2 24hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339694 | daf-2_PA14_4 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339695 | pa14 sma6 7/30 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339696 | pa14 4/22 n2 24hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339697 | daf-2_PA14_2 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339698 | pa14 629new 4hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339699 | pa14 4/23 n2 24hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339700 | pa14 sma6 7/2 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339701 | op50 5/07 N2 4hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339702 | op50 4/22 n2 24hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339703 | daf-2_OP50_3 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339704 | daf-2_PA14_3 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339705 | op50 6/29 N2 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339706 | op50 4/29 sma6 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339707 | pa14 5/7 n2 4hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339708 | daf-2_PA14_1 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339709 | daf-2_OP50_4 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339710 | op50 sma6 7/2 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339711 | pa14 4/29 sma6 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339712 | op50 sma6 7/30 4hrs (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339713 | pa14 5/29 n2 4hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339714 | op50 n2 11/19 24hr (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM339715 | daf-2_OP50_2 (GSE13473: Response of C. elegans immune pathway mutants to P. aeruginosa infection) | Synchronized C. elegans cultures of three geontypes -- wildype N2, daf-2(e1370) and sma-6(wk7) -- were prepared using standard techniques (http://cmgm.stanford.edu/~kimlab/index_methods.html). Live young adult worms were split between NG plates pre-seeded with the non-pathogenic E. coli strain OP50 or the Pseudomonas aeruginosa clinical isolate PA14 and incubated at 25C for 4 or 24 hours before harvesting. This experiment was repeated at least three times on independent occasions. cDNA probes were prepared from experimental samples and from reference mRNA extracted from mixed stage wild type worms grown at 25C, and were labeled with Cy3 or Cy5, as indicated. A reference experiement design type is where all samples are compared to a common reference. Elapsed Time: Time Infection: Exposure to the non-pathogenic E. coli strain OP50 or to the pathogenic Pseudomonas aeruginosa strain PA14 Strain Name: C. elegans wildtype strain N2 or the immune pathway mutants daf-2(e1370) or sma-6(wk7) Keywords: reference_design |
| GSM360090 | f1 v f13 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360313 | f1 v f26 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360317 | f13 v f1 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360318 | f1 v N2 (wild-type) (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360319 | f13 v f26 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360332 | f13 v N2 (wild-type) (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360333 | f26 v f1 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360334 | f26 v f13 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360335 | f26 v N2 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360336 | N2 (wild-type) v f1 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360337 | N2 (wild-type) v f13 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM360338 | N2 (wild-type) v f26 (GSE14432: A C. elegans LSD1 Demethylase Contributes to Germline Immortality by Reprogramming Epigenetic Memory) | Microarray-based expression profiling of mixed stage populations taken from generation 1,13 and 26 spr-5 mutant animals as well as wild-type animals reveals a large class of spermatogenesis-expressed genes whose expression coordinately increased from generations 1 to 13 and then decreased from generations 13 to 26 in spr-5(by101) mutants. These results suggest that a failure to reset spermatogenesis acquired H3K4me2 may result in the progressive sterility that is observed in spr-5 mutants. |
| GSM365572 | XO_TY2222-E_080307_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365573 | XO_TY2222-E_080307_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365574 | XO_TY2222-E_080307_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365575 | XO_TY2222-E-022208_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365576 | XO_TY2222-E-022208_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365577 | XO_TY2222-E-022208_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365578 | XO_TY2222-E-022208_D (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365579 | XO_TY2222-E-022208_E (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365580 | XX_WT-E_080307_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365581 | XX_WT-E_080307_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365582 | XX_WT-E_080307_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365583 | XX_WT-E_090707_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365584 | XX_WT-E_090707_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365585 | XX_WT-E_090707_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365586 | XX_SDC2Y93R-P-022208_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365587 | XX_SDC2Y93R-P-022208_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365588 | XX_SDC2Y93R-P-022208_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365589 | XX_WT-P_081407_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365590 | XX_WT-P_081407_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365591 | XX_WT-P_081407_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365592 | XX_DPY27-N_042807_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365593 | XX_DPY27-N_042807_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365594 | XX_DPY27-N_042807_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365595 | XX_WT-N_080307_A (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365596 | XX_WT-N_080307_B (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM365597 | XX_WT-N_080307_C (GSE14649: DCC binding and function (Expression Analysis)) | In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics C. elegans |
| GSM372570 | Wild type embryo, 2-cell stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372571 | Wild type embryo, 2-cell stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372572 | Wild type embryo, 2-cell stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372573 | Wild type embryo, 2E stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372574 | Wild type embryo, 2E stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372575 | Wild type embryo, 2E stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372576 | Wild type embryo, 4E stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372577 | Wild type embryo, 4E stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372578 | Wild type embryo, 4E stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372579 | Wild type embryo, 8E stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372580 | Wild type embryo, 8E stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372581 | Wild type embryo, 8E stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372582 | mes-2 embryo, 2E stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372583 | mes-2 embryo, 2E stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372584 | mes-2 embryo, 2E stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372585 | mes-2 embryo, 4E stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372586 | mes-2 embryo, 4E stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372587 | mes-2 embryo, 4E stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372588 | mes-2 embryo, 8E stage, Replicate 1 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372589 | mes-2 embryo, 8E stage, Replicate 2 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM372590 | mes-2 embryo, 8E stage, Replicate 3 (GSE14913: C. elegans embryos: control vs. mes-2 mutant) | Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. |
| GSM375499 | young adult_not exposured_rep1 (GSE15016: Ecotoxicogenomic analysis on the soil nematode Caenorhabditis elegans exposed to BPA, DEHP and NP ) | Gene expression analysis was conducted on the wildtype Caenorhabditis elegans exposed to bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP) and nonylphenol (NP) using whole genome microarray. The microarray study was conducted in an ecotoxicological context, by investigating the response of global gene expression with that of classical toxicological endpoints, such as, mortality, growth, reproduction and development. Results provide insight into global transcription response of C.elegans to these endocrine disrupting chemicals exposure and also contribute to enhance the potential of C.elegans microarray in ecotoxicology (ecotoxicogenomics). key word : ecotoxicogenomics |
| GSM375500 | young adult_24hr BPA exposure_rep1 (GSE15016: Ecotoxicogenomic analysis on the soil nematode Caenorhabditis elegans exposed to BPA, DEHP and NP ) | Gene expression analysis was conducted on the wildtype Caenorhabditis elegans exposed to bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP) and nonylphenol (NP) using whole genome microarray. The microarray study was conducted in an ecotoxicological context, by investigating the response of global gene expression with that of classical toxicological endpoints, such as, mortality, growth, reproduction and development. Results provide insight into global transcription response of C.elegans to these endocrine disrupting chemicals exposure and also contribute to enhance the potential of C.elegans microarray in ecotoxicology (ecotoxicogenomics). key word : ecotoxicogenomics |
| GSM375501 | young adult_24hr DEHP exposure_rep1 (GSE15016: Ecotoxicogenomic analysis on the soil nematode Caenorhabditis elegans exposed to BPA, DEHP and NP ) | Gene expression analysis was conducted on the wildtype Caenorhabditis elegans exposed to bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP) and nonylphenol (NP) using whole genome microarray. The microarray study was conducted in an ecotoxicological context, by investigating the response of global gene expression with that of classical toxicological endpoints, such as, mortality, growth, reproduction and development. Results provide insight into global transcription response of C.elegans to these endocrine disrupting chemicals exposure and also contribute to enhance the potential of C.elegans microarray in ecotoxicology (ecotoxicogenomics). key word : ecotoxicogenomics |
| GSM375502 | young adult_24hr NP exposure_rep1 (GSE15016: Ecotoxicogenomic analysis on the soil nematode Caenorhabditis elegans exposed to BPA, DEHP and NP ) | Gene expression analysis was conducted on the wildtype Caenorhabditis elegans exposed to bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP) and nonylphenol (NP) using whole genome microarray. The microarray study was conducted in an ecotoxicological context, by investigating the response of global gene expression with that of classical toxicological endpoints, such as, mortality, growth, reproduction and development. Results provide insight into global transcription response of C.elegans to these endocrine disrupting chemicals exposure and also contribute to enhance the potential of C.elegans microarray in ecotoxicology (ecotoxicogenomics). key word : ecotoxicogenomics |
| GSM378577 | glp-1_UV_2008_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378578 | glp-1_UV_2008_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378579 | N2_control_2007_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378580 | N2_control_2007_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378581 | N2_UV_2007_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378582 | N2_UV_2007_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378583 | glp-1_control_2007_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378584 | glp-1_control_2007_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378585 | glp-1_UV_2007_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378586 | glp-1_UV_2007_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378587 | xpa-1_control_2007_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378588 | xpa-1_control_2007_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378589 | xpa-1_UV_2007_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378590 | xpa-1_UV_2007_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378591 | xpa-1_control_2008_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378592 | xpa-1_control_2008_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378593 | xpa-1_UV_2008_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378594 | xpa-1_UV_2008_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378595 | N2_control_2008_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378596 | N2_control_2008_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378597 | N2_UV_2008_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378598 | N2_UV_2008_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378599 | glp-1_control_2008_rep1 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM378600 | glp-1_control_2008_rep2 (GSE15159: Transcriptomic response of young adult N2, xpa1, and glp1 nematodes 3h after exposure to 50 J/m2 UVC radiation at 25°C) | We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains. |
| GSM389220 | dbl-1 L4 worm, biological rep1 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389221 | dbl-1 L4 worm, biological rep2 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389222 | dbl-1 L4 worm, biological rep3 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389223 | dbl-1 L4 worm, biological rep4 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389224 | dbl-1 L4 worm, biological rep5 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389225 | sma-6 L4 worm, biological rep1 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389226 | sma-6 L4 worm, biological rep2 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389227 | sma-6 L4 worm, biological rep3 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389228 | sma-6 L4 worm, biological rep4 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389229 | sma-6 L4 worm, biological rep5 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM389230 | sma-6 L4 worm, biological rep6 (GSE15527: Regulation of genes affecting body size and innate immunity by the DBL-1/BMP-like pathway in Caenorhabditis elegans) | Compare the global gene expression profiles of Sma-6 and Dbl-1 in L4 stage C. elegans |
| GSM39425 | pp0-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39426 | pp41-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39427 | pp53-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39428 | pp66-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39429 | pp83-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39430 | pp122-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39431 | pp143-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39432 | pp186-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39433 | pp0-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39434 | pp23-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39435 | pp41-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39436 | pp53-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39437 | pp66-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39438 | pp143-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39439 | pp186-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39440 | ms41-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39441 | ms66-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39442 | ms122-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39443 | ms53-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39444 | ms101-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39445 | ms0-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39446 | ms66-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39447 | ms83-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39448 | ms122-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39449 | ms143-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39450 | ms186-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39451 | ms0-6 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39452 | ms53-6 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39453 | ms83-6 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39454 | ms186-6 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39455 | ms83-7 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39456 | ms83-8 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39457 | ms186-7 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39458 | ms186-8 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39459 | p23-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39460 | p41-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39461 | p53-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39462 | p66-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39463 | p83-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39464 | p101-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39465 | p122-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39466 | p143-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39467 | p186-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39468 | p0-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39469 | p23-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39470 | p41-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39471 | p53-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39472 | p66-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39473 | p101-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39474 | p122-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39475 | p143-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39476 | p186-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39477 | p0-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39478 | p23-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39479 | p41-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39480 | p83-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39481 | p101-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39482 | p122-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39483 | p143-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39484 | p186-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39485 | pp0-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39486 | pp23-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39487 | pp41-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39488 | pp53-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39489 | pp66-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39490 | pp83-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39491 | pp101-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39492 | pp122-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39493 | pp143-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39494 | pp186-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39495 | pp0-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39496 | pp23-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39497 | pp41-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39498 | pp66-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39499 | pp83-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39500 | pp101-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39501 | pp122-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39502 | pp122-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39503 | pp186-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39504 | ms0-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39505 | ms23-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39506 | ms41-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39507 | ms122-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39508 | ms23-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39509 | ms41-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39510 | ms101-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39511 | ms122-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39512 | ms143-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39513 | 00B (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39514 | 00C (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39515 | 00P (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39516 | 23-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39517 | 23-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39518 | 23-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39519 | 23-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39520 | 41D (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39521 | 41E (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39522 | 53-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39523 | 53-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39524 | 53-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39525 | 66-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39526 | 66-5 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39527 | 83-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39528 | 83-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39529 | 83-3 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39530 | 66O (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39531 | 66I (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39532 | 101G (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39533 | 101R (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39534 | 122-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39535 | 122-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39536 | 143L (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39537 | 143M (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39538 | 143Q (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39539 | 186-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39540 | 186-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39541 | 186-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39542 | 41S (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39543 | 53-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39544 | 83-4 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39545 | 101H (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39546 | 122-2 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM39547 | p66-1 (GSE2180: C. elegans embryonic timecourse in wt and mutant embryos) | This series of samples comprises multiple early embryonic time courses for C. elegans. Time courses consisting of 10 time points each for 4 different genotypes are included: wild-type (strain N2 grown on E. coli strain OP50), pie-1(zu154) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain OP50), pie-1(zu154);pal-1(RNAi) (progeny of homozygous mutant mothers [Unc] of strain JJ532 grown on E. coli strain HT115 expressing pal-1 hairpin RNA), and mex-3(zu155);skn-1(RNAi) (progeny of homozygous mutant mothers [Dpy] of strain JJ518 grown on E. coli strain HT115 expressing skn-1 hairpin RNA). Embryos were manually staged by morphology at the 4-cell stage and allowed to develop in water for defined amounts of time at 22 degrees C. RNA was amplified as described (Baugh et al. Development, 2003; Baugh et al. Nucleic Acids Research, 2001). This series of samples comprises all replicate data reported by Baugh et al. (Development, 2005). Keywords: time-course |
| GSM395631 | N2-1 (GSE15762: Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms) | The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. |
| GSM395632 | N2-2 (GSE15762: Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms) | The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. |
| GSM395633 | N2-3 (GSE15762: Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms) | The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. |
| GSM395634 | hlh-30(tm1978)-1 (GSE15762: Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms) | The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. |
| GSM395635 | hlh-30(tm1978)-2 (GSE15762: Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms) | The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. |
| GSM395636 | hlh-30(tm1978)-3 (GSE15762: Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms) | The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor. |
| GSM401793 | MT_GFPp_rep1 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401794 | MT_GFPm_rep1 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401795 | WT_GFPp_rep1 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401796 | WT_GFPm_rep1 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401797 | MT_GFPp_rep2 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401798 | MT_GFPm_rep2 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401799 | WT_GFPp_rep2 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401800 | WT_GFPm_rep2 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401801 | MT_GFPp_rep3 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401802 | MT_GFPm_rep3 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401803 | WT_GFPp_rep3 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM401804 | WT_GFPm_rep3 (GSE16050: The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans) | We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. |
| GSM40306 | tom-1(nu468) Sample 1 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40307 | tom-1(nu468) Sample 2 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40308 | Wild type Sample 1 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40309 | Wild type Sample 2 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40310 | Wild type Sample 3 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40311 | Wild type Sample 4 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40312 | unc-43(n1186) Sample 1 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40313 | unc-43(n1186) Sample 2 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM40314 | unc-43(n1186) Sample 3 (GSE2210: Microarray-assisted Cloning of Mutants: Expression Profiling of tom-1 and unc-43) | Analysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning. Keywords: other |
| GSM412179 | nth-1_1 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412180 | nth-1_2 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412181 | nth-1_3 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412182 | nth-1;xpa-1_1 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412183 | nth-1;xpa-1_2 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412184 | xpa-1_1 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412185 | xpa-1_2 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412186 | N2_1 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM412187 | N2_2 (GSE16405: Transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1) | Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways. Results: The gene expression signatures from nth-1, xpa-1 and nth-1;xpa-1 are deciphered. We find that the single mutants are more similar in overall transcriptomic activity compared to the double mutant and their corresponding wild-type (N2). Interestingly, of the enriched Gene Ontology terms for respective mutants are aging and proteolysis for nth-1, aging, energy production and unfolded protein response for xpa-1, and DNA repair and regulation of M-phase for nth-1;xpa-1. We also find striking similarities between the biological processes found to be enriched in the single mutants, which show a shared response in genes associated with aging and insulin signaling. Loss of either BER or NER induces an oxidative stress response, but does not confer resistance to heat shock. Conclusion: Taken together, our study provides a general overview about the global transcriptional changes in the absence of nth-1, xpa-1 and nth-1;xpa-1. Our results also point to a two-tiered global response to combat the effects of decreased DNA repair capacity. |
| GSM418149 | Control vs. DZN (1mg/ml). Replicate 1 (GSE16686: C. elegans : Control vs. Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418150 | Control vs. DZN (1mg/ml). Replicate 2 (GSE16686: C. elegans : Control vs. Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418151 | Control vs. DZN (1mg/ml). Replicate 3 (GSE16686: C. elegans : Control vs. Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418152 | DZN (1mg/ml) vs. Control. Replicate 1 (GSE16686: C. elegans : Control vs. Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418153 | DZN (1mg/ml) vs. Control. Replicate 2 (GSE16686: C. elegans : Control vs. Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418154 | DZN (1mg/ml) vs. Control. Replicate 3 (GSE16686: C. elegans : Control vs. Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418156 | Control vs. CPF (0.5mg/ml). Replicate 1 (GSE16688: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5mg/ml of Chorpyrifos (CPF) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418157 | Control vs. CPF (0.5mg/ml). Replicate 2 (GSE16688: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5mg/ml of Chorpyrifos (CPF) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418158 | Control vs. CPF (0.5mg/ml). Replicate 3 (GSE16688: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5mg/ml of Chorpyrifos (CPF) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418159 | CPF (0.5mg/ml) vs. Control. Replicate 1 (GSE16688: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5mg/ml of Chorpyrifos (CPF) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418160 | CPF (0.5mg/ml) vs. Control. Replicate 2 (GSE16688: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5mg/ml of Chorpyrifos (CPF) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418161 | CPF (0.5mg/ml) vs. Control. Replicate 3 (GSE16688: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5mg/ml of Chorpyrifos (CPF) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418248 | Control vs. CPF (0.5mg/ml) + DZN (1mg/ml). Replicate 1 (GSE16698: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) + Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5 mg/ml of Chlorpyrifos and 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418249 | Control vs. CPF (0.5mg/ml) + DZN (1mg/ml). Replicate 2 (GSE16698: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) + Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5 mg/ml of Chlorpyrifos and 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418250 | Control vs. CPF (0.5mg/ml) + DZN (1mg/ml). Replicate 3 (GSE16698: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) + Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5 mg/ml of Chlorpyrifos and 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418251 | CPF (0.5mg/ml) + DZN (1mg/ml) vs. Control. Replicate 1 (GSE16698: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) + Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5 mg/ml of Chlorpyrifos and 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418252 | CPF (0.5mg/ml) + DZN (1mg/ml) vs. Control. Replicate 2 (GSE16698: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) + Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5 mg/ml of Chlorpyrifos and 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM418253 | CPF (0.5mg/ml) + DZN (1mg/ml) vs. Control. Replicate 3 (GSE16698: C. elegans : Control vs. Chlorpyrifos (0.5mg/ml) + Diazinon (1 mg/ml) treatment) | Transcriptional profile of C. elegans comparing control vs. nematodes treated with 0.5 mg/ml of Chlorpyrifos and 1mg/ml of Diazinon (DZN) at 16°C. Toxicant was added to agar and nematode culture on petri dishes for 72h before harvesting. |
| GSM419959 | Wild-type young adult biological rep 3 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419960 | Wild-type young adult biological rep 4 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419961 | Wild-type young adult biological rep 5 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419962 | Wild-type young adult biological rep 6 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419963 | fer-1 (hc1ts) mutant young adult biological rep 1 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419964 | fer-1 (hc1ts) mutant young adult biological rep 2 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419965 | fer-1 (hc1ts) mutant young adult biological rep 5 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419966 | fer-1 (hc1ts) mutant young adult biological rep 6 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419967 | fer-1 (hc24ts) mutant young adult biological rep 1 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419968 | fer-1 (hc24ts) mutant young adult biological rep 2 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419969 | fer-1 (hc24ts) mutant young adult biological rep 3 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM419970 | fer-1 (hc24ts) mutant young adult biological rep 5 (GSE16753: C. elegans fer-1 mutant gene expression profile) | In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. |
| GSM424861 | C.elegans control sample replicate 1 (GSE16975: Hydrogen sulfide (H2S) modulates lifespan of C.elegans) | Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated. |
| GSM424862 | C.elegans control sample replicate 2 (GSE16975: Hydrogen sulfide (H2S) modulates lifespan of C.elegans) | Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated. |
| GSM424863 | C.elegans control sample replicate 3 (GSE16975: Hydrogen sulfide (H2S) modulates lifespan of C.elegans) | Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated. |
| GSM424864 | C.elegans hydrogen sulfide sample replicate 1 (GSE16975: Hydrogen sulfide (H2S) modulates lifespan of C.elegans) | Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated. |
| GSM424865 | C.elegans hydrogen sulfide sample replicate 2 (GSE16975: Hydrogen sulfide (H2S) modulates lifespan of C.elegans) | Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated. |
| GSM424866 | C.elegans hydrogen sulfide sample replicate 3 (GSE16975: Hydrogen sulfide (H2S) modulates lifespan of C.elegans) | Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated. |
| GSM427104 | WN8 vs. WN41 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427105 | WN60 vs. WN77 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427106 | WN9 vs. WN62 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427107 | WN71 vs. WN79 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427108 | WN27 vs. WN56 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427109 | WN46 vs. WN69 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427110 | WN68 vs. WN37 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427111 | WN13 vs. WN21 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427112 | WN20 vs. WN53 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427113 | WN57 vs. WN32 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427114 | WN19 vs. WN39 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427115 | WN76 vs. WN59 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427116 | WN28 vs. WN50 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427117 | WN44 vs. WN2 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427118 | WN24 vs. WN16 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427119 | WN11 vs. WN25 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427120 | WN19 vs. WN1 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427121 | WN33 vs. WN3 T1 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427122 | WN8 vs. WN41 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427123 | WN60 vs. WN77 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427124 | WN9 vs. WN62 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427125 | WN71 vs. WN79 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427126 | WN27 vs. WN56 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427127 | WN46 vs. WN69 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427128 | WN68 vs. WN37 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427129 | WN13 vs. WN21 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427130 | WN20 vs. WN53 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427131 | WN57 vs. WN32 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427132 | WN19 vs. WN39 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427133 | WN76 vs. WN59 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427134 | WN28 vs. WN50 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427135 | WN44 vs. WN2 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427136 | WN24 vs. WN16 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427137 | WN11 vs. WN25 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427138 | WN19 vs. WN1 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427139 | WN33 vs. WN3 T2 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427140 | WN8 vs. WN41 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427141 | WN60 vs. WN77 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427142 | WN9 vs. WN62 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427143 | WN71 vs. WN79 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427144 | WN27 vs. WN56 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427145 | WN46 vs. WN69 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427146 | WN68 vs. WN37 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427147 | WN13 vs. WN21 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427148 | WN20 vs. WN53 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427149 | WN57 vs. WN32 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427150 | WN19 vs. WN39 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427151 | WN76 vs. WN59 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427152 | WN28 vs. WN50 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427153 | WN44 vs. WN2 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427154 | WN24 vs. WN16 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427155 | WN11 vs. WN25 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427156 | WN19 vs. WN1 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM427157 | WN33 vs. WN3 T3 (GSE17071: Dynamic gene expression of Recombinant Inbred Lines (RILs) in C. elegans) | We mapped quantitative trait loci for genome-wide gene expression (eQTL) in juvenile, reproductive and senescent C. elegans recombinant inbred lines, to determine heritable transcript dynamics |
| GSM436 | fem-3(q23) (red, channel 2) vs. fem-1(hc17) (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM437 | fem-3(q23) (red, channel 2) vs. fem-1(hc17) (green, channel 1)- repeat #1 (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM438 | vjr N2 mixed control (red, channel 2) vs N2-3 T4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM439 | vjr N2 mixed control (red, channel 2) vs bn2-1 T5 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM440 | vjr N2 mixed control (red, channel 2) vs bn2-3 T4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM441 | vjr N2 mixed control (red, channel 2) vs N2-2 T4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM442 | vjr N2 mixed control (red, channel 2) vs N2-4 T4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM443 | vjr N2 mixed control (red, channel 2) vs bn2-2 T4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM444 | vjr N2 mixed control (red, channel 2) vs bn2-4 T4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM445 | vjr N2 mixed control (red, channel 2) vs N2-2 T2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM446 | vjr mixed control (red, channel 2) vs N2-2 T3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM447 | vjr mixed contol (red, channel 2) vs bn2-2 T2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM448 | vjr mixed control (red, channel 2) vs bn2-2 T3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM449 | vjr N2 mixed control (red, channel 2) vs N2-4 T2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM450 | vjr mixed control (red, channel 2) vs N2-4 T3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM451 | vjr mixed contol (red, channel 2) vs bn2-4 T2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM452 | vjr mixed control (red, channel 2) vs bn2-4 T3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM453398 | WT Starved L1, biological rep1 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453399 | WT Starved L1, biological rep2 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453400 | WT Starved L1, biological rep3 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453401 | Ogt starved L1, biological replicate 1 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453402 | Ogt starved L1, biological replicate 2 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453403 | Ogt starved L1, biological replicate 3 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453404 | Oga starved L1, biological replicate 1 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453405 | Oga starved L1, biological replicate 2 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453406 | Oga starved L1, biological replicate 3 (GSE18130: Expression from C. elegans L1 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453407 | WT Fed L4, biological rep1 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453408 | WT Fed L4, biological rep2 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453409 | WT Fed L4, biological rep3 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453410 | Ogt Fed L4, biological replicate 1 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453411 | Ogt Fed L4, biological replicate 2 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453412 | Ogt Fed L4, biological replicate 3 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453413 | Oga Fed L4, biological replicate 1 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453414 | Oga Fed L4, biological replicate 2 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453415 | Oga Fed L4, biological replicate 3 (GSE18131: Expression from C. elegans L4 animals) | Nutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Whole genome transcriptional profiling of the O-GlcNAc cycling mutants confirmed dramatic deregulation of genes in these key pathways. As predicted, the O-GlcNAc cycling mutants show phenotypically altered lifespan and susceptibility to UV stress. |
| GSM453876 | Caenorhabditis elegans grown with sufficient Biotin 1 (GSE18157: Gene expression underlying the effects of biotin deficiency in rat liver, worms and yeast) | Biotin is cofactor of crucial enzymes for intermediary metabolism, and its deficiency affects the transcription of some critical genes of mammalian glucose metabolism. However, the precise mechanisms of biotin starvation on gene expression are unknown. Here we show that metabolic changes ushered by deficiency of this vitamin sets in motion extensive reorganization of carbon metabolism gene expression, consistent across three diverse eukaryotes, that is mediated through a regulatory circuitry at the genome level similar in the three species. We used affymetrix microarrays to detail the global gene expression underlying the effects of biotin deficiency in Rattus norvegicus liver, Caenorhabditis elegans and Saccharomyces cerevisiae and identified distinct classes of up-regulated genes during this event. |
| GSM453877 | Caenorhabditis elegans grown with sufficient Biotin 2 (GSE18157: Gene expression underlying the effects of biotin deficiency in rat liver, worms and yeast) | Biotin is cofactor of crucial enzymes for intermediary metabolism, and its deficiency affects the transcription of some critical genes of mammalian glucose metabolism. However, the precise mechanisms of biotin starvation on gene expression are unknown. Here we show that metabolic changes ushered by deficiency of this vitamin sets in motion extensive reorganization of carbon metabolism gene expression, consistent across three diverse eukaryotes, that is mediated through a regulatory circuitry at the genome level similar in the three species. We used affymetrix microarrays to detail the global gene expression underlying the effects of biotin deficiency in Rattus norvegicus liver, Caenorhabditis elegans and Saccharomyces cerevisiae and identified distinct classes of up-regulated genes during this event. |
| GSM453878 | Caenorhabditis elegans in biotin deficiency 1 (GSE18157: Gene expression underlying the effects of biotin deficiency in rat liver, worms and yeast) | Biotin is cofactor of crucial enzymes for intermediary metabolism, and its deficiency affects the transcription of some critical genes of mammalian glucose metabolism. However, the precise mechanisms of biotin starvation on gene expression are unknown. Here we show that metabolic changes ushered by deficiency of this vitamin sets in motion extensive reorganization of carbon metabolism gene expression, consistent across three diverse eukaryotes, that is mediated through a regulatory circuitry at the genome level similar in the three species. We used affymetrix microarrays to detail the global gene expression underlying the effects of biotin deficiency in Rattus norvegicus liver, Caenorhabditis elegans and Saccharomyces cerevisiae and identified distinct classes of up-regulated genes during this event. |
| GSM453879 | Caenorhabditis elegans in biotin deficiency 2 (GSE18157: Gene expression underlying the effects of biotin deficiency in rat liver, worms and yeast) | Biotin is cofactor of crucial enzymes for intermediary metabolism, and its deficiency affects the transcription of some critical genes of mammalian glucose metabolism. However, the precise mechanisms of biotin starvation on gene expression are unknown. Here we show that metabolic changes ushered by deficiency of this vitamin sets in motion extensive reorganization of carbon metabolism gene expression, consistent across three diverse eukaryotes, that is mediated through a regulatory circuitry at the genome level similar in the three species. We used affymetrix microarrays to detail the global gene expression underlying the effects of biotin deficiency in Rattus norvegicus liver, Caenorhabditis elegans and Saccharomyces cerevisiae and identified distinct classes of up-regulated genes during this event. |
| GSM453880 | Caenorhabditis elegans in biotin deficiency 3 (GSE18157: Gene expression underlying the effects of biotin deficiency in rat liver, worms and yeast) | Biotin is cofactor of crucial enzymes for intermediary metabolism, and its deficiency affects the transcription of some critical genes of mammalian glucose metabolism. However, the precise mechanisms of biotin starvation on gene expression are unknown. Here we show that metabolic changes ushered by deficiency of this vitamin sets in motion extensive reorganization of carbon metabolism gene expression, consistent across three diverse eukaryotes, that is mediated through a regulatory circuitry at the genome level similar in the three species. We used affymetrix microarrays to detail the global gene expression underlying the effects of biotin deficiency in Rattus norvegicus liver, Caenorhabditis elegans and Saccharomyces cerevisiae and identified distinct classes of up-regulated genes during this event. |
| GSM453 | REF-vjr (red, channel 2) vs N2 #3 L3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM454 | REF-vjr (red, channel 2) vs N2 #3 L4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM455141 | age-1(mg44)_rep1 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455142 | intestine_age-1_rep1 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455143 | neuron_age-1_rep1 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455144 | age-1(mg44)_rep2 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455145 | intestine_age-1_rep2 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455146 | neuron_age-1_rep2 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455147 | intestine_age-1_rep3 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455148 | neuron_age-1_rep3 (GSE18200: Gene expression C. elegans age-1 mutants with neuron- or intestine-restricted age-1 activity) | The goal of this experiment was to identify transcripts regulated non-autonomously by age-1 activity in neurons or intestine. Comparisons of gene expression were made between age-1(mg44) null adults and CY251 (age-1(mg44); bvIs2) and CY262 (age-1(mg44); bvIs1); all were relative to wildtype (N2). The integrated transgenes, bvIs2 and bvIs1, carry the age-1 cDNA expressed from the neuronal ric-19 promoter (bvIs2) or intestinal ges-1 promoter (bvIs1). Transcripts upregulated in age-1(mg44) adults compared to wildtype (>;=1.5 fold; p<0.05) or downregulated (<0.6 fold; p<0.05) were considered to be age-1 target genes. Rescue in CY251 or CY262 was determined by change in the transgenic background versus age-1(mg44) (all relative to N2 wildtype). Non-autonomous rescue of a target gene was usually determined by transcript levels that were at least 50% rescued compared to wildtype. |
| GSM455149 | wildtype vs cde-1, young adults (GSE18202: Variation in germline gene expression in cde-1 mutant) | analysis of germline gene expression in wildtype and cde-1 mutant C. elegans. |
| GSM455156 | cde-1 vs wildtype, young adults (GSE18202: Variation in germline gene expression in cde-1 mutant) | analysis of germline gene expression in wildtype and cde-1 mutant C. elegans. |
| GSM455157 | wildtype vs cde-1, aged adults (GSE18202: Variation in germline gene expression in cde-1 mutant) | analysis of germline gene expression in wildtype and cde-1 mutant C. elegans. |
| GSM455158 | cde-1 vs wildtype, aged adults (GSE18202: Variation in germline gene expression in cde-1 mutant) | analysis of germline gene expression in wildtype and cde-1 mutant C. elegans. |
| GSM455 | REF-vjr (red, channel 2) vs bn2 #3 L3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM456 | REF-vjr (red, channel 2) vs bn2 #3 L4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM457 | REF-vjr (red, channel 2) vs N2 #1 L4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM458 | REF-vjr (red, channel 2) vs bn2 #1 L4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM459 | REF-vjr (red, channel 2) vs bn2 #1 L3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM460 | REF-vjr (red, channel 2) vs N2 #1 L2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM461962 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 1 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461963 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 2 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461964 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 3 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461965 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 4 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461966 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 5 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461967 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 6 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461968 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 7 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461969 | daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi replicate 8 (GSE18561: Adult C. elegans: Control daf-2 mutants treated with daf-16 RNAi vs. daf-2 mutants treated with empty vector RNAi) | Transcriptional profiling of adult C. elegans comparing daf-16(-); daf-2(-) animals with adult daf-2(-) animals. |
| GSM461970 | Control animals vs. glucose-fed animals replicate 1 (GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture) | Transcriptional profiling of adult C. elegans comparing normally cultured control animals with adult animals that were cultured on diet supplemented with 2% D-glucose. |
| GSM461971 | Control animals vs. glucose-fed animals replicate 2 (GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture) | Transcriptional profiling of adult C. elegans comparing normally cultured control animals with adult animals that were cultured on diet supplemented with 2% D-glucose. |
| GSM461972 | Control animals vs. glucose-fed animals replicate 3 (GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture) | Transcriptional profiling of adult C. elegans comparing normally cultured control animals with adult animals that were cultured on diet supplemented with 2% D-glucose. |
| GSM461973 | Control animals vs. glucose-fed animals replicate 4 (GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture) | Transcriptional profiling of adult C. elegans comparing normally cultured control animals with adult animals that were cultured on diet supplemented with 2% D-glucose. |
| GSM461974 | Control animals vs. glucose-fed animals replicate 5 (GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture) | Transcriptional profiling of adult C. elegans comparing normally cultured control animals with adult animals that were cultured on diet supplemented with 2% D-glucose. |
| GSM461975 | Control animals vs. glucose-fed animals replicate 6 (GSE18562: Adult C. elegans: Control OP50 culture vs. OP50 + 2% glucose culture) | Transcriptional profiling of adult C. elegans comparing normally cultured control animals with adult animals that were cultured on diet supplemented with 2% D-glucose. |
| GSM461 | REF-vjr (red, channel 2) vs N2 #2 L2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM462 | REF-vjr (red, channel 2) vs N2 #3 L2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM463 | REF-vjr (red, channel 2) vs glp-4 #1 L2 (green, channel1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM464 | REF-vjr (red, channel 2) vs glp-4 #2 and #4 L2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM465 | REF-vjr (red, channel 2) vs glp-4 #3 L2 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM466 | REF-vjr (red, channel 2) vs N2 #1 L3 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM467 | fem3 #4 (red, channel 2) vs. fem1 #4 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM468 | fem3 #5 (red, channel 2) vs. fem1 #5 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM469 | fem3 #1 (red, channel 2) fem1 #1 (green, channel 1) (GSE5: Global profile of germline gene expression in C. elegans) | We used DNA microarrays to profile gene expression patterns in the C. elegans germline and identified 1416 germline-enriched transcripts that define three groups. The sperm-enriched group contains an unusually large number of protein kinases and phosphatases. The oocyte-enriched group includes potentially new components of embryonic signaling pathways. The germline-intrinsic group, defined as genes expressed similarly in germlines making only sperm or only oocytes, contains a family of piwi-related genes that may be important for stem cell proliferation. Finally, examination of the chromosomal location of germline transcripts revealed that sperm-enriched and germline-intrinsic genes are nearly absent from the X chromosome, but oocyte-enriched genes are not. This research has been described more fully in Reinke V et al.(2000) Mol Cell 6:605-16 Keywords: other |
| GSM474531 | ALG-1(-) 1 (GSE19138: Comprehensive discovery of endogenous Argonaute binding sites in C. elegans) | Comprehensive discovery of endogenous Argonaute binding sites in C. elegans |
| GSM474532 | ALG-1(-) 2 (GSE19138: Comprehensive discovery of endogenous Argonaute binding sites in C. elegans) | Comprehensive discovery of endogenous Argonaute binding sites in C. elegans |
| GSM474533 | ALG-1(-) 3 (GSE19138: Comprehensive discovery of endogenous Argonaute binding sites in C. elegans) | Comprehensive discovery of endogenous Argonaute binding sites in C. elegans |
| GSM474534 | WT1 (GSE19138: Comprehensive discovery of endogenous Argonaute binding sites in C. elegans) | Comprehensive discovery of endogenous Argonaute binding sites in C. elegans |
| GSM474535 | WT2 (GSE19138: Comprehensive discovery of endogenous Argonaute binding sites in C. elegans) | Comprehensive discovery of endogenous Argonaute binding sites in C. elegans |
| GSM474536 | WT3 (GSE19138: Comprehensive discovery of endogenous Argonaute binding sites in C. elegans) | Comprehensive discovery of endogenous Argonaute binding sites in C. elegans |
| GSM479867 | N2 at iso, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479868 | N2 at iso, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479869 | N2 at iso, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479870 | N2 at 200 for 15min, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479871 | N2 at 200 for 15min, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479872 | N2 at 200 for 15min, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479873 | N2 at 200 for 1 hour, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479874 | N2 at 200 for 1 hour, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479875 | N2 at 200 for 1 hour, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479876 | N2 at 200 for 6 hours, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479877 | N2 at 200 for 6 hours, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479878 | N2 at 200 for 6 hours, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479879 | N2 at 200 for 1 generation, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479880 | N2 at 200 for 1 generation, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479881 | N2 at 200 for 1 generation, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479882 | osm-7(n1515) at iso, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479883 | osm-7(n1515) at iso, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479884 | osm-7(n1515) at iso, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479885 | osm-8(n1518) at iso, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479886 | osm-8(n1518) at iso, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479887 | osm-8(n1518) at iso, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479888 | osm-11(n1604) at iso, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479889 | osm-11(n1604) at iso, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479890 | osm-11(n1604) at iso, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479891 | dpy-9(e12) at iso, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479892 | dpy-9(e12) at iso, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479893 | dpy-9(e12) at iso, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479894 | dpy-10(e128) at iso, rep1 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479895 | dpy-10(e128) at iso, rep2 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM479896 | dpy-10(e128) at iso, rep3 (GSE19310: Expression data from wild type C. elegans and 5 osmotic stress resistant mutants exposed to hyper/isotonic environments) | Adaptation of C. elegans to hypertonic environments involves the accumulation of the organic osmolyte glycerol via transcriptional upregulation of the glycerol biosynthestic enzyme gpdh-1. A number of mutants, termed osmotic stress resistant (osr) mutants, have been identified. osr mutants cause constitutive upregulation of gpdh-1 and confer extreme resistance to hypertonicity. We tested the hypothesis that osr mutants broadly activate a gene expression program normally activated by osmotic stress in wild type animals using Affymterix microarray analysis of the hypertonic stress response in wild type animals and of constituitive gene expression changes in five osr mutants. |
| GSM498038_FBF_GFP_IP__biological_replicate_1 | FBF-GFP IP, biological replicate 1 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498039_TUB_GFP_IP__biological_replicate_1 | TUB-GFP IP, biological replicate 1 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498040_FBF_GFP_IP__biological_replicate_2 | FBF-GFP IP, biological replicate 2 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498041_TUB_GFP_IP__biological_replicate_2 | TUB-GFP IP, biological replicate 2 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498042_FBF_GFP_IP__biological_replicate_3 | FBF-GFP IP, biological replicate 3 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498043_TUB_GFP_IP__biological_replicate_3 | TUB-GFP IP, biological replicate 3 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498044_FBF_GFP_IP__biological_replicate_4 | FBF-GFP IP, biological replicate 4 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM498045_TUB_GFP_IP__biological_replicate_4 | TUB-GFP IP, biological replicate 4 (GSE19922: FBF-IP/TUB-IP log2 ratios) | The PUF family of RNA binding proteins has a conserved role in maintaining stem cell self-renewal. FBF is a C. elegans PUF that is required to maintain germline stem cells (GSCs). To understand how FBF controls GSCs, we sought to identify is target mRNAs. Briefly, we immunoprecipitated FBF-mRNA complexes from worm extracts and then used microarrays to identify the FBF-associated mRNAs. To focus on germline targets of FBF, we used a FBF-GFP transgene under the control of a germline promoter and we used an anti-GFP antibody to purify FBF-GFP from worm extracts. In parallel, we also processed a strain expressing TUBULIN-GFP in the germline to control for mRNAs that non-specifically co-purify with GFP. We found that FBF associates with >;1,000 unique mRNAs and likely controls a broad network of key cellular and developmental regulators. |
| GSM499032_N2_1 | control wild type N2_1 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499033_N2_2 | control wild type N2_2 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499034_N2_3 | control wild type N2_3 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499035_JS62_1 | transgenic aex-3::his-SUMO-1 JS62_1 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499036_JS62_2 | transgenic aex-3::his-SUMO-1 JS62_2 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499037_JS62_3 | transgenic aex-3::his-SUMO-1 JS62_3 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499038_JS63_1 | transgenic myo-4::his-SUMO-1 JS63_1 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499039_JS63_2 | transgenic myo-4::his-SUMO-1 JS63_2 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM499040_JS63_3 | transgenic myo-4::his-SUMO-1 JS63_3 (GSE19972: Expression Data from Ectopic expression of SUMO-1 in C. elegans) | Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. |
| GSM501248 | C. elegans N2_Y. pestis KIM5_24h_Sample A (GSE20053: C. elegans gene expression in response to Y. pestis KIM5 infection) | The response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h. |
| GSM501268 | C. elegans N2_Y. pestis KIM5_24h_Sample B (GSE20053: C. elegans gene expression in response to Y. pestis KIM5 infection) | The response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h. |
| GSM501269 | C. elegans N2_Y. pestis KIM5_24h_Sample C (GSE20053: C. elegans gene expression in response to Y. pestis KIM5 infection) | The response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h. |
| GSM501270 | C. elegans N2_E. coli OP50_24h_Sample A (GSE20053: C. elegans gene expression in response to Y. pestis KIM5 infection) | The response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h. |
| GSM501271 | C. elegans N2_E. coli OP50_24h_Sample B (GSE20053: C. elegans gene expression in response to Y. pestis KIM5 infection) | The response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h. |
| GSM501272 | C. elegans N2_E. coli OP50_24h_Sample C (GSE20053: C. elegans gene expression in response to Y. pestis KIM5 infection) | The response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h. |
| GSM516621 | N2 vs. mir-243_Replicate1 (GSE20558: Adult Caenorhabditis elegans: wild-type (N2) and mir-243 mutant worms) | Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. |
| GSM516622 | N2 vs. mir-243_Replicate1_dye swap (GSE20558: Adult Caenorhabditis elegans: wild-type (N2) and mir-243 mutant worms) | Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. |
| GSM516623 | N2 vs. mir-243_Replicate2 (GSE20558: Adult Caenorhabditis elegans: wild-type (N2) and mir-243 mutant worms) | Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. |
| GSM516624 | N2 vs. mir-243_Replicate2_dye swap (GSE20558: Adult Caenorhabditis elegans: wild-type (N2) and mir-243 mutant worms) | Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. |
| GSM516625 | N2 vs. mir-243_Replicate3 (GSE20558: Adult Caenorhabditis elegans: wild-type (N2) and mir-243 mutant worms) | Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. |
| GSM516626 | N2 vs. mir-243_Replicate3_dye swap (GSE20558: Adult Caenorhabditis elegans: wild-type (N2) and mir-243 mutant worms) | Transcriptional profiling of N2 vs. mir-243 worms, aiming to identify direct and indirect targets of the microRNA. |
| GSM524942 | Adult C. elegans strain GE-31 control, replicate 4 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524943 | Adult C. elegans strain GE-31 control, replicate 5 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524944 | Adult C. elegans strain GE-31 control, replicate 6 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524945 | Adult C. elegans strain GE-31 control, replicate 7 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524946 | Adult C. elegans strain GE-31 control, replicate 8 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524947 | Adult C. elegans strain GE-31 exposed to 5 mg/L Atrazine, replicate 1 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524948 | Adult C. elegans strain GE-31 exposed to 5 mg/L Atrazine, replicate 2 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524949 | Adult C. elegans strain GE-31 exposed to 5 mg/L Atrazine, replicate 3 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524950 | Adult C. elegans strain GE-31 exposed to 5 mg/L Atrazine, replicate 4 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524951 | Adult C. elegans strain GE-31 exposed to 5 mg/L Atrazine, replicate 5 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524952 | Adult C. elegans strain GE-31 exposed to 25 mg/L Atrazine, replicate 1 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524953 | Adult C. elegans strain GE-31 exposed to 25 mg/L Atrazine, replicate 2 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524954 | Adult C. elegans strain GE-31 exposed to 25 mg/L Atrazine, replicate 3 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524955 | Adult C. elegans strain GE-31 exposed to 25 mg/L Atrazine, replicate 4 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524956 | Adult C. elegans strain GE-31 exposed to 25 mg/L Atrazine, replicate 5 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524957 | Adult C. elegans strain GE-31 exposed to 75 mg/L Atrazine, replicate 1 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524958 | Adult C. elegans strain GE-31 exposed to 75 mg/L Atrazine, replicate 2 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524959 | Adult C. elegans strain GE-31 exposed to 75 mg/L Atrazine, replicate 5 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524960 | Adult C. elegans strain GE-31 exposed to 150 mg/L Atrazine, replicate 1 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524961 | Adult C. elegans strain GE-31 exposed to 150 mg/L Atrazine, replicate 2 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524962 | Adult C. elegans strain GE-31 exposed to 150 mg/L Atrazine, replicate 3 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524963 | Adult C. elegans strain GE-31 exposed to 150 mg/L Atrazine, replicate 4 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524964 | Adult C. elegans strain GE-31 exposed to 150 mg/L Atrazine, replicate 5 (GSE21008: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: atrazine) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to atrazine (AZ). For AZ, the physiological mode of action predicted by DEBtox was increased cost for maintenance. The transcriptional analysis demonstrated that this increase resulted from effects on DNA integrity as indicated by changes in the expression of genes chromosomal repair. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524965 | Adult C. elegans strain GE-31 control, replicate 1 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524966 | Adult C. elegans strain GE-31 control, replicate 2 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524967 | Adult C. elegans strain GE-31 control, replicate 3 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524968 | Adult C. elegans strain GE-31 control, replicate 4b (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524969 | Adult C. elegans strain GE-31 control, replicate 5b (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524970 | Adult C. elegans strain GE-31 exposed to 10 mg/L Cadmium, replicate 1 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524971 | Adult C. elegans strain GE-31 exposed to 10 mg/L Cadmium, replicate 2 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524972 | Adult C. elegans strain GE-31 exposed to 10 mg/L Cadmium, replicate 3 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524973 | Adult C. elegans strain GE-31 exposed to 10 mg/L Cadmium, replicate 4 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524974 | Adult C. elegans strain GE-31 exposed to 20 mg/L Cadmium, replicate 1 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524975 | Adult C. elegans strain GE-31 exposed to 20 mg/L Cadmium, replicate 2 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524976 | Adult C. elegans strain GE-31 exposed to 20 mg/L Cadmium, replicate 3 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524977 | Adult C. elegans strain GE-31 exposed to 20 mg/L Cadmium, replicate 4 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524978 | Adult C. elegans strain GE-31 exposed to 40 mg/L Cadmium, replicate 1 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524979 | Adult C. elegans strain GE-31 exposed to 40 mg/L Cadmium, replicate 2 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524980 | Adult C. elegans strain GE-31 exposed to 40 mg/L Cadmium, replicate 3 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524981 | Adult C. elegans strain GE-31 exposed to 40 mg/L Cadmium, replicate 4 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524982 | Adult C. elegans strain GE-31 exposed to 40 mg/L Cadmium, replicate 5 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524983 | Adult C. elegans strain GE-31 exposed to 60 mg/L Cadmium, replicate 1 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524984 | Adult C. elegans strain GE-31 exposed to 60 mg/L Cadmium, replicate 2 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524985 | Adult C. elegans strain GE-31 exposed to 60 mg/L Cadmium, replicate 3 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524986 | Adult C. elegans strain GE-31 exposed to 60 mg/L Cadmium, replicate 4 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524987 | Adult C. elegans strain GE-31 exposed to 60 mg/L Cadmium, replicate 5 (GSE21010: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: cadmium) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to cadmium. For Cd, the physiological mode of action as indicated by DEBtox model fitting was an effect on energy assimilation from food, suggesting that the transcriptional response to exposure should be dominated by changes in the expression of transcripts associated with energy metabolism and the mitochondria. While evidence for effect on genes associated with energy production were seen, an ontological analysis also indicated an effect of Cd exposure on DNA integrity and transcriptional activity. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524988 | Adult C. elegans strain GE-31 control, replicate 2b (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524989 | Adult C. elegans strain GE-31 control, replicate 3b (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524990 | Adult C. elegans strain GE-31 control, replicate 4c (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524991 | Adult C. elegans strain GE-31 control, replicate 5c (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524992 | Adult C. elegans strain GE-31 control, replicate 6b (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524993 | Adult C. elegans strain GE-31 control, replicate 7b (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524994 | Adult C. elegans strain GE-31 control, replicate 8b (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524995 | Adult C. elegans strain GE-31 exposed to 100 mg/L Fluoranthene, replicate 1 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524996 | Adult C. elegans strain GE-31 exposed to 100 mg/L Fluoranthene, replicate 2 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524997 | Adult C. elegans strain GE-31 exposed to 100 mg/L Fluoranthene, replicate 3 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524998 | Adult C. elegans strain GE-31 exposed to 100 mg/L Fluoranthene, replicate 4 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM524999 | Adult C. elegans strain GE-31 exposed to 250 mg/L Fluoranthene, replicate 1 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525000 | Adult C. elegans strain GE-31 exposed to 250 mg/L Fluoranthene, replicate 2 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525001 | Adult C. elegans strain GE-31 exposed to 250 mg/L Fluoranthene, replicate 3 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525002 | Adult C. elegans strain GE-31 exposed to 250 mg/L Fluoranthene, replicate 4 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525003 | Adult C. elegans strain GE-31 exposed to 250 mg/L Fluoranthene, replicate 5 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525004 | Adult C. elegans strain GE-31 exposed to 500 mg/L Fluoranthene, replicate 1 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525005 | Adult C. elegans strain GE-31 exposed to 500 mg/L Fluoranthene, replicate 2 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525006 | Adult C. elegans strain GE-31 exposed to 500 mg/L Fluoranthene, replicate 3 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525007 | Adult C. elegans strain GE-31 exposed to 500 mg/L Fluoranthene, replicate 4 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525008 | Adult C. elegans strain GE-31 exposed to 500 mg/L Fluoranthene, replicate 5 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525009 | Adult C. elegans strain GE-31 exposed to 1000 mg/L Fluoranthene, replicate 1 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525010 | Adult C. elegans strain GE-31 exposed to 1000 mg/L Fluoranthene, replicate 2 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525011 | Adult C. elegans strain GE-31 exposed to 1000 mg/L Fluoranthene, replicate 3 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525012 | Adult C. elegans strain GE-31 exposed to 1000 mg/L Fluoranthene, replicate 4 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM525013 | Adult C. elegans strain GE-31 exposed to 1000 mg/L Fluoranthene, replicate 5 (GSE21011: Linking toxicant physiological mode of action with induced gene expression changes in Caenorhabditis elegans: fluoranthene) | Physiologically based modelling using DEBtox (dynamic energy budget in toxicology) and transcriptional profiling were used in Caenorhabditis elegans to identify how physiological modes of action, as indicated by effects on system level resource allocation were associated with changes in gene expression following exposure to fluoranthene (FA). DEBtox modelling showed an effect of FA on costs for growth and reproduction (i.e. for production of new and differentiated biomass). The microarray analysis supported this effect, showing an effect of FA on protein integrity and turnover that would be expected to have consequences for rates of somatic growth. Our results have established that outputs from process based models and transcriptomics analyses can help to link mechanisms of action of toxic chemicals with resulting demographic effects. Such complimentary analyses can assist in the categorisation of chemicals for risk assessment purposes. |
| GSM529725 | PVD and OLL neurons, biological rep1 (GSE21162: Expression data from the PVD and OLL neurons in C. elegans) | Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. |
| GSM529726 | PVD and OLL neurons, biological rep2 (GSE21162: Expression data from the PVD and OLL neurons in C. elegans) | Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. |
| GSM529727 | PVD and OLL neurons, biological rep3 (GSE21162: Expression data from the PVD and OLL neurons in C. elegans) | Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. |
| GSM529728 | L3/L4 stage whole animal reference, rep1 (GSE21162: Expression data from the PVD and OLL neurons in C. elegans) | Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. |
| GSM529729 | L3/L4 stage whole animal reference, rep2 (GSE21162: Expression data from the PVD and OLL neurons in C. elegans) | Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. |
| GSM529730 | L3/L4 stage whole animal reference, rep3 (GSE21162: Expression data from the PVD and OLL neurons in C. elegans) | Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. |
| GSM534207 | L1 larvae treated with let-418(RNAi), replicate 3 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534208 | L1 larvae treated with mep-1(RNAi), replicate 3 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534209 | L1 larvae treated with gfp(RNAi), replicate 3 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534210 | L1 larvae treated with let-418(RNAi), replicate 2 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534211 | L1 larvae treated with mep-1(RNAi), replicate 2 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534212 | L1 larvae treated with gfp(RNAi), replicate 2 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534213 | L1 larvae treated with let-418(RNAi), replicate 1 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534214 | L1 larvae treated with mep-1(RNAi), replicate 1 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM534215 | L1 larvae treated with gfp(RNAi), replicate 1 (GSE21376: Developmental Roles of MEC and NuRD Complexes in Caenorhabditis elegans.) | Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself. |
| GSM536248 | ung-1, biological rep1 (GSE21467: Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.) | The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. |
| GSM536249 | ung-1, biological rep2 (GSE21467: Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.) | The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. |
| GSM536250 | ung-1, biological rep3 (GSE21467: Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.) | The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. |
| GSM536251 | wild type N2, biological rep1 (GSE21467: Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.) | The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. |
| GSM536252 | wild type N2, biological rep2 (GSE21467: Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.) | The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. |
| GSM536253 | wild type N2, biological rep3 (GSE21467: Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.) | The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. |
| GSM539007_ci20070213ce_U_01_Input_IP8_65 | Input_1 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539008_ci20070213ce_U_02_Input_IP9_65 | Input_2 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539009_ci20070213ce_U_03_Input_IP10_65 | Input_3 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539010_ci20070213ce_U_04_MYC_IP8_65 | aMYC_1 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539011_ci20070213ce_U_05_MYC_IP9_65 | aMYC_2 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539012_ci20070213ce_U_06_MYC_IP10_65 | aMYC_3 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539013_ci20070213ce_U_07_FLAG_IP8_65 | aFLAG_1 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539014_ci20070213ce_U_08_FLAG_IP9_65 | aFLAG_2 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539015_ci20070213ce_U_09_FLAG_IP10_65 | aFLAG_3 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539016_ci20070530ce_U_03_N2_IP_109 | N2_aFLAG_1 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539017_ci20070530ce_U_07_N2_IP_109 | N2_aFLAG_2 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539018_ci20070530ce_U_11_N2_IP_109 | N2_aFLAG_3 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539019_ci20070530ce_U_04_gld1_gfp_flag_IP_109 | GGF_aFLAG_1 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539020_ci20070530ce_U_08_gld1_gfp_flag_IP_109 | GGF_aFLAG_2 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM539021_ci20070530ce_U_12_gld1_gfp_flag_IP_109 | GGF_aFLAG_3 (GSE21591: RNA immunoprecipitation of GLD-1 followed by microarray analysis of the co-IP'ed mRNAs) | RNA-binding proteins (RBPs) are critical regulators of gene expression and elucidating the interactions of RBPs with their RNA targets is necessary to understand how combinations of RBPs control transcriptome expression. The Quaking-related (QR) sub-family of STAR domain RBPs includes developmental regulators and tumor suppressors such as C. elegans GLD-1, which functions as a master regulator of germ line development. To understand how GLD-1 interacts with the transcriptome, we identified GLD-1 associated mRNAs by a ribonomic approach. The scale of GLD-1 mRNA interactions allowed us to determine rules governing GLD-1 target selection and to derive a predictive model where GLD-1 association with mRNA is based on the number and strength of 7-mer GLD-1 binding elements (GBEs) within UTRs. GLD-1/mRNA interactions were quantified, and predictions were verified both in vitro and in live animals, including by ‘transplantation’ experiments where ‘weak’ and ‘strong’ GBEs imposed translational repression of increasing strength on a non-target mRNA.Importantly, this study provides a unique quantitative picture of how an RBP interacts with its mRNA targets. As combinatorial regulation by multiple RBPs is thought to regulate gene expression, quantification of RBP/mRNA interactions should be a way to predict and potentially modify biological outcomes of complex posttranscriptional regulatory networks, and our analysis suggests that such an approach is possible. |
| GSM542288_C_elegans_ABZ_1 | albendazole exposure, biological rep 1 (GSE21747: Expression data from Caenorhabditis elegans exposed to albendazole) | We have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole; an important anthelmintic for human and animal parasite control. The transcriptional response of the mutant strain CB3474 ben-1(e1880)III, which is highly resistant to benzimidazoles due to a null mutation in the ?-tubulin drug target, was examined. This approach was successful in minimizing transcriptional responses associated with non-specific stress or with the drug mode of action, resulting in only in a small subset of genes showing differential expression in response to drug exposure. |
| GSM542289_C_elegans_ABZ_2 | albendazole exposure, biological rep 2 (GSE21747: Expression data from Caenorhabditis elegans exposed to albendazole) | We have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole; an important anthelmintic for human and animal parasite control. The transcriptional response of the mutant strain CB3474 ben-1(e1880)III, which is highly resistant to benzimidazoles due to a null mutation in the ?-tubulin drug target, was examined. This approach was successful in minimizing transcriptional responses associated with non-specific stress or with the drug mode of action, resulting in only in a small subset of genes showing differential expression in response to drug exposure. |
| GSM542290_C_elegans_ABZ_3 | albendazole exposure, biological rep 3 (GSE21747: Expression data from Caenorhabditis elegans exposed to albendazole) | We have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole; an important anthelmintic for human and animal parasite control. The transcriptional response of the mutant strain CB3474 ben-1(e1880)III, which is highly resistant to benzimidazoles due to a null mutation in the ?-tubulin drug target, was examined. This approach was successful in minimizing transcriptional responses associated with non-specific stress or with the drug mode of action, resulting in only in a small subset of genes showing differential expression in response to drug exposure. |
| GSM542291_C_elegans_CONT_1 | no albendazole exposure, biological rep 1 (GSE21747: Expression data from Caenorhabditis elegans exposed to albendazole) | We have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole; an important anthelmintic for human and animal parasite control. The transcriptional response of the mutant strain CB3474 ben-1(e1880)III, which is highly resistant to benzimidazoles due to a null mutation in the ?-tubulin drug target, was examined. This approach was successful in minimizing transcriptional responses associated with non-specific stress or with the drug mode of action, resulting in only in a small subset of genes showing differential expression in response to drug exposure. |
| GSM542292_C_elegans_CONT_2 | no albendazole exposure, biological rep 2 (GSE21747: Expression data from Caenorhabditis elegans exposed to albendazole) | We have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole; an important anthelmintic for human and animal parasite control. The transcriptional response of the mutant strain CB3474 ben-1(e1880)III, which is highly resistant to benzimidazoles due to a null mutation in the ?-tubulin drug target, was examined. This approach was successful in minimizing transcriptional responses associated with non-specific stress or with the drug mode of action, resulting in only in a small subset of genes showing differential expression in response to drug exposure. |
| GSM542293_C_elegans_CONT_3 | no albendazole exposure, biological rep 3 (GSE21747: Expression data from Caenorhabditis elegans exposed to albendazole) | We have investigated how the model nematode Caenorhabditis elegans responds to and metabolizes albendazole; an important anthelmintic for human and animal parasite control. The transcriptional response of the mutant strain CB3474 ben-1(e1880)III, which is highly resistant to benzimidazoles due to a null mutation in the ?-tubulin drug target, was examined. This approach was successful in minimizing transcriptional responses associated with non-specific stress or with the drug mode of action, resulting in only in a small subset of genes showing differential expression in response to drug exposure. |
| GSM542652_AA049_268N2L4_Celegans_ | L4 larvae, biological rep1 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542653_AA052_272N2L4_Celegans_ | L4 larvae, biological rep2 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542654_AA055_291N2L4_Celegans_ | L4 larvae, biological rep3 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542655_AA050_268N2d6_Celegans_ | day 6 adults, biological rep 1 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542656_AA053_272N2d6_Celegans_ | day 6 adults, biological rep 2 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542657_AA056_291N2d6_Celegans_ | day 6 adults, biological rep 3 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542658_AA051_268N2d15_Celegans_ | day 15 adults, biological rep 1 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542659_AA054_272N2d15_Celegans_ | day 15 adults, biological rep 2 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM542660_AA057_291N2d15_Celegans_ | day 15 adults, biological rep 3 (GSE21784: Genome-wide expression analysis during aging in C. elegans) | Aging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression. |
| GSM543285 | CELEGANS_OP50_8H_REP1 (GSE21819: Caenorhabditis elegans infected with Staphylococcus aureus) | Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions |
| GSM543286 | CELEGANS_OP50_8H_REP2 (GSE21819: Caenorhabditis elegans infected with Staphylococcus aureus) | Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions |
| GSM543287 | CELEGANS_OP50_8H_REP3 (GSE21819: Caenorhabditis elegans infected with Staphylococcus aureus) | Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions |
| GSM543288 | CELEGANS_RN6390_8H_REP1 (GSE21819: Caenorhabditis elegans infected with Staphylococcus aureus) | Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions |
| GSM543289 | CELEGANS_RN6390_8H_REP2 (GSE21819: Caenorhabditis elegans infected with Staphylococcus aureus) | Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions |
| GSM543290 | CELEGANS_RN6390_8H_REP3 (GSE21819: Caenorhabditis elegans infected with Staphylococcus aureus) | Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions |
| GSM543590 | N2 vs ok165 (rep1) (GSE21851: Gene Expression Profiling of C. elegans - ets-4 Mutant Animals Vs Wild-type) | The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals |
| GSM543591 | N2 vs uz1 (rep1) (GSE21851: Gene Expression Profiling of C. elegans - ets-4 Mutant Animals Vs Wild-type) | The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals |
| GSM543592 | N2 vs ok165 (rep2) (GSE21851: Gene Expression Profiling of C. elegans - ets-4 Mutant Animals Vs Wild-type) | The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals |
| GSM543593 | N2 vs uz1 (rep2) (GSE21851: Gene Expression Profiling of C. elegans - ets-4 Mutant Animals Vs Wild-type) | The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals |
| GSM543594 | N2 vs ok165 (rep3) (GSE21851: Gene Expression Profiling of C. elegans - ets-4 Mutant Animals Vs Wild-type) | The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals |
| GSM543595 | N2 vs uz1 (rep3) (GSE21851: Gene Expression Profiling of C. elegans - ets-4 Mutant Animals Vs Wild-type) | The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals |
| GSM562065_C_elegans_IVM100ng_1 | 100ng/ml ivermectin exposure, biological rep 1 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562066_C_elegans_IVM100ng_2 | 100ng/ml ivermectin exposure, biological rep 2 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562067_C_elegans_IVM100ng_3 | 100ng/ml ivermectin exposure, biological rep 3 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562068_C_elegans_IVM100ng_4 | 100ng/ml ivermectin exposure, biological rep 4 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562069_C_elegans_IVM100ng_5 | 100ng/ml ivermectin exposure, biological rep 5 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562070_C_elegans_IVM100ng_CONT_1 | 100ng/ml DMSO control, biological rep 1 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562071_C_elegans_IVM100ng_CONT_2 | 100ng/ml DMSO control, biological rep 2 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562072_C_elegans_IVM100ng_CONT_3 | 100ng/ml DMSO control, biological rep 3 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562073_C_elegans_IVM100ng_CONT_4 | 100ng/ml DMSO control, biological rep 4 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562074_C_elegans_IVM100ng_CONT_5 | 100ng/ml DMSO control, biological rep 5 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562075_C_elegans_IVM1ug_1 | 1ug/ml ivermectin exposure, biological rep 1 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562076_C_elegans_IVM1ug_2 | 1ug/ml ivermectin exposure, biological rep 2 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562077_C_elegans_IVM1ug_3 | 1ug/ml ivermectin exposure, biological rep 3 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562078_C_elegans_IVM1ug_4 | 1ug/ml ivermectin exposure, biological rep 4 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562079_C_elegans_IVM1ug_5 | 1ug/ml ivermectin exposure, biological rep 5 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562080_C_elegans_IVM1ug_CONT_1 | 1ug/ml DMSO control, biological rep 1 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562081_C_elegans_IVM1ug_CONT_2 | 1ug/ml DMSO control, biological rep 2 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562082_C_elegans_IVM1ug_CONT_3 | 1ug/ml DMSO control, biological rep 3 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562083_C_elegans_IVM1ug_CONT_4 | 1ug/ml DMSO control, biological rep 4 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM562084_C_elegans_IVM1ug_CONT_5 | 1ug/ml DMSO control, biological rep 5 (GSE22660: Expression data from Caenorhabditis elegans exposed to ivermectin) | We have investigated the transcriptomic response of the model nematode Caenorhabditis elegans to ivermectin (IVM); an important anthelmintic for human and animal parasite control. The transcriptomic response of the mutant strain DA1316 avr-14(ad1302); avr-15(ad1250); glc-1(pk54), which is highly resistant to ivermectin due to null mutations in three glutamate-gated chloride channel subunits, was examined. Despite the resistant nature of this strain, pharyngeal pumping rate was decreased following 4 hrs exposure to 100ng/ml and 1?g/ml ivermectin resulting in significant change in the expression level of genes associated with a fasting response. |
| GSM567790 | young adult_not exposed_rep1 (GSE24923: mRNA microarray analysis on young adult Caenorhabditis elegans, Drosophila melanogaster, and Danio rerio exposed to benzene, toluene, and formaldehyde) | This SuperSeries is composed of the SubSeries listed below. |
| GSM567791 | young adult_24hr Benzene exposure_rep1 (GSE24923: mRNA microarray analysis on young adult Caenorhabditis elegans, Drosophila melanogaster, and Danio rerio exposed to benzene, toluene, and formaldehyde) | This SuperSeries is composed of the SubSeries listed below. |
| GSM567792 | young adult_24hr Toluene exposure_rep1 (GSE24923: mRNA microarray analysis on young adult Caenorhabditis elegans, Drosophila melanogaster, and Danio rerio exposed to benzene, toluene, and formaldehyde) | This SuperSeries is composed of the SubSeries listed below. |
| GSM567793 | young adult_24hr Formaldehyde exposure_rep1 (GSE24923: mRNA microarray analysis on young adult Caenorhabditis elegans, Drosophila melanogaster, and Danio rerio exposed to benzene, toluene, and formaldehyde) | This SuperSeries is composed of the SubSeries listed below. |
| GSM567794 | young adult_24hr BTF mix exposure_rep1 (GSE24923: mRNA microarray analysis on young adult Caenorhabditis elegans, Drosophila melanogaster, and Danio rerio exposed to benzene, toluene, and formaldehyde) | This SuperSeries is composed of the SubSeries listed below. |
| GSM575204 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #1 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575205 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #2 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575206 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #3 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575207 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #4 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575208 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #5 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575209 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #6 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575210 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #8 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575211 | sma-2;fem-1 oocyte D8 vs fem-1 oocyte D8 array #9 SL2.6.09 (GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte) | To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. |
| GSM575212 | sma-2x3 L4 vs N2 L4 #1 WS 4.6.07 (GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4) | To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans. |
| GSM575213 | N2 L4 v sma-2x3 L4 #2 DF WS 4.6.07 (GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4) | To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans. |
| GSM575214 | sma-2x3 L4 v N2 L4 #3 WS 4.6.07 (GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4) | To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans. |
| GSM575215 | sma-4(e729) L4 v N2 L4 #1 WS 4.10.7 (GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4) | To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans. |
| GSM575216 | fem-1 oocyte D3 vs fem-1 oocyte D8 array #3 SL9.13.08 (GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte) | To find genes in C. elegans oocytes associated with reproductive aging. |
| GSM575217 | fem-1 oocyte D3 vs fem-1 oocyte D8 array #5 SL12.02.08 (GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte) | To find genes in C. elegans oocytes associated with reproductive aging. |
| GSM575218 | fem-1 oocyte D3 vs fem-1 oocyte D8 array #6 SL12.02.08 (GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte) | To find genes in C. elegans oocytes associated with reproductive aging. |
| GSM575219 | fem-1 oocyte D3 vs fem-1 oocyte D8 array #7 SL12.02.08 (GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte) | To find genes in C. elegans oocytes associated with reproductive aging. |
| GSM575220 | fem-1 oocyte D3 vs fem-1 oocyte D8 array #8 SL12.02.08 (GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte) | To find genes in C. elegans oocytes associated with reproductive aging. |
| GSM587853_GLD_2_wt_IP_1 | GLD-2 wt-IP, biological replicate 1 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587854_GLD_2_wt_IP_2 | GLD-2 wt-IP, biological replicate 2 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587855_GLD_2_wt_IP_3 | GLD-2 wt-IP, biological replicate 3 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587856_GLD_2_wt_IP_4 | GLD-2 wt-IP, biological replicate 4 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587857_GLD_2_gld_2_RNAi__IP_1 | GLD-2 gld-2(RNAi)-IP, biological replicate 1 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587858_GLD_2_gld_2_RNAi__IP_2 | GLD-2 gld-2(RNAi)-IP, biological replicate 2 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587859_GLD_2_gld_2_RNAi__IP_3 | GLD-2 gld-2(RNAi)-IP, biological replicate 3 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587860_GLD_2_gld_2_RNAi__IP_4 | GLD-2 gld-2(RNAi)-IP, biological replicate 4 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587861_RNP_8_wt_IP_1 | RNP-8 wt-IP, biological replicate 1 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587862_RNP_8_wt_IP_2 | RNP-8 wt-IP, biological replicate 2 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587863_RNP_8_wt_IP_3 | RNP-8 wt-IP, biological replicate 3 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587864_RNP_8_rnp_8_q784__IP_1 | RNP-8 rnp-8(q784)-IP, biological replicate 1 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587865_RNP_8_rnp_8_q784__IP_2 | RNP-8 rnp-8(q784)-IP, biological replicate 2 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587866_RNP_8_rnp_8_q784__IP_3 | RNP-8 rnp-8(q784)-IP, biological replicate 3 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587867_wild_type_total_RNA_1 | wild-type total RNA, biological replicate 1 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587868_wild_type_total_RNA_2 | wild-type total RNA, biological replicate 2 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587869_wild_type_total_RNA_3 | wild-type total RNA, biological replicate 3 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587870_wild_type_total_RNA_4 | wild-type total RNA, biological replicate 4 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587871_gld_2_RNAi_total_RNA_1 | gld-2(RNAi), biological replicate 1 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587872_gld_2_RNAi_total_RNA_2 | gld-2(RNAi), biological replicate 2 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM587873_gld_2_RNAi_total_RNA_3 | gld-2(RNAi), biological replicate 3 (GSE23843: RIP-chip analysis of the C. elegans GLD-2 and RNP-8 protein) | C. elegans GLD-2 forms an active PAP with multiple RNA-binding partners to regulate diverse aspects of germline and early embryonic development. One GLD-2 partner, RNP-8, was previously shown to influence oocyte fate specification. To identify transcripts selectively associated with both GLD-2 and RNP-8, we employ a genomic approach using the method of RNA immunoprecipitation followed by microarray analysis (RIP-chip). We used microarrays to identify mRNAs selectively associated with either GLD-2 or RNP-8. |
| GSM588088 | Strain QX1 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588089 | Strain QX194 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588090 | Strain QX195 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588091 | Strain QX197 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588092 | Strain QX199 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588093 | Strain QX200 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588094 | Strain QX202 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588095 | Strain QX203 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588096 | Strain QX204 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588097 | Strain QX209 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588098 | Strain QX20 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588099 | Strain QX21 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588100 | Strain QX212 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588101 | Strain QX213 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588102 | Strain QX216 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588103 | Strain QX217 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588104 | Strain QX220 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588105 | Strain QX222 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588106 | Strain QX223 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588107 | Strain QX224 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588108 | Strain QX226 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588109 | Strain QX227 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588110 | Strain QX228 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588111 | Strain QX233 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588112 | Strain QX235 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588113 | Strain QX25 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588114 | Strain QX26 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588115 | Strain QX28 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588116 | Strain QX29 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588117 | Strain QX30 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588118 | Strain QX31 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588119 | Strain QX32 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588120 | Strain QX33 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588121 | Strain QX37 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588122 | Strain QX3 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588123 | Strain QX41 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588124 | Strain QX44 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588125 | Strain QX45 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588126 | Strain QX47 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588127 | Strain QX48 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588128 | Strain QX51 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588129 | Strain QX52 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588130 | Strain QX53 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588131 | Strain QX56 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588132 | Strain QX4 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588133 | Strain QX58 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588134 | Strain QX60 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588135 | Strain QX64 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588136 | Strain QX65 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588137 | Strain QX66 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588138 | Strain QX67 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588139 | Strain QX68 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588140 | Strain QX69 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588141 | Strain QX70 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588142 | Strain QX72 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588143 | Strain QX74 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588144 | Strain QX6 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588145 | Strain QX81 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588146 | Strain QX82 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588147 | Strain QX83 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588148 | Strain QX85 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588149 | Strain QX86 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588150 | Strain QX87 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588151 | Strain QX88 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588152 | Strain QX90 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588153 | Strain QX91 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588154 | Strain QX93 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588155 | Strain QX94 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588156 | Strain QX98 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588157 | Strain QX103 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588158 | Strain QX107 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588159 | Strain QX108 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588160 | Strain QX111 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588161 | Strain QX113 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588162 | Strain QX115 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588163 | Strain QX11 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588164 | Strain QX119 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588165 | Strain QX120 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588166 | Strain QX121 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588167 | Strain QX128 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588168 | Strain QX132 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588169 | Strain QX134 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588170 | Strain QX13 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588171 | Strain QX135 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588172 | Strain QX136 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588173 | Strain QX140 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588174 | Strain QX141 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588175 | Strain QX142 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588176 | Strain QX144 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588177 | Strain QX145 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588178 | Strain QX148 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588179 | Strain QX150 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588180 | Strain QX151 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588181 | Strain QX154 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588182 | Strain QX15 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588183 | Strain QX158 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588184 | Strain QX159 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588185 | Strain QX161 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588186 | Strain QX162 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588187 | Strain QX164 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588188 | Strain QX165 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588189 | Strain QX166 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588190 | Strain QX167 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588191 | Strain QX168 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588192 | Strain QX169 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588193 | Strain QX170 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588194 | Strain QX172 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588195 | Strain QX174 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588196 | Strain QX16 (Cy5) vs Common Reference (Cy3) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588197 | Strain QX19 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588198 | Strain QX196 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588199 | Strain QX198 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588200 | Strain QX205 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588201 | Strain QX206 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588202 | Strain QX207 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588203 | Strain QX208 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588204 | Strain QX210 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588205 | Strain QX211 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588206 | Strain QX214 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588207 | Strain QX215 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588208 | Strain QX218 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588209 | Strain QX221 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588210 | Strain QX22 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588211 | Strain QX225 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588212 | Strain QX229 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588213 | Strain QX230 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588214 | Strain QX231 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588215 | Strain QX232 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588216 | Strain QX234 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588217 | Strain QX236 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588218 | Strain QX24 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588219 | Strain QX237 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588220 | Strain QX27 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588221 | Strain QX34 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588222 | Strain QX38 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588223 | Strain QX2 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588224 | Strain QX39 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588225 | Strain QX40 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588226 | Strain QX42 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588227 | Strain QX43 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588228 | Strain QX49 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588229 | Strain QX54 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588230 | Strain QX55 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588231 | Strain QX5 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588232 | Strain QX59 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588233 | Strain QX61 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588234 | Strain QX62 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588235 | Strain QX63 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588236 | Strain QX71 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588237 | Strain QX73 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588238 | Strain QX76 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588239 | Strain QX77 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588240 | Strain QX7 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588241 | Strain QX78 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588242 | Strain QX79 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588243 | Strain QX80 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588244 | Strain QX84 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588245 | Strain QX92 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588246 | Strain QX95 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588247 | Strain QX8 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588248 | Strain QX9 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588249 | Strain QX96 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588250 | Strain QX97 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588251 | Strain QX99 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588252 | Strain QX100 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588253 | Strain QX101 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588254 | Strain QX102 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588255 | Strain QX104 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588256 | Strain QX106 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588257 | Strain QX109 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588258 | Strain QX112 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588259 | Strain QX114 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588260 | Strain QX10 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588261 | Strain QX117 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588262 | Strain QX124 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588263 | Strain QX125 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588264 | Strain QX127 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588265 | Strain QX129 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588266 | Strain QX131 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588267 | Strain QX133 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588268 | Strain QX12 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588269 | Strain QX137 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588270 | Strain QX138 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588271 | Strain QX139 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588272 | Strain QX143 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588273 | Strain QX147 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588274 | Strain QX149 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588275 | Strain QX153 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588276 | Strain QX14 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588277 | Strain QX156 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588278 | Strain QX157 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588279 | Strain QX160 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588280 | Strain QX163 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588281 | Strain QX171 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588282 | Strain QX173 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588283 | Strain QX177 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588284 | Strain QX178 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588285 | Strain QX179 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588286 | Strain QX180 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588287 | Strain QX181 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588288 | Strain QX182 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588289 | Strain QX183 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588290 | Strain QX184 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588291 | Strain QX185 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588292 | Strain QX187 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588293 | Strain QX189 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588294 | Strain QX192 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM588295 | Strain QX193 (Cy3) vs Common Reference (Cy5) (GSE23857: QX recombinant inbred advanced intercross lines of C. elegans) | Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, while mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTL) influencing transcript abundance traits in a cross of two C. elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci. |
| GSM627440 | WT (1) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627441 | WT (2) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627442 | WT (3) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627443 | crh-1 null (1) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627444 | crh-1 null (2) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627445 | crh-1 null (3) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627446 | tax-6 null (1) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627447 | tax-6 null (2) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627448 | tax-6 null (3) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627449 | aak-2 o/e (1) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627450 | aak-2 o/e (2) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627451 | aak-2 o/e (3) (GSE25513: AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB) | AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. |
| GSM627491_3X_D1 | daf-19,daf-12#1 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627492_3X_D2 | daf-19,daf-12#2 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627493_3X_D3 | daf-19,daf-12#3 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627494_3X_D4 | daf-19,daf-12#4 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627495_3X_S1 | daf-12#1 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627496_3X_S2 | daf-12#2 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627497_3X_S3 | daf-12#3 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627498_3X_S4 | daf-12#4 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627499_3X_WT1 | WT#1 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627500_3X_WT2 | WT#2 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627501_3X_WT3 | WT#3 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM627502_3X_WT4 | WT#4 (GSE25633: Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport.) | Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. |
| GSM62934 | C. elegans_1_1 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62935 | C. elegans_1_2 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62936 | C. elegans_1_3 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62937 | C. elegans_1_4 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62938 | C. elegans_2-1 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62939 | C. elegans_2_2 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62940 | C. elegans_2_3 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62941 | C. elegans_2_4 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62942 | C. elegans_3_1 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62943 | C. elegans_2_2 (2) (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62944 | C. elegans_3_3 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM62945 | C. elegans_3_4 (GSE2862: Twist Heat Shock in C. elegans) | Three biological replicates of each treatment were generated and the expression profiles were determined using Affymetrix C. elegans arrays. Comparisons between the sample groups allow the identification of genes expression patterns. Keywords: repeat |
| GSM631538 | Hpl1_KO_Mutant_Replicate1 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631539 | Hpl1_KO_Mutant_Replicate2 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631540 | Hpl2_KO_Mutant_Replicate1 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631541 | Hpl2_KO_Mutant_Replicate2 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631542 | His24_KO_Mutant_Replicate1 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631543 | His24_KO_Mutant_Replicate2 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631544 | WildType_Replicate1 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631545 | WildType_Replicate2 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631546 | WildType_Replicate3 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM631547 | WildType_Replicate4 (GSE25714: Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response) | Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. |
| GSM634543 | WT_fedL1_rep1 (GSE25834: An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression) | This SuperSeries is composed of the SubSeries listed below. |
| GSM634544 | WT_fedL1_rep2 (GSE25834: An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression) | This SuperSeries is composed of the SubSeries listed below. |
| GSM634545 | WT_fedL1_rep3 (GSE25834: An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression) | This SuperSeries is composed of the SubSeries listed below. |
| GSM635241 | mixed embryo XX_WT-N_080307_A (GSE25834: An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression) | This SuperSeries is composed of the SubSeries listed below. |
| GSM635242 | mixed embryo XX_WT-N_080307_B (GSE25834: An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression) | This SuperSeries is composed of the SubSeries listed below. |
| GSM635243 | mixed embryo XX_WT-N_080307_C (GSE25834: An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression) | This SuperSeries is composed of the SubSeries listed below. |
| GSM640611 | Control 1 (GSE26094: Life span-extending effects of royal jelly and its related substances on the nematode Caenorhabditis elegans) | One of the most important issues in the study of aging is to discover compounds with longevity-promoting activity and to unravel their underlying mechanisms. Queen honey bees are continuously fed royal jelly (RJ), and they live more than 10 times longer than hive workers, derived from the same diploid genome, which are fed it only for a short period of time during their larval stages. Therefore, RJ is likely to contain longevity-promoting agents for queens. RJ has been reported to possess diverse pharmacological properties. Furthermore, protease-treated RJ (pRJ) has additional beneficial activities. How RJ and pRJ exert these effects and which components in them play a critical role is largely unknown. The evolutionally conserved mechanisms that control lifespan have been indicated. The nematode Caenorhabditis elegans has been widely used for study of aging and longevity, due to its relatively short lifespan and well-established genetic pathways. The purpose of the present study was to elucidate whether RJ and its related substances contain the life span-extending activity in C. elegans and to obtain some insight into the active agents and their mechanisms. We found that both RJ and pRJ extended the lifespan of C. elegans. The life span-extending activity of pRJ was enriched by ODS column chromatography (pRJ-Fraction 5). pRJ-Fr. 5 extended the life span partly by acting through the FOXO transcription factor DAF-16, the activation of which is known to promote longevity in C. elegans by reducing insulin/IGF-1 signaling (IIS). pRJ-Fr. 5 induced changes in the expression of 3 genes encoding insulin-like peptides. Moreover, pRJ-Fr. 5 and reduced IIS shared some common features in terms of their effect on gene expression, such as up-regulation of dod-3 and down-regulation of dod-19, dao-4 and fkb-4. The dod-19 is a previously identified life span determinant in C. elegans, and the fkb-4 encodes a homologue of the mammalian FK506-binding protein. 10-Hydroxy-2-decenoic acid (10-HDA), which was present in high concentration in pRJ-Fr. 5, increased the lifespan independently of DAF-16 activity.These results demonstrate that RJ and its related substances extended the life span in C. elegans, suggesting that RJ may contain longevity-promoting factors common to diverse species across phyla. pRJ-Fr. 5 had higher life span-extending activity than either RJ or pRJ and extended the life span in part through the IIS-DAF-16 pathway. We provide the first evidence that 10-HDA, a defined natural product in RJ, extended organismal lifespan. It is noteworthy that 10-HDA performed its lifespan-extending function through a mechanism totally different from the IIS-DAF-16 pathway. Further search and characterization of the lifespan-extending agents in RJ and pRJ may broaden our understanding of the gene network of longevity regulation in diverse species and provide the possibility for nutraceutical interventions in the aging process. |
| GSM640612 | Control 2 (GSE26094: Life span-extending effects of royal jelly and its related substances on the nematode Caenorhabditis elegans) | One of the most important issues in the study of aging is to discover compounds with longevity-promoting activity and to unravel their underlying mechanisms. Queen honey bees are continuously fed royal jelly (RJ), and they live more than 10 times longer than hive workers, derived from the same diploid genome, which are fed it only for a short period of time during their larval stages. Therefore, RJ is likely to contain longevity-promoting agents for queens. RJ has been reported to possess diverse pharmacological properties. Furthermore, protease-treated RJ (pRJ) has additional beneficial activities. How RJ and pRJ exert these effects and which components in them play a critical role is largely unknown. The evolutionally conserved mechanisms that control lifespan have been indicated. The nematode Caenorhabditis elegans has been widely used for study of aging and longevity, due to its relatively short lifespan and well-established genetic pathways. The purpose of the present study was to elucidate whether RJ and its related substances contain the life span-extending activity in C. elegans and to obtain some insight into the active agents and their mechanisms. We found that both RJ and pRJ extended the lifespan of C. elegans. The life span-extending activity of pRJ was enriched by ODS column chromatography (pRJ-Fraction 5). pRJ-Fr. 5 extended the life span partly by acting through the FOXO transcription factor DAF-16, the activation of which is known to promote longevity in C. elegans by reducing insulin/IGF-1 signaling (IIS). pRJ-Fr. 5 induced changes in the expression of 3 genes encoding insulin-like peptides. Moreover, pRJ-Fr. 5 and reduced IIS shared some common features in terms of their effect on gene expression, such as up-regulation of dod-3 and down-regulation of dod-19, dao-4 and fkb-4. The dod-19 is a previously identified life span determinant in C. elegans, and the fkb-4 encodes a homologue of the mammalian FK506-binding protein. 10-Hydroxy-2-decenoic acid (10-HDA), which was present in high concentration in pRJ-Fr. 5, increased the lifespan independently of DAF-16 activity.These results demonstrate that RJ and its related substances extended the life span in C. elegans, suggesting that RJ may contain longevity-promoting factors common to diverse species across phyla. pRJ-Fr. 5 had higher life span-extending activity than either RJ or pRJ and extended the life span in part through the IIS-DAF-16 pathway. We provide the first evidence that 10-HDA, a defined natural product in RJ, extended organismal lifespan. It is noteworthy that 10-HDA performed its lifespan-extending function through a mechanism totally different from the IIS-DAF-16 pathway. Further search and characterization of the lifespan-extending agents in RJ and pRJ may broaden our understanding of the gene network of longevity regulation in diverse species and provide the possibility for nutraceutical interventions in the aging process. |
| GSM640613 | Control 3 (GSE26094: Life span-extending effects of royal jelly and its related substances on the nematode Caenorhabditis elegans) | One of the most important issues in the study of aging is to discover compounds with longevity-promoting activity and to unravel their underlying mechanisms. Queen honey bees are continuously fed royal jelly (RJ), and they live more than 10 times longer than hive workers, derived from the same diploid genome, which are fed it only for a short period of time during their larval stages. Therefore, RJ is likely to contain longevity-promoting agents for queens. RJ has been reported to possess diverse pharmacological properties. Furthermore, protease-treated RJ (pRJ) has additional beneficial activities. How RJ and pRJ exert these effects and which components in them play a critical role is largely unknown. The evolutionally conserved mechanisms that control lifespan have been indicated. The nematode Caenorhabditis elegans has been widely used for study of aging and longevity, due to its relatively short lifespan and well-established genetic pathways. The purpose of the present study was to elucidate whether RJ and its related substances contain the life span-extending activity in C. elegans and to obtain some insight into the active agents and their mechanisms. We found that both RJ and pRJ extended the lifespan of C. elegans. The life span-extending activity of pRJ was enriched by ODS column chromatography (pRJ-Fraction 5). pRJ-Fr. 5 extended the life span partly by acting through the FOXO transcription factor DAF-16, the activation of which is known to promote longevity in C. elegans by reducing insulin/IGF-1 signaling (IIS). pRJ-Fr. 5 induced changes in the expression of 3 genes encoding insulin-like peptides. Moreover, pRJ-Fr. 5 and reduced IIS shared some common features in terms of their effect on gene expression, such as up-regulation of dod-3 and down-regulation of dod-19, dao-4 and fkb-4. The dod-19 is a previously identified life span determinant in C. elegans, and the fkb-4 encodes a homologue of the mammalian FK506-binding protein. 10-Hydroxy-2-decenoic acid (10-HDA), which was present in high concentration in pRJ-Fr. 5, increased the lifespan independently of DAF-16 activity.These results demonstrate that RJ and its related substances extended the life span in C. elegans, suggesting that RJ may contain longevity-promoting factors common to diverse species across phyla. pRJ-Fr. 5 had higher life span-extending activity than either RJ or pRJ and extended the life span in part through the IIS-DAF-16 pathway. We provide the first evidence that 10-HDA, a defined natural product in RJ, extended organismal lifespan. It is noteworthy that 10-HDA performed its lifespan-extending function through a mechanism totally different from the IIS-DAF-16 pathway. Further search and characterization of the lifespan-extending agents in RJ and pRJ may broaden our understanding of the gene network of longevity regulation in diverse species and provide the possibility for nutraceutical interventions in the aging process. |
| GSM640614 | pRJ-FR. 5 fed 1 (GSE26094: Life span-extending effects of royal jelly and its related substances on the nematode Caenorhabditis elegans) | One of the most important issues in the study of aging is to discover compounds with longevity-promoting activity and to unravel their underlying mechanisms. Queen honey bees are continuously fed royal jelly (RJ), and they live more than 10 times longer than hive workers, derived from the same diploid genome, which are fed it only for a short period of time during their larval stages. Therefore, RJ is likely to contain longevity-promoting agents for queens. RJ has been reported to possess diverse pharmacological properties. Furthermore, protease-treated RJ (pRJ) has additional beneficial activities. How RJ and pRJ exert these effects and which components in them play a critical role is largely unknown. The evolutionally conserved mechanisms that control lifespan have been indicated. The nematode Caenorhabditis elegans has been widely used for study of aging and longevity, due to its relatively short lifespan and well-established genetic pathways. The purpose of the present study was to elucidate whether RJ and its related substances contain the life span-extending activity in C. elegans and to obtain some insight into the active agents and their mechanisms. We found that both RJ and pRJ extended the lifespan of C. elegans. The life span-extending activity of pRJ was enriched by ODS column chromatography (pRJ-Fraction 5). pRJ-Fr. 5 extended the life span partly by acting through the FOXO transcription factor DAF-16, the activation of which is known to promote longevity in C. elegans by reducing insulin/IGF-1 signaling (IIS). pRJ-Fr. 5 induced changes in the expression of 3 genes encoding insulin-like peptides. Moreover, pRJ-Fr. 5 and reduced IIS shared some common features in terms of their effect on gene expression, such as up-regulation of dod-3 and down-regulation of dod-19, dao-4 and fkb-4. The dod-19 is a previously identified life span determinant in C. elegans, and the fkb-4 encodes a homologue of the mammalian FK506-binding protein. 10-Hydroxy-2-decenoic acid (10-HDA), which was present in high concentration in pRJ-Fr. 5, increased the lifespan independently of DAF-16 activity.These results demonstrate that RJ and its related substances extended the life span in C. elegans, suggesting that RJ may contain longevity-promoting factors common to diverse species across phyla. pRJ-Fr. 5 had higher life span-extending activity than either RJ or pRJ and extended the life span in part through the IIS-DAF-16 pathway. We provide the first evidence that 10-HDA, a defined natural product in RJ, extended organismal lifespan. It is noteworthy that 10-HDA performed its lifespan-extending function through a mechanism totally different from the IIS-DAF-16 pathway. Further search and characterization of the lifespan-extending agents in RJ and pRJ may broaden our understanding of the gene network of longevity regulation in diverse species and provide the possibility for nutraceutical interventions in the aging process. |
| GSM640615 | pRJ-FR. 5 fed 2 (GSE26094: Life span-extending effects of royal jelly and its related substances on the nematode Caenorhabditis elegans) | One of the most important issues in the study of aging is to discover compounds with longevity-promoting activity and to unravel their underlying mechanisms. Queen honey bees are continuously fed royal jelly (RJ), and they live more than 10 times longer than hive workers, derived from the same diploid genome, which are fed it only for a short period of time during their larval stages. Therefore, RJ is likely to contain longevity-promoting agents for queens. RJ has been reported to possess diverse pharmacological properties. Furthermore, protease-treated RJ (pRJ) has additional beneficial activities. How RJ and pRJ exert these effects and which components in them play a critical role is largely unknown. The evolutionally conserved mechanisms that control lifespan have been indicated. The nematode Caenorhabditis elegans has been widely used for study of aging and longevity, due to its relatively short lifespan and well-established genetic pathways. The purpose of the present study was to elucidate whether RJ and its related substances contain the life span-extending activity in C. elegans and to obtain some insight into the active agents and their mechanisms. We found that both RJ and pRJ extended the lifespan of C. elegans. The life span-extending activity of pRJ was enriched by ODS column chromatography (pRJ-Fraction 5). pRJ-Fr. 5 extended the life span partly by acting through the FOXO transcription factor DAF-16, the activation of which is known to promote longevity in C. elegans by reducing insulin/IGF-1 signaling (IIS). pRJ-Fr. 5 induced changes in the expression of 3 genes encoding insulin-like peptides. Moreover, pRJ-Fr. 5 and reduced IIS shared some common features in terms of their effect on gene expression, such as up-regulation of dod-3 and down-regulation of dod-19, dao-4 and fkb-4. The dod-19 is a previously identified life span determinant in C. elegans, and the fkb-4 encodes a homologue of the mammalian FK506-binding protein. 10-Hydroxy-2-decenoic acid (10-HDA), which was present in high concentration in pRJ-Fr. 5, increased the lifespan independently of DAF-16 activity.These results demonstrate that RJ and its related substances extended the life span in C. elegans, suggesting that RJ may contain longevity-promoting factors common to diverse species across phyla. pRJ-Fr. 5 had higher life span-extending activity than either RJ or pRJ and extended the life span in part through the IIS-DAF-16 pathway. We provide the first evidence that 10-HDA, a defined natural product in RJ, extended organismal lifespan. It is noteworthy that 10-HDA performed its lifespan-extending function through a mechanism totally different from the IIS-DAF-16 pathway. Further search and characterization of the lifespan-extending agents in RJ and pRJ may broaden our understanding of the gene network of longevity regulation in diverse species and provide the possibility for nutraceutical interventions in the aging process. |
| GSM640616 | pRJ-FR. 5 fed 3 (GSE26094: Life span-extending effects of royal jelly and its related substances on the nematode Caenorhabditis elegans) | One of the most important issues in the study of aging is to discover compounds with longevity-promoting activity and to unravel their underlying mechanisms. Queen honey bees are continuously fed royal jelly (RJ), and they live more than 10 times longer than hive workers, derived from the same diploid genome, which are fed it only for a short period of time during their larval stages. Therefore, RJ is likely to contain longevity-promoting agents for queens. RJ has been reported to possess diverse pharmacological properties. Furthermore, protease-treated RJ (pRJ) has additional beneficial activities. How RJ and pRJ exert these effects and which components in them play a critical role is largely unknown. The evolutionally conserved mechanisms that control lifespan have been indicated. The nematode Caenorhabditis elegans has been widely used for study of aging and longevity, due to its relatively short lifespan and well-established genetic pathways. The purpose of the present study was to elucidate whether RJ and its related substances contain the life span-extending activity in C. elegans and to obtain some insight into the active agents and their mechanisms. We found that both RJ and pRJ extended the lifespan of C. elegans. The life span-extending activity of pRJ was enriched by ODS column chromatography (pRJ-Fraction 5). pRJ-Fr. 5 extended the life span partly by acting through the FOXO transcription factor DAF-16, the activation of which is known to promote longevity in C. elegans by reducing insulin/IGF-1 signaling (IIS). pRJ-Fr. 5 induced changes in the expression of 3 genes encoding insulin-like peptides. Moreover, pRJ-Fr. 5 and reduced IIS shared some common features in terms of their effect on gene expression, such as up-regulation of dod-3 and down-regulation of dod-19, dao-4 and fkb-4. The dod-19 is a previously identified life span determinant in C. elegans, and the fkb-4 encodes a homologue of the mammalian FK506-binding protein. 10-Hydroxy-2-decenoic acid (10-HDA), which was present in high concentration in pRJ-Fr. 5, increased the lifespan independently of DAF-16 activity.These results demonstrate that RJ and its related substances extended the life span in C. elegans, suggesting that RJ may contain longevity-promoting factors common to diverse species across phyla. pRJ-Fr. 5 had higher life span-extending activity than either RJ or pRJ and extended the life span in part through the IIS-DAF-16 pathway. We provide the first evidence that 10-HDA, a defined natural product in RJ, extended organismal lifespan. It is noteworthy that 10-HDA performed its lifespan-extending function through a mechanism totally different from the IIS-DAF-16 pathway. Further search and characterization of the lifespan-extending agents in RJ and pRJ may broaden our understanding of the gene network of longevity regulation in diverse species and provide the possibility for nutraceutical interventions in the aging process. |
| GSM64838 | wild-type (red, channel 2) vs. VHL mutant (ok161) (green, channel 1) (GSE2963: Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans) | The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways that are distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Bishop T, Lau KW, Epstein AC, Kim SK, Jiang M, O'rourke D, Pugh CW, Gleadle JM, Taylor MS, Hodgkin J, Ratcliffe PJ, Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans., Bishop T, et al. (2004) PLoS Biol 2(10):e289, 2004-10-01, http://biology.plosjournals.org/plosonline/?request=get-document&doi=10.1371/journal.pbio.0020289 Keywords: Logical Set |
| GSM64839 | hif-1 (red, channel 2) vs.hif-1; vhl-1 (green, channel 1) repeat no. 1 (GSE2963: Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans) | The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways that are distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Bishop T, Lau KW, Epstein AC, Kim SK, Jiang M, O'rourke D, Pugh CW, Gleadle JM, Taylor MS, Hodgkin J, Ratcliffe PJ, Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans., Bishop T, et al. (2004) PLoS Biol 2(10):e289, 2004-10-01, http://biology.plosjournals.org/plosonline/?request=get-document&doi=10.1371/journal.pbio.0020289 Keywords: Logical Set |
| GSM64840 | hif-1 (red, channel 2) vs. hif-1; vhl-1 (green, channel 1) repeat no. 2 (GSE2963: Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans) | The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways that are distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Bishop T, Lau KW, Epstein AC, Kim SK, Jiang M, O'rourke D, Pugh CW, Gleadle JM, Taylor MS, Hodgkin J, Ratcliffe PJ, Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans., Bishop T, et al. (2004) PLoS Biol 2(10):e289, 2004-10-01, http://biology.plosjournals.org/plosonline/?request=get-document&doi=10.1371/journal.pbio.0020289 Keywords: Logical Set |
| GSM64841 | hif-1 (red, channel 2) vs. hif-1; vhl-1 (green, channel 1) repeat no. 3 (GSE2963: Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans) | The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways that are distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Bishop T, Lau KW, Epstein AC, Kim SK, Jiang M, O'rourke D, Pugh CW, Gleadle JM, Taylor MS, Hodgkin J, Ratcliffe PJ, Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans., Bishop T, et al. (2004) PLoS Biol 2(10):e289, 2004-10-01, http://biology.plosjournals.org/plosonline/?request=get-document&doi=10.1371/journal.pbio.0020289 Keywords: Logical Set |
| GSM64906 | N2 control #1 (red, channel 2) vs. testosterone 10e-09 (green, channel 1) (GSE2970: Caenorhabditis elegans as an environmental monitor using DNA microarray analysis.) | In order to assist in the identification of possible endocrine disrupting chemicals (EDC) in groundwater, we are developing Caenorhabolitis elegans as a high throughput bioassay system in which responses to EDC may be detected by gene expression using DNA microarray analysis. As a first step we examined gene expression patterns and vitellogenin responses of this organism to vertebrate steroids, in liquid culture. Western blotting showed the expected number and size of vitellogenin translation products after estrogen exposure. At 10(-9) M, vitellogenin decreased, but at 10(-7) and 10(-5), vitellogenin was increased. Testosterone (10(-5) M) increased the synthesis of vitellogenin, but progesterone-treated cultures (10(-5) M) had less vitellogenin. Using DNA microarray analysis, we examined the pattern of gene expression after progesterone (10(-5), 10(-7), and 10(-9) M), estrogen (10(-5) M), and testosterone (10(-9) M) exposure, with special attention to the traditional biomarker genes used in environmental studies [vitellogenin, cytochrome P450 (CYP), glutathione s-transferase (GST), metallothionein (MT), and heat shock proteins (HSP)]. GST and P450 genes were affected by estrogen (10(-5) M) and progesterone (10(-5) and 10(-7) M) treatments. For vitellogenin genes, estrogen treatment (10(-5) M) caused overexpression of the vit-2 and vit-6 genes (2.68 and 3.25 times, respectively). After progesterone treatment (10(-7) M), the vit-5 and vit-6 were down-regulated and vit-1 up-regulated (3.59-fold). Concentrations of testosterone and progesterone at 10(-9) M did not influence the expression of the vit, CYP, or GST genes. Although the analysis is incomplete, and low doses and combinations of EDC need to be tested, these preliminary results indicate C. elegans may be a useful laboratory and field model for screening EDC. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM64907 | N2 control #1 (red, channel 2) vs. progesterone 10e-09 (green, channel 1) (GSE2970: Caenorhabditis elegans as an environmental monitor using DNA microarray analysis.) | In order to assist in the identification of possible endocrine disrupting chemicals (EDC) in groundwater, we are developing Caenorhabolitis elegans as a high throughput bioassay system in which responses to EDC may be detected by gene expression using DNA microarray analysis. As a first step we examined gene expression patterns and vitellogenin responses of this organism to vertebrate steroids, in liquid culture. Western blotting showed the expected number and size of vitellogenin translation products after estrogen exposure. At 10(-9) M, vitellogenin decreased, but at 10(-7) and 10(-5), vitellogenin was increased. Testosterone (10(-5) M) increased the synthesis of vitellogenin, but progesterone-treated cultures (10(-5) M) had less vitellogenin. Using DNA microarray analysis, we examined the pattern of gene expression after progesterone (10(-5), 10(-7), and 10(-9) M), estrogen (10(-5) M), and testosterone (10(-9) M) exposure, with special attention to the traditional biomarker genes used in environmental studies [vitellogenin, cytochrome P450 (CYP), glutathione s-transferase (GST), metallothionein (MT), and heat shock proteins (HSP)]. GST and P450 genes were affected by estrogen (10(-5) M) and progesterone (10(-5) and 10(-7) M) treatments. For vitellogenin genes, estrogen treatment (10(-5) M) caused overexpression of the vit-2 and vit-6 genes (2.68 and 3.25 times, respectively). After progesterone treatment (10(-7) M), the vit-5 and vit-6 were down-regulated and vit-1 up-regulated (3.59-fold). Concentrations of testosterone and progesterone at 10(-9) M did not influence the expression of the vit, CYP, or GST genes. Although the analysis is incomplete, and low doses and combinations of EDC need to be tested, these preliminary results indicate C. elegans may be a useful laboratory and field model for screening EDC. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM64908 | N2 control #1 (red, channel 2) vs. progesterone 10e-07 (green, channel 1) (GSE2970: Caenorhabditis elegans as an environmental monitor using DNA microarray analysis.) | In order to assist in the identification of possible endocrine disrupting chemicals (EDC) in groundwater, we are developing Caenorhabolitis elegans as a high throughput bioassay system in which responses to EDC may be detected by gene expression using DNA microarray analysis. As a first step we examined gene expression patterns and vitellogenin responses of this organism to vertebrate steroids, in liquid culture. Western blotting showed the expected number and size of vitellogenin translation products after estrogen exposure. At 10(-9) M, vitellogenin decreased, but at 10(-7) and 10(-5), vitellogenin was increased. Testosterone (10(-5) M) increased the synthesis of vitellogenin, but progesterone-treated cultures (10(-5) M) had less vitellogenin. Using DNA microarray analysis, we examined the pattern of gene expression after progesterone (10(-5), 10(-7), and 10(-9) M), estrogen (10(-5) M), and testosterone (10(-9) M) exposure, with special attention to the traditional biomarker genes used in environmental studies [vitellogenin, cytochrome P450 (CYP), glutathione s-transferase (GST), metallothionein (MT), and heat shock proteins (HSP)]. GST and P450 genes were affected by estrogen (10(-5) M) and progesterone (10(-5) and 10(-7) M) treatments. For vitellogenin genes, estrogen treatment (10(-5) M) caused overexpression of the vit-2 and vit-6 genes (2.68 and 3.25 times, respectively). After progesterone treatment (10(-7) M), the vit-5 and vit-6 were down-regulated and vit-1 up-regulated (3.59-fold). Concentrations of testosterone and progesterone at 10(-9) M did not influence the expression of the vit, CYP, or GST genes. Although the analysis is incomplete, and low doses and combinations of EDC need to be tested, these preliminary results indicate C. elegans may be a useful laboratory and field model for screening EDC. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM64909 | N2 control #2 (red, channel 2) vs. estrogen 10e-05 (green, channel 1) (GSE2970: Caenorhabditis elegans as an environmental monitor using DNA microarray analysis.) | In order to assist in the identification of possible endocrine disrupting chemicals (EDC) in groundwater, we are developing Caenorhabolitis elegans as a high throughput bioassay system in which responses to EDC may be detected by gene expression using DNA microarray analysis. As a first step we examined gene expression patterns and vitellogenin responses of this organism to vertebrate steroids, in liquid culture. Western blotting showed the expected number and size of vitellogenin translation products after estrogen exposure. At 10(-9) M, vitellogenin decreased, but at 10(-7) and 10(-5), vitellogenin was increased. Testosterone (10(-5) M) increased the synthesis of vitellogenin, but progesterone-treated cultures (10(-5) M) had less vitellogenin. Using DNA microarray analysis, we examined the pattern of gene expression after progesterone (10(-5), 10(-7), and 10(-9) M), estrogen (10(-5) M), and testosterone (10(-9) M) exposure, with special attention to the traditional biomarker genes used in environmental studies [vitellogenin, cytochrome P450 (CYP), glutathione s-transferase (GST), metallothionein (MT), and heat shock proteins (HSP)]. GST and P450 genes were affected by estrogen (10(-5) M) and progesterone (10(-5) and 10(-7) M) treatments. For vitellogenin genes, estrogen treatment (10(-5) M) caused overexpression of the vit-2 and vit-6 genes (2.68 and 3.25 times, respectively). After progesterone treatment (10(-7) M), the vit-5 and vit-6 were down-regulated and vit-1 up-regulated (3.59-fold). Concentrations of testosterone and progesterone at 10(-9) M did not influence the expression of the vit, CYP, or GST genes. Although the analysis is incomplete, and low doses and combinations of EDC need to be tested, these preliminary results indicate C. elegans may be a useful laboratory and field model for screening EDC. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM64910 | N2 control #2 (red, channel 2) vs. cholesterol 10e-09 (green, channel 1) (GSE2970: Caenorhabditis elegans as an environmental monitor using DNA microarray analysis.) | In order to assist in the identification of possible endocrine disrupting chemicals (EDC) in groundwater, we are developing Caenorhabolitis elegans as a high throughput bioassay system in which responses to EDC may be detected by gene expression using DNA microarray analysis. As a first step we examined gene expression patterns and vitellogenin responses of this organism to vertebrate steroids, in liquid culture. Western blotting showed the expected number and size of vitellogenin translation products after estrogen exposure. At 10(-9) M, vitellogenin decreased, but at 10(-7) and 10(-5), vitellogenin was increased. Testosterone (10(-5) M) increased the synthesis of vitellogenin, but progesterone-treated cultures (10(-5) M) had less vitellogenin. Using DNA microarray analysis, we examined the pattern of gene expression after progesterone (10(-5), 10(-7), and 10(-9) M), estrogen (10(-5) M), and testosterone (10(-9) M) exposure, with special attention to the traditional biomarker genes used in environmental studies [vitellogenin, cytochrome P450 (CYP), glutathione s-transferase (GST), metallothionein (MT), and heat shock proteins (HSP)]. GST and P450 genes were affected by estrogen (10(-5) M) and progesterone (10(-5) and 10(-7) M) treatments. For vitellogenin genes, estrogen treatment (10(-5) M) caused overexpression of the vit-2 and vit-6 genes (2.68 and 3.25 times, respectively). After progesterone treatment (10(-7) M), the vit-5 and vit-6 were down-regulated and vit-1 up-regulated (3.59-fold). Concentrations of testosterone and progesterone at 10(-9) M did not influence the expression of the vit, CYP, or GST genes. Although the analysis is incomplete, and low doses and combinations of EDC need to be tested, these preliminary results indicate C. elegans may be a useful laboratory and field model for screening EDC. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM64911 | N2 control #2 (red, channel 2) vs. progesterone 10e-05 (green, channel 1) (GSE2970: Caenorhabditis elegans as an environmental monitor using DNA microarray analysis.) | In order to assist in the identification of possible endocrine disrupting chemicals (EDC) in groundwater, we are developing Caenorhabolitis elegans as a high throughput bioassay system in which responses to EDC may be detected by gene expression using DNA microarray analysis. As a first step we examined gene expression patterns and vitellogenin responses of this organism to vertebrate steroids, in liquid culture. Western blotting showed the expected number and size of vitellogenin translation products after estrogen exposure. At 10(-9) M, vitellogenin decreased, but at 10(-7) and 10(-5), vitellogenin was increased. Testosterone (10(-5) M) increased the synthesis of vitellogenin, but progesterone-treated cultures (10(-5) M) had less vitellogenin. Using DNA microarray analysis, we examined the pattern of gene expression after progesterone (10(-5), 10(-7), and 10(-9) M), estrogen (10(-5) M), and testosterone (10(-9) M) exposure, with special attention to the traditional biomarker genes used in environmental studies [vitellogenin, cytochrome P450 (CYP), glutathione s-transferase (GST), metallothionein (MT), and heat shock proteins (HSP)]. GST and P450 genes were affected by estrogen (10(-5) M) and progesterone (10(-5) and 10(-7) M) treatments. For vitellogenin genes, estrogen treatment (10(-5) M) caused overexpression of the vit-2 and vit-6 genes (2.68 and 3.25 times, respectively). After progesterone treatment (10(-7) M), the vit-5 and vit-6 were down-regulated and vit-1 up-regulated (3.59-fold). Concentrations of testosterone and progesterone at 10(-9) M did not influence the expression of the vit, CYP, or GST genes. Although the analysis is incomplete, and low doses and combinations of EDC need to be tested, these preliminary results indicate C. elegans may be a useful laboratory and field model for screening EDC. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM64916 | C18-2 (GSE2971: muscle mRNA tagging) | We present a global overview of muscle gene expression in C. elegans using a novel technique called mRNA-tagging, and have identified genes involved in contraction, muscle structure, and energy utilization. Furthermore, we found that muscle-expressed genes are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome in which the order of genes along the chromosome is correlated with their expression in specific tissues. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM64917 | C18-3 (GSE2971: muscle mRNA tagging) | We present a global overview of muscle gene expression in C. elegans using a novel technique called mRNA-tagging, and have identified genes involved in contraction, muscle structure, and energy utilization. Furthermore, we found that muscle-expressed genes are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome in which the order of genes along the chromosome is correlated with their expression in specific tissues. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM64918 | C18-4 (GSE2971: muscle mRNA tagging) | We present a global overview of muscle gene expression in C. elegans using a novel technique called mRNA-tagging, and have identified genes involved in contraction, muscle structure, and energy utilization. Furthermore, we found that muscle-expressed genes are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome in which the order of genes along the chromosome is correlated with their expression in specific tissues. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM64919 | C18-5 (GSE2971: muscle mRNA tagging) | We present a global overview of muscle gene expression in C. elegans using a novel technique called mRNA-tagging, and have identified genes involved in contraction, muscle structure, and energy utilization. Furthermore, we found that muscle-expressed genes are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome in which the order of genes along the chromosome is correlated with their expression in specific tissues. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM64920 | C18-6 (GSE2971: muscle mRNA tagging) | We present a global overview of muscle gene expression in C. elegans using a novel technique called mRNA-tagging, and have identified genes involved in contraction, muscle structure, and energy utilization. Furthermore, we found that muscle-expressed genes are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome in which the order of genes along the chromosome is correlated with their expression in specific tissues. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM64921 | C18-1 (GSE2971: muscle mRNA tagging) | We present a global overview of muscle gene expression in C. elegans using a novel technique called mRNA-tagging, and have identified genes involved in contraction, muscle structure, and energy utilization. Furthermore, we found that muscle-expressed genes are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome in which the order of genes along the chromosome is correlated with their expression in specific tissues. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65025 | New N2 mixed stage (red, channel 2) vs.L2 Ras T30.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65026 | New N2 mixed stage (red, channel 2) vs.L2 Ras T1.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65027 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0new.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65028 | New N2 mixed stage (red, channel 2) vs.L2 N2 T2new.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65029 | New N2 mixed stage (red, channel 2) vs.L2 Ras T2.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65030 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0new.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65031 | New N2 mixed stage (red, channel 2) vs.L2 Ras T30.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65032 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0new.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65033 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65034 | New N2 mixed stage (red, channel 2) vs.L2 N2 T2new.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65035 | New N2 mixed stage (red, channel 2) vs.L2 N2 T30.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65036 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0new.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65037 | New N2 mixed stage (red, channel 2) vs.L2 N2 T1.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65038 | New N2 mixed stage (red, channel 2) vs.L2 N2 T2new.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65039 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65040 | New N2 mixed stage (red, channel 2) vs.L2 N2 T30.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65041 | New N2 mixed stage (red, channel 2) vs.L2 N2 T1.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65042 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65043 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65044 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0new.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65045 | New N2 mixed stage (red, channel 2) vs.L2 Ras T30.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65046 | New N2 mixed stage (red, channel 2) vs.L2 Ras T2.4bis (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65047 | New N2 mixed stage (red, channel 2) vs.L2 Ras T1.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65048 | New N2 mixed stage (red, channel 2) vs.L2 Ras T2.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65049 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65050 | New N2 mixed stage (red, channel 2) vs.L2 Ras T1.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65051 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65052 | New N2 mixed stage (red, channel 2) vs.L2 Ras T30.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65053 | New N2 mixed stage (red, channel 2) vs.L2 Ras T1.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65054 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65055 | New N2 mixed stage (red, channel 2) vs.L2 N2 T30.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65056 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65057 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0new.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65058 | New N2 mixed stage (red, channel 2) vs.L2 N2 T1.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65059 | New N2 mixed stage (red, channel 2) vs.L2 Ras T2.1 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65060 | New N2 mixed stage (red, channel 2) vs.L2 Ras T0new.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65061 | New N2 mixed stage (red, channel 2) vs.L2 N2 T1.4(green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65062 | New N2 mixed stage (red, channel 2) vs.L2 N2 T30.4 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65063 | New N2 mixed stage (red, channel 2) vs.L2 N2 T2new.2 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65064 | New N2 mixed stage (red, channel 2) vs.L2 N2 T0new.3 (green, channel 1) (GSE2974: Downstream targets of let-60 Ras in Caenorhabditis elegans) | In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65065 | mixed stage N2 (red, channel 2) vs. SL2-amplified N2 (repeat #4) (green, channel 1) (GSE2975: Global analysis of Caenorhabditis elegans operons) | Caenorhabditis elegans and its relatives are unique among animals, possibly even among eukaryotes, in having operons. In these regulated multigene transcription units, a polycistronic pre-mRNA is processed to monocistronic mRNAs by 3' end formation and trans-splicing utilizing a special snRNP, the SL2 snRNP, for downstream mRNAs1. Previously, the correlation between downstream location in an operon and SL2 trans-splicing has been strong, but anecdotal. Although only 28 operons have been reported previously, the complete sequence of the genome reveals numerous gene clusters. To determine how many represent operons, we probed full-genome microarrays for SL2-containing mRNAs. We found significant enrichment for about 1200 genes including most of a group of several hundred genes represented by cDNAs that contain SL2 sequence. Analysis of their genomic arrangements indicates that >;90% are downstream genes, falling in 790 distinct operons. We conclude that the genome contains at least 1000 operons, 2- 8 genes in length, that contain ~15% of C. elegans genes. Most of the operons have not been reported previously, and numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal heretofore unknown functional relationships. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65066 | mixed stage N2 (red channel 2) vs. SL2-amplified mixed stage N2 (green, channel 1) (GSE2975: Global analysis of Caenorhabditis elegans operons) | Caenorhabditis elegans and its relatives are unique among animals, possibly even among eukaryotes, in having operons. In these regulated multigene transcription units, a polycistronic pre-mRNA is processed to monocistronic mRNAs by 3' end formation and trans-splicing utilizing a special snRNP, the SL2 snRNP, for downstream mRNAs1. Previously, the correlation between downstream location in an operon and SL2 trans-splicing has been strong, but anecdotal. Although only 28 operons have been reported previously, the complete sequence of the genome reveals numerous gene clusters. To determine how many represent operons, we probed full-genome microarrays for SL2-containing mRNAs. We found significant enrichment for about 1200 genes including most of a group of several hundred genes represented by cDNAs that contain SL2 sequence. Analysis of their genomic arrangements indicates that >;90% are downstream genes, falling in 790 distinct operons. We conclude that the genome contains at least 1000 operons, 2- 8 genes in length, that contain ~15% of C. elegans genes. Most of the operons have not been reported previously, and numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal heretofore unknown functional relationships. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65067 | mixed stage N2 (red, channel 2) vs. SL2-amplified N2 (repeat #1) (green, channel 1) (GSE2975: Global analysis of Caenorhabditis elegans operons) | Caenorhabditis elegans and its relatives are unique among animals, possibly even among eukaryotes, in having operons. In these regulated multigene transcription units, a polycistronic pre-mRNA is processed to monocistronic mRNAs by 3' end formation and trans-splicing utilizing a special snRNP, the SL2 snRNP, for downstream mRNAs1. Previously, the correlation between downstream location in an operon and SL2 trans-splicing has been strong, but anecdotal. Although only 28 operons have been reported previously, the complete sequence of the genome reveals numerous gene clusters. To determine how many represent operons, we probed full-genome microarrays for SL2-containing mRNAs. We found significant enrichment for about 1200 genes including most of a group of several hundred genes represented by cDNAs that contain SL2 sequence. Analysis of their genomic arrangements indicates that >;90% are downstream genes, falling in 790 distinct operons. We conclude that the genome contains at least 1000 operons, 2- 8 genes in length, that contain ~15% of C. elegans genes. Most of the operons have not been reported previously, and numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal heretofore unknown functional relationships. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65068 | mixed stage N2 (red, channel 2) vs. SL2-amplified N2 (repeat #2) (green, channel 1) (GSE2975: Global analysis of Caenorhabditis elegans operons) | Caenorhabditis elegans and its relatives are unique among animals, possibly even among eukaryotes, in having operons. In these regulated multigene transcription units, a polycistronic pre-mRNA is processed to monocistronic mRNAs by 3' end formation and trans-splicing utilizing a special snRNP, the SL2 snRNP, for downstream mRNAs1. Previously, the correlation between downstream location in an operon and SL2 trans-splicing has been strong, but anecdotal. Although only 28 operons have been reported previously, the complete sequence of the genome reveals numerous gene clusters. To determine how many represent operons, we probed full-genome microarrays for SL2-containing mRNAs. We found significant enrichment for about 1200 genes including most of a group of several hundred genes represented by cDNAs that contain SL2 sequence. Analysis of their genomic arrangements indicates that >;90% are downstream genes, falling in 790 distinct operons. We conclude that the genome contains at least 1000 operons, 2- 8 genes in length, that contain ~15% of C. elegans genes. Most of the operons have not been reported previously, and numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal heretofore unknown functional relationships. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM65069 | mixed stage N2 (red, channel 2) vs. SL2-amplified N2 (repeat #3) (green, channel 1) (GSE2975: Global analysis of Caenorhabditis elegans operons) | Caenorhabditis elegans and its relatives are unique among animals, possibly even among eukaryotes, in having operons. In these regulated multigene transcription units, a polycistronic pre-mRNA is processed to monocistronic mRNAs by 3' end formation and trans-splicing utilizing a special snRNP, the SL2 snRNP, for downstream mRNAs1. Previously, the correlation between downstream location in an operon and SL2 trans-splicing has been strong, but anecdotal. Although only 28 operons have been reported previously, the complete sequence of the genome reveals numerous gene clusters. To determine how many represent operons, we probed full-genome microarrays for SL2-containing mRNAs. We found significant enrichment for about 1200 genes including most of a group of several hundred genes represented by cDNAs that contain SL2 sequence. Analysis of their genomic arrangements indicates that >;90% are downstream genes, falling in 790 distinct operons. We conclude that the genome contains at least 1000 operons, 2- 8 genes in length, that contain ~15% of C. elegans genes. Most of the operons have not been reported previously, and numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal heretofore unknown functional relationships. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM675861 | C.elegans_8days_1G1-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675862 | C.elegans_8days_1G2-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675863 | C.elegans_8days_1G3-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675864 | C.elegans_8days_microG1-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675865 | C.elegans_8days_microG2-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675866 | C.elegans_8days_microG3-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675867 | C.elegans_8days_GC1-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675868 | C.elegans_8days_GC2-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675869 | C.elegans_8days_GC3-2 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675870 | C.elegans_8days_1G1-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675871 | C.elegans_8days_1G2-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675872 | C.elegans_8days_1G3-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675873 | C.elegans_8days_microG1-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675874 | C.elegans_8days_microG2-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675875 | C.elegans_8days_microG3-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675876 | C.elegans_8days_GC1-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675877 | C.elegans_8days_GC2-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM675878 | C.elegans_8days_GC3-1 (GSE27338: Microgravity effect on C. elegans N2/VC (CERISE, 8days)) | Microgravity effect on C. elegans gene expression was analysed by whole genome microarray. The worms were cultivated under microgravity for 8days in the Japanese Module of the International Space Station. |
| GSM677582_C | C. albicans alive #1 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677583_C | C. albicans alive #2 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677584_C | C. albicans alive #3 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677585_Heat_Killed_C | Heat Killed C. albicans #1 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677586_Heat_Killed_C | Heat Killed C. albicans #2 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677587_Heat_Killed_C | Heat Killed C. albicans #3 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677588_Heat_Killed_E_coli__1 | Heat Killed E coli #1 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677589_Heat_Killed_E_coli__2 | Heat Killed E coli #2 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM677590_Heat_Killed_E_coli__3 | Heat Killed E coli #3 (GSE27401: Caenorhabditis elegans infection with Candida albicans) | N2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen. |
| GSM685476 | N2, Fed 0 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685477 | N2, Fed 0 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685478 | N2, Fed 24 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685479 | N2, Fed 24 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685480 | N2, Fed 48 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685481 | N2, Fed 48 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685482 | N2, Fast 3 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685483 | N2, Fast 3 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685484 | N2, Fast 6 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685485 | N2, Fast 6 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685486 | N2, Fast 9 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685487 | N2, Fast 9 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685488 | N2, Fast 12 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685489 | N2, Fast 12 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685490 | N2, Fast 18 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685491 | N2, Fast 18 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685492 | N2, Fast 24 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685493 | N2, Fast 24 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685494 | N2, Fast 36 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685495 | N2, Fast 36 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685496 | N2, Fast 48 h, rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685497 | N2, Fast 48 h, rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685498 | N2, Fed , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685499 | N2, Fed , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685500 | N2, Fed , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685501 | N2, Fast , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685502 | N2, Fast , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685503 | N2, Fast , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685504 | kgb-1, Fed , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685505 | kgb-1, Fed , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685506 | kgb-1, Fed , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685507 | kgb-1, Fast , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685508 | kgb-1, Fast , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685509 | kgb-1, Fast , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685510 | jun-1, Fed , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685511 | jun-1, Fed , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685512 | jun-1, Fed , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685513 | jun-1, Fast , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685514 | jun-1, Fast , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685515 | jun-1, Fast , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685516 | daf-16, Fed , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685517 | daf-16, Fed , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685518 | daf-16, Fed , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685519 | daf-16, Fast , rep 1 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685520 | daf-16, Fast , rep 2 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM685521 | daf-16, Fast , rep 3 (GSE27677: A conserved JNK/AP-1 module is a key mediator of intermittent fasting-induced longevity in C. elegans) | Dietary restriction extends lifespan and delays the age-related physiological decline in many species. Intermittent fasting (IF) is one of the most effective dietary restriction regimens that extends lifespan in C. elegans and mammals1,2. In C. elegans, the FOXO transcription factor DAF-16 is implicated in fasting-induced gene expression changes and the longevity response to IF3; however, the mechanisms that sense and transduce fasting-stress stimuli have remained largely unknown. Here we show that a KGB-1/AP1 (activator protein 1) module is a key signalling pathway that mediates fasting-induced transcriptional changes and IF-induced longevity. Our promoter analysis coupled to genome-wide microarray results has shown that the AP-1-binding site, together with the FOXO-binding site, is highly over-represented in the promoter regions of fasting-induced genes. We find that JUN-1 (C. elegans c-Jun) and FOS-1 (C. elegans c-Fos), which constitute the AP-1 transcription factor complex, are required for IF-induced longevity. We also find that KGB-1 acts as a direct activator of JUN-1 and FOS-1, is activated in response to fasting, and, among the three C. elegans JNKs, is specifically required for IF-induced longevity. Our results demonstrate that most fasting-induced upregulated genes, including almost all of the DAF-16-dependent genes, require KGB-1 and JUN-1 function for their induction, and that the loss of kgb-1 suppresses the fasting-induced upregulation of DAF-16 target genes without affecting fasting-induced DAF-16 nuclear translocation. These findings identify the evolutionarily conserved JNK/AP-1 module as a key mediator of fasting-stress responses, and suggest a model in which two fasting-induced signalling pathways leading to DAF-16 nuclear translocation and KGB-1/AP-1 activation, respectively, integrate in the nucleus to coordinately mediate fasting-induced transcriptional changes and IF-induced longevity. To delineate the whole picture of transcriptional changes in response to fasting, we performed genome-wide gene expression analyses during 2 days (48 h) fasting. |
| GSM68696 | D2 4-1 (daf-2 expt.4 t.p.1) (red, channel 2) vs. D16 4-1 (daf-16 expt.4 t.p.1) (green, channel 1) (GSE3089: Transcriptional outputs of the Caenorhabditis elegans forkhead protein DAF-16) | To identify DAF-16-dependent transcriptional alterations that occur in a long-lived C. elegans strain, we used cDNA microarrays and genomic analysis to identify putative direct and indirect DAF-16 transcriptional target genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM68697 | D2 3-1 (daf-2 expt.3 t.p.1) (red, channel 2) vs. D16 3-1 (daf-16 expt.3 t.p.1) (green, channel 1) (GSE3089: Transcriptional outputs of the Caenorhabditis elegans forkhead protein DAF-16) | To identify DAF-16-dependent transcriptional alterations that occur in a long-lived C. elegans strain, we used cDNA microarrays and genomic analysis to identify putative direct and indirect DAF-16 transcriptional target genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM68698 | D2 1-1 (daf-2 timepoint 1) (red, channel 2) vs. D16 1-1 (daf-16 timepoint 1) (green, channel 1) (GSE3089: Transcriptional outputs of the Caenorhabditis elegans forkhead protein DAF-16) | To identify DAF-16-dependent transcriptional alterations that occur in a long-lived C. elegans strain, we used cDNA microarrays and genomic analysis to identify putative direct and indirect DAF-16 transcriptional target genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM68699 | D2 2-1 (daf-2 expt2 t.p.1) (red, channel 2) vs. D16 2-1 (daf-16 expt2 t.p.1) (green, channel 1) (GSE3089: Transcriptional outputs of the Caenorhabditis elegans forkhead protein DAF-16) | To identify DAF-16-dependent transcriptional alterations that occur in a long-lived C. elegans strain, we used cDNA microarrays and genomic analysis to identify putative direct and indirect DAF-16 transcriptional target genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM688037_2246_4774_27844_wt_A_Celegans | wt, biological rep1 (GSE27867: Expression data from C. elegans (wild type vs. tag-24)) | To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa. |
| GSM688038_2246_4774_27845_wt_B_Celegans | wt, biological rep2 (GSE27867: Expression data from C. elegans (wild type vs. tag-24)) | To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa. |
| GSM688039_2246_4774_27846_wt_C_Celegans | wt, biological rep3 (GSE27867: Expression data from C. elegans (wild type vs. tag-24)) | To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa. |
| GSM688040_2246_4774_27838_tag24_A_Celegans | tag-24, biological rep1 (GSE27867: Expression data from C. elegans (wild type vs. tag-24)) | To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa. |
| GSM688041_2246_4774_27839_tag24_B_Celegans | tag-24, biological rep2 (GSE27867: Expression data from C. elegans (wild type vs. tag-24)) | To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa. |
| GSM688042_2246_4774_27840_tag24_C_Celegans | tag-24, biological rep3 (GSE27867: Expression data from C. elegans (wild type vs. tag-24)) | To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa. |
| GSM69759 | mutant sorted touch cell (red, channel 2) vs. wt sorted touch cell (green, channel 1) (GSE3121: Identification of genes expressed in C. elegans touch receptor neurons) | By culturing and isolating wild-type and mec-3 mutant cells from embryos and applying their amplified RNA to DNA microarrays, here we have identified genes that are known to be expressed in touch receptors, a previously uncloned gene (mec-17) that is needed for maintaining touch receptor differentiation, and more than 50 previously unknown mec-3-dependent genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM69760 | mutant sorted touch cell (red, channel 2) vs. wt sorted touch cell (repeat #4) (green, channel 1) (GSE3121: Identification of genes expressed in C. elegans touch receptor neurons) | By culturing and isolating wild-type and mec-3 mutant cells from embryos and applying their amplified RNA to DNA microarrays, here we have identified genes that are known to be expressed in touch receptors, a previously uncloned gene (mec-17) that is needed for maintaining touch receptor differentiation, and more than 50 previously unknown mec-3-dependent genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM69761 | mutant sorted touch cell (red, channel 2) vs. wt sorted touch cell (repeat #1) (green, channel 1) (GSE3121: Identification of genes expressed in C. elegans touch receptor neurons) | By culturing and isolating wild-type and mec-3 mutant cells from embryos and applying their amplified RNA to DNA microarrays, here we have identified genes that are known to be expressed in touch receptors, a previously uncloned gene (mec-17) that is needed for maintaining touch receptor differentiation, and more than 50 previously unknown mec-3-dependent genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM69762 | mutant sorted touch cell (red, channel 2) vs. wt sorted touch cell (repeat #2) (green, channel 1) (GSE3121: Identification of genes expressed in C. elegans touch receptor neurons) | By culturing and isolating wild-type and mec-3 mutant cells from embryos and applying their amplified RNA to DNA microarrays, here we have identified genes that are known to be expressed in touch receptors, a previously uncloned gene (mec-17) that is needed for maintaining touch receptor differentiation, and more than 50 previously unknown mec-3-dependent genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM69763 | wt sorted touch cell (red, channel 2) vs. mutant sorted touch cell (green, channel 1) (GSE3121: Identification of genes expressed in C. elegans touch receptor neurons) | By culturing and isolating wild-type and mec-3 mutant cells from embryos and applying their amplified RNA to DNA microarrays, here we have identified genes that are known to be expressed in touch receptors, a previously uncloned gene (mec-17) that is needed for maintaining touch receptor differentiation, and more than 50 previously unknown mec-3-dependent genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM69764 | mutant sorted touch cell (red, channel 2) vs. wt sorted touch cell (repeat #3) (green, channel 1) (GSE3121: Identification of genes expressed in C. elegans touch receptor neurons) | By culturing and isolating wild-type and mec-3 mutant cells from embryos and applying their amplified RNA to DNA microarrays, here we have identified genes that are known to be expressed in touch receptors, a previously uncloned gene (mec-17) that is needed for maintaining touch receptor differentiation, and more than 50 previously unknown mec-3-dependent genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM705443_Emb_wt_1 | wild-type N2 embryo 1 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705444_Emb_wt_2 | wild-type N2 embryo 2 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705445_Emb_wt_3 | wild-type N2 embryo 3 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705446_Emb_mutant_1 | lin-54(n2990) embryo 1 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705447_Emb_mutant_2 | lin-54(n2990) embryo 2 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705448_Emb_mutant_3 | lin-54(n2990) embryo 3 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705449_G_wt_1 | wild-type N2 dissected germline 1 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705450_G_wt_2 | wild-type N2 dissected germline 2 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705451_G_wt_3 | wild-type N2 dissected germline 3 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705452_G_mutant_1 | lin-54(n3423) dissected germline 1 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705453_G_mutant_2 | lin-54(n3423) dissected germline 2 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM705454_G_mutant_3 | lin-54(n3423) dissected germline 3 (GSE28853: Chromosome-biased binding and gene regulation by the C. elegans DRM complex) | This SuperSeries is composed of the SubSeries listed below. |
| GSM70919 | L1 MTC#1T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70920 | L1 MTC#2T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70921 | Dauer MTC#4T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70922 | L1 MTC#1T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70923 | L1 MTC#2T2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70924 | L1 MTC#1T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70925 | L1 MTC#2T3 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70926 | L1 MTC#1T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70927 | L1 MTC#2T4 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70928 | L1 MTC#4T3 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70929 | L1 MTC#1T12 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70930 | L1 MTC#4T4 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70931 | L1 MTC#4T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70932 | Dauer MTC#2T3-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70933 | Dauer MTC#2T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70934 | L1 MTC#4T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70935 | Dauer MTC#2T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70936 | Dauer MTC#2T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70937 | Dauer MTC#2T12 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70938 | Dauer MTC#3T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70939 | Dauer MTC#3T2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70940 | Dauer MTC#3T4 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70941 | Dauer MTC#3T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70942 | Dauer MTC#3T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70943 | Dauer Adjust #1 T0 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70944 | Dauer Adjust #1 T12 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70945 | Dauer MTC#1T0-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70946 | L1 MTC#2T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70947 | Dauer MTC#1T2-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70948 | Dauer MTC#1T4-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70949 | Dauer MTC#2T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70950 | Dauer MTC#2T2-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70951 | L1 MTC#2T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70952 | Dauer MTC#2T8-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70953 | L1 MTC#2T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70954 | Dauer MTC#3T0-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70955 | L1 MTC#2T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70956 | L1 MTC#2T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70957 | L1 MTC#4T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70958 | L1 MTC#2T12 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70959 | L1 MTC#4T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70960 | L1 MTC#4T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70961 | L1 MTC#4T12 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70962 | Dauer MTC#3T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70963 | Dauer MTC#3T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70964 | Dauer MTC#3T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70965 | Dauer Adjust #2 T0 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70966 | Dauer MTC#3T12-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70967 | Dauer MTC#4T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70968 | Dauer Adjust #2 T12 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70969 | Dauer Adjust #4 T0 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70970 | Dauer MTC#1T3 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70971 | Dauer Adjust #4 T12 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70972 | Dauer Adjust #3 T0 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70973 | L1 MTC#3T0 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70974 | L1 MTC#3T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70975 | L1 MTC#3T3 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70976 | L1 MTC#3T4 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70977 | L1 MTC#3T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70978 | L1 MTC#3T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70979 | L1 MTC#3T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70980 | Dauer MTC#3T3-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70981 | Dauer MTC#4T0-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70982 | Dauer MTC#4T2-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70983 | Dauer MTC#4T3-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70984 | Dauer MTC#4T5-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70985 | L1 MTC#1T0 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70986 | Dauer MTC#4T6-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70987 | L1 MTC#1T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70988 | Dauer MTC#4T7 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70989 | L1 MTC#1T2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70990 | L1 MTC#1T3 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70991 | Dauer MTC#1T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70992 | L1 MTC#1T4 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70993 | L1 MTC#1T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM70994 | Dauer Adjust #3 T12 (red, channel 2) vs RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71121 | Dauer MTC#2T0 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71122 | L1 MTC#2T0 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71123 | Dauer MTC#1T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71124 | L1 MTC#3T8 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71125 | L1 MTC#3T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71126 | L1 MTC#3T12 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71127 | L1 MTC#4T0 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71128 | L1 MTC#4T1 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71129 | L1 MTC#4T2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71130 | Dauer MTC#2T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71131 | Dauer MTC#4T4 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71132 | L1 MTC#3T2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71133 | Dauer MTC#4T10-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71134 | Dauer MTC#1T5 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71135 | Dauer MTC#4T12-2 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71136 | Dauer MTC#1T6 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71137 | Dauer MTC#1T10 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM71138 | Dauer MTC#1T12 (red, channel 2) vs. RefB-JW (green, channel 1) (GSE3169: Global analysis of dauer gene expression in Caenorhabditis elegans) | These are the 94 microarray experiments that are published in the paper: John Wang and Stuart K. Kim. Global analysis of dauer gene expression in Caenorhabditis elegans, Development 2003 130: 1621-1634. There are 94 individual microarray experiments divided into 3 broad experiments. The first experiment is a time course of dauer exit; each time course is labeled as Dauer MTC#. The second experiment is a time course of L1 development after starvation arrest; each time couse is labeled L1 MTC#. The final experiment is a comparison of pure dauers (0 hours) versus 12 hours after dauer exit and are labeled Dauer Adjust. Every time course was repeated 4 times (#N)however for the dauer 4 and 7 hour time points there are only 3 replicates. For instance, all the time points labeled as Dauer MTC#1 are from the same starting pool of dauer worms that were aliquoted into 10 fractions and analyzed at the time indicated. Every sample is compared to a common reference RNA that is used throughout all the hybridizations. In some cases there is a -2 after the hour designation; this means the first hybridization failed for some technical reason and thus the second hybridization (same RNA) is reported. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM714598_08022901 | Wild-type 0 h after shifting temperature rep1 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714599_08022902 | Wild-type 4 h after shifting temperature rep1 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714600_08022903 | Wild-type 0 h after shifting temperature rep2 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714601_08022904 | Wild-type 4 h after shifting temperature rep2 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714602_08030501 | Wild-type 0 h after shifting temperature rep3 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714603_08030502 | Wild-type 4 h after shifting temperature rep3 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714604_08030701 | Wild-type 0 h after shifting temperature rep4 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714605_08030702 | Wild-type 4 h after shifting temperature rep4 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714606_08031101 | Wild-type 1 h after shifting temperature rep1 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714607_08031102 | Wild-type 2 h after shifting temperature rep1 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714608_08031201 | Wild-type 1 h after shifting temperature rep2 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM714609_08031202 | Wild-type 2 h after shifting temperature rep2 (GSE28856: Expression data of wild-type C. elegans shifted from 23 degrees to 17 degrees) | C. elegans exhibits thermotaxis, where most of the animals that had been cultivated at a particular temperature ranging from 15°C to 25°C for a few hours with a food source and then placed on a thermal gradient for an hour migrate to the cultivation temperature. In addition, animals that were previously conditioned to migrate to a certain temperature are capable of migrating to a new cultivation temperature a few hours after the cultivation temperature was shifted to the new temperature To gain the detailed molecular insight into thermotactic behavior, the genome-wide microarray analysis during behavioral conditioning was performed. We compared the transcriptional profile of animals conditioned to migrate to the new temperature 17°C with that of animals conditioned to migrate to the previous temperature 23°C |
| GSM742037 | Control 1 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742038 | Control 7 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742039 | Control 9 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742040 | Control 10 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742041 | 1 Gy 2 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742042 | 1 Gy 3 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742043 | 1 Gy 5 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM742044 | 1 Gy 15 (GSE29979: Radiation-Induced Genomic Instability in Caenorhabditis Elegans) | Significant impacts on gene expression were observed generations after exposure in ionising radiation exposed nematodes. |
| GSM767758 | C. elegans: Dauers vs Mix-Stage, Biological replicate 1 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767759 | C. elegans: Dauers vs Mix-Stage, Biological replicate 2 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767760 | C. elegans: Dauers vs Mix-Stage, Biological replicate 3 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767761 | C. elegans: Dauers vs Mix-Stage, Biological replicate 4 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767762 | C. elegans: Dauer-Exit (12hrs) vs Mix-Stage, Biological replicate 1 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767763 | C. elegans: Dauer-Exit (12hrs) vs Mix-Stage, Biological replicate 2 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767764 | C. elegans: Dauer-Exit (12hrs) vs Mix-Stage, Biological replicate 3 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM767765 | C. elegans: Dauer-Exit (12hrs) vs Mix-Stage, Biological replicate 4 (GSE36644: Pristionchus pacificus and Caenorhabditis elegans: Dauer and Dauer exit versus mix-stage comparisons) | This SuperSeries is composed of the SubSeries listed below. |
| GSM769062 | F4 +/+ (from +/+) #1 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769063 | F4 +/+ (from +/+) #2 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769064 | F4 +/+ (from +/+) #3 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769065 | F4 +/+ (from +/+) #4 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769066 | F4 +/+ (from +/+) #5 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769067 | F4 +/+ (from +/+) #6 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769068 | F4 +/+ (from wdr-5) #1 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769069 | F4 +/+ (from wdr-5) #2 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769070 | F4 +/+ (from wdr-5) #3 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769071 | F4 +/+ (from wdr-5) #4 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769072 | F4 +/+ (from wdr-5) #5 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769073 | F4 +/+ (from wdr-5) #6 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769074 | F4 wdr-5/wdr-5 #1 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769075 | F4 wdr-5/wdr-5 #2 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769076 | F4 wdr-5/wdr-5 #3 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769077 | F4 wdr-5/wdr-5 #4 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769078 | F4 wdr-5/wdr-5 #5 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769079 | F4 wdr-5/wdr-5 #6 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769080 | F5 +/+ (from +/+) #1 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769081 | F5 +/+ (from +/+) #2 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769082 | F5 +/+ (from +/+) #3 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769083 | F5 +/+ (from +/+) #4 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769084 | F5 +/+ (from +/+) #5 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769085 | F5 +/+ (from +/+) #6 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769086 | F5 +/+ (from wdr-5) #1 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769087 | F5 +/+ (from wdr-5) #2 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769088 | F5 +/+ (from wdr-5) #4 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769089 | F5 +/+ (from wdr-5) #5 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769090 | F5 +/+ (from wdr-5) #6 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769091 | F5 wdr-5/wdr-5 #1 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769092 | F5 wdr-5/wdr-5 #2 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769093 | F5 wdr-5/wdr-5 #3 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769094 | F5 wdr-5/wdr-5 #4 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769095 | F5 wdr-5/wdr-5 #5 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM769096 | F5 wdr-5/wdr-5 #6 (GSE31043: Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans) | Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. |
| GSM794220_08_02_04_Krause_Celegans_C1 | Control, biological rep1 (GSE32031: Expression data in C. elegans L2 larvae after nhr-23 inhibition and in controls) | NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. |
| GSM794221_08_02_04_Krause_Celegans_C2 | Control, biological rep2 (GSE32031: Expression data in C. elegans L2 larvae after nhr-23 inhibition and in controls) | NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. |
| GSM794222_08_02_04_Krause_Celegans_C3 | Control, biological rep3 (GSE32031: Expression data in C. elegans L2 larvae after nhr-23 inhibition and in controls) | NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. |
| GSM794223_08_02_04_Krause_Celegans_E1 | Exerimental (nhr-23 RNAi), biological rep1 (GSE32031: Expression data in C. elegans L2 larvae after nhr-23 inhibition and in controls) | NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. |
| GSM794224_08_02_04_Krause_Celegans_E2 | Exerimental (nhr-23 RNAi), biological rep2 (GSE32031: Expression data in C. elegans L2 larvae after nhr-23 inhibition and in controls) | NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. |
| GSM794225_08_02_04_Krause_Celegans_E3 | Exerimental (nhr-23 RNAi), biological rep3 (GSE32031: Expression data in C. elegans L2 larvae after nhr-23 inhibition and in controls) | NHR-23, a conserved member of the nuclear receptor family of transcription factors, is required for normal development in C. elegans where it plays a critical role in growth and molting. In a search for NHR-23 dependent genes, we performed whole genome comparative expression microarrays on both control and nhr-23 inhibited synchronized larvae. Genes that decreased in response to nhr-23 RNAi included several collagen genes. Unexpectedly, several hedgehog-related genes were also down-regulated after nhr-23 RNAi. A homozygous nhr-23 deletion allele was used to confirm the RNAi knockdown phenotypes and the changes in gene expression. Our results indicate that NHR-23 is a critical coregulator of functionally linked genes involved in growth and molting and reveal evolutionary parallels among the ecdysozoa. |
| GSM800976 | Larval Mutant, biological rep1 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800977 | Larval Mutant, biological rep2 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800978 | Adult Wild-type, biological rep1 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800979 | Adult Wild-type, biological rep2 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800980 | Larval Wild-type, biological rep1 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800981 | Adult Mutant, biological rep1 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800982 | Adult Mutant, biological rep2 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800983 | Adult Mutant, biological rep3 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800984 | Larval Wild-type, biological rep2 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM800985 | Adult Wild-type, biological rep3 (GSE32339: Comparison between Caenorhabditis elegans wild-type and Nep-1 mutant strains) | RET/GDNF and ET3/EDNRB regulate cell survival, differentiation and migration of neural crest-derived cells. Many signalling mediators of RET have been characterized but the target genes at the end of the signalling cascade are largely unknown. Since the RET/EDNRB crosstalk has been previously shown, we used a Caenorhabditis elegans knockout strain of Nep-1, a homologue of human ECE1 (endothelin-converting enzyme-1), to identify new target genes. Transcriptome comparison between wild-type and Nep-1 strains at different stages identified vit-3 as a differentially expressed gene. Molecular studies of the vit3 mammalian homologue, Apoliporotein B (APOB), were performed in the murine Neuro2a cell line, a model of ENS development. Apob expression in Neuro2a is specifically activated by the RET/GDNF signalling pathway, since Ret silencing abolished Apob increase, and this effect is induced by MAPK P38 kinase activation. Mouse Apob promoter study revealed that there is a p53-dependent repressor element in the promoter region which blocks Apob expression and we show that actually p53 binds to this region. We demonstrated that RET/GDNF and EDNRB/endothelin 3 (ET-3) cooperate in inducing neuronal differentiation resulting in Apob activation. We also show that Apob expression is downregulated in mouse embryos homozygous for the mutation RetC620R and presenting a severe HSCR phenotype, whereas heterozygous mice, phenotypically normal, present a significant increase in Apob expression. These data suggest that Apob has an important role in RET-mediated neuronal development and APOB decrease may have an impact in human disorders where RET absence has been already identified, such as HSCR and Parkinson disease. Gene expression analysis using Affymetrix GeneChip C. elegans arrays in order to identify genes up- or down-regulated in nep-1 strains, homologue of human ECE1 (endothelin-converting enzyme 1). |
| GSM803567 | wildtype A-class, biological rep1 (GSE32467: Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans) | In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord. |
| GSM803568 | wildtype A-class, biological rep2 (GSE32467: Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans) | In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord. |
| GSM803569 | wildtype A-class, biological rep3 (GSE32467: Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans) | In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord. |
| GSM803570 | unc-37(e262) A-class, biological rep1 (GSE32467: Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans) | In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord. |
| GSM803571 | unc-37(e262) A-class, biological rep2 (GSE32467: Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans) | In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord. |
| GSM803572 | unc-37(e262) A-class, biological rep3 (GSE32467: Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans) | In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord. |
| GSM805419_C1_030210_Celegans_ | Control Replicate1 (GSE32521: Toxicogenomic responses of C. elegans to gold nanoparticles) | We used Au nanoparticles (Au-NPs) as a model for studying particle specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, free living nematode Caenorhabditis elegans. Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC10 (5.9 mg L-1) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Activation of 26 pqn/abu genes from noncanonical Unfolded Protein Response (UPR) pathway and up-regulation of molecular chaperones (hsp-16.1, hsp-70, hsp-3 and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Inhibition of abu-11 with RNAi showed increase in mortality in Au-NP exposed nematodes suggesting possible involvement of abu-11 (a gene associated with specific to C. elegans UPR) in a protective mechanism against Au-NPs. Exposure to Au-NPs also caused activation of genes involved in apoptosis and necrosis and resulted ultimately in 10% mortality. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to a model ecoreceptor which activate both general and specific biological pathways. |
| GSM805420_C2_030210_Celegans_ | Control Replicate2 (GSE32521: Toxicogenomic responses of C. elegans to gold nanoparticles) | We used Au nanoparticles (Au-NPs) as a model for studying particle specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, free living nematode Caenorhabditis elegans. Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC10 (5.9 mg L-1) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Activation of 26 pqn/abu genes from noncanonical Unfolded Protein Response (UPR) pathway and up-regulation of molecular chaperones (hsp-16.1, hsp-70, hsp-3 and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Inhibition of abu-11 with RNAi showed increase in mortality in Au-NP exposed nematodes suggesting possible involvement of abu-11 (a gene associated with specific to C. elegans UPR) in a protective mechanism against Au-NPs. Exposure to Au-NPs also caused activation of genes involved in apoptosis and necrosis and resulted ultimately in 10% mortality. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to a model ecoreceptor which activate both general and specific biological pathways. |
| GSM805421_C3_030210_Celegans_ | Control Replicate3 (GSE32521: Toxicogenomic responses of C. elegans to gold nanoparticles) | We used Au nanoparticles (Au-NPs) as a model for studying particle specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, free living nematode Caenorhabditis elegans. Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC10 (5.9 mg L-1) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Activation of 26 pqn/abu genes from noncanonical Unfolded Protein Response (UPR) pathway and up-regulation of molecular chaperones (hsp-16.1, hsp-70, hsp-3 and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Inhibition of abu-11 with RNAi showed increase in mortality in Au-NP exposed nematodes suggesting possible involvement of abu-11 (a gene associated with specific to C. elegans UPR) in a protective mechanism against Au-NPs. Exposure to Au-NPs also caused activation of genes involved in apoptosis and necrosis and resulted ultimately in 10% mortality. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to a model ecoreceptor which activate both general and specific biological pathways. |
| GSM805422_A1_030210_Celegans_ | Au-NP Replicate1 (GSE32521: Toxicogenomic responses of C. elegans to gold nanoparticles) | We used Au nanoparticles (Au-NPs) as a model for studying particle specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, free living nematode Caenorhabditis elegans. Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC10 (5.9 mg L-1) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Activation of 26 pqn/abu genes from noncanonical Unfolded Protein Response (UPR) pathway and up-regulation of molecular chaperones (hsp-16.1, hsp-70, hsp-3 and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Inhibition of abu-11 with RNAi showed increase in mortality in Au-NP exposed nematodes suggesting possible involvement of abu-11 (a gene associated with specific to C. elegans UPR) in a protective mechanism against Au-NPs. Exposure to Au-NPs also caused activation of genes involved in apoptosis and necrosis and resulted ultimately in 10% mortality. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to a model ecoreceptor which activate both general and specific biological pathways. |
| GSM805423_A2_030210_Celegans_ | Au-NP Replicate2 (GSE32521: Toxicogenomic responses of C. elegans to gold nanoparticles) | We used Au nanoparticles (Au-NPs) as a model for studying particle specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, free living nematode Caenorhabditis elegans. Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC10 (5.9 mg L-1) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Activation of 26 pqn/abu genes from noncanonical Unfolded Protein Response (UPR) pathway and up-regulation of molecular chaperones (hsp-16.1, hsp-70, hsp-3 and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Inhibition of abu-11 with RNAi showed increase in mortality in Au-NP exposed nematodes suggesting possible involvement of abu-11 (a gene associated with specific to C. elegans UPR) in a protective mechanism against Au-NPs. Exposure to Au-NPs also caused activation of genes involved in apoptosis and necrosis and resulted ultimately in 10% mortality. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to a model ecoreceptor which activate both general and specific biological pathways. |
| GSM805424_A3_030210_Celegans_ | Au-NP Replicate3 (GSE32521: Toxicogenomic responses of C. elegans to gold nanoparticles) | We used Au nanoparticles (Au-NPs) as a model for studying particle specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, free living nematode Caenorhabditis elegans. Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC10 (5.9 mg L-1) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Activation of 26 pqn/abu genes from noncanonical Unfolded Protein Response (UPR) pathway and up-regulation of molecular chaperones (hsp-16.1, hsp-70, hsp-3 and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Inhibition of abu-11 with RNAi showed increase in mortality in Au-NP exposed nematodes suggesting possible involvement of abu-11 (a gene associated with specific to C. elegans UPR) in a protective mechanism against Au-NPs. Exposure to Au-NPs also caused activation of genes involved in apoptosis and necrosis and resulted ultimately in 10% mortality. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to a model ecoreceptor which activate both general and specific biological pathways. |
| GSM815851_HENGCEL_01_081006 | WS5041 (mir 58(n4640); alg 1(tm492); opIs205). Replicate 1 (GSE32944: Identification of miRNA target genes in C. elegans by RIP-chip-SRM) | RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans RNA binding protein immunopurification + microarray + targeted protein quantification via Selected Reaction Monitoring This SuperSeries is composed of the SubSeries listed below. |
| GSM815852_HENGCEL_02_081006 | WS4303 (alg 1(tm492); opIs205). Replicate 1 (GSE32944: Identification of miRNA target genes in C. elegans by RIP-chip-SRM) | RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans RNA binding protein immunopurification + microarray + targeted protein quantification via Selected Reaction Monitoring This SuperSeries is composed of the SubSeries listed below. |
| GSM815853_HENGCEL_03_081006 | WS5041 (mir 58(n4640); alg 1(tm492); opIs205). Replicate 2 (GSE32944: Identification of miRNA target genes in C. elegans by RIP-chip-SRM) | RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans RNA binding protein immunopurification + microarray + targeted protein quantification via Selected Reaction Monitoring This SuperSeries is composed of the SubSeries listed below. |
| GSM815854_HENGCEL_04_081006 | WS4303 (alg 1(tm492); opIs205). Replicate 2 (GSE32944: Identification of miRNA target genes in C. elegans by RIP-chip-SRM) | RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans RNA binding protein immunopurification + microarray + targeted protein quantification via Selected Reaction Monitoring This SuperSeries is composed of the SubSeries listed below. |
| GSM815855_HENGCEL_05_081006 | WS5041 (mir 58(n4640); alg 1(tm492); opIs205). Replicate 3 (GSE32944: Identification of miRNA target genes in C. elegans by RIP-chip-SRM) | RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans RNA binding protein immunopurification + microarray + targeted protein quantification via Selected Reaction Monitoring This SuperSeries is composed of the SubSeries listed below. |
| GSM815856_HENGCEL_06_081006 | WS4303 (alg 1(tm492); opIs205). Replicate 3 (GSE32944: Identification of miRNA target genes in C. elegans by RIP-chip-SRM) | RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans RNA binding protein immunopurification + microarray + targeted protein quantification via Selected Reaction Monitoring This SuperSeries is composed of the SubSeries listed below. |
| GSM815900_C | C. elegans exposed to space condition, technical rep1 (GSE32949: Expression data from C. elegans) | We used microarrays to investigate the effects of microgravity and space radiation on the genome-wide expression of the C. elegans. |
| GSM815901_160508_C | C. elegans exposed to space condition, technical rep2 (GSE32949: Expression data from C. elegans) | We used microarrays to investigate the effects of microgravity and space radiation on the genome-wide expression of the C. elegans. |
| GSM815902_160508_C | C. elegans exposed to space condition, technical rep3 (GSE32949: Expression data from C. elegans) | We used microarrays to investigate the effects of microgravity and space radiation on the genome-wide expression of the C. elegans. |
| GSM815903_C | C. elegans ground control, technical rep1 (GSE32949: Expression data from C. elegans) | We used microarrays to investigate the effects of microgravity and space radiation on the genome-wide expression of the C. elegans. |
| GSM815904_C | C. elegans ground control, technical rep2 (GSE32949: Expression data from C. elegans) | We used microarrays to investigate the effects of microgravity and space radiation on the genome-wide expression of the C. elegans. |
| GSM815905_160508_C | C. elegans ground control, technical rep3 (GSE32949: Expression data from C. elegans) | We used microarrays to investigate the effects of microgravity and space radiation on the genome-wide expression of the C. elegans. |
| GSM824416 | Hpl2 His24 KO 1 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824417 | Hpl2 His24 KO 2 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824418 | Hpl1 His24 KO 1 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824419 | Hpl1 His24 KO 2 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824420 | Hpl1 Hpl2 KO 1 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824421 | Hpl1 Hpl2 KO 2 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824422 | Hpl1 Hpl2 His24 KO 1 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM824423 | Hpl1 Hpl2 His24 KO 2 (GSE33339: Transcriptional repression of Hox genes by binding of HP1 and methylated H1 to H3K27me3 in C. elegans) | Elucidation of the biological role of H1 and HP1 in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Therefore we decided to study the function of HP1 (HPL-1 and HPL-2) and H1 (HIS-24) related proteins in C. elegans, since hpls and his-24 deficient nematodes are viable. Global transcriptional analysis of the mutant animals revealed that expression of only a small number of genes was affected and HPLs, and HIS-24 appear to influence the expression of genes through either activation or repression. Interestingly, knockout of HPL-2 and HIS-24 caused chromatin structure changes in the germline without altering core histone modifications. Furthermore, the mutant animals showed abnormal development of the male tail and the ectopic expression of C. elegans HOM-C genes (egl-5 and mab-5) involved in the developmental patterning of the mating structures. Surprisingly, H3K27me3 chromatin mark presented at the C. elegans HOM-C gene promoters was recognized by HPL-2 and methylated form of HIS-24. We propose that methylated HIS-24 and HPL-2 bind independently to PcG target loci that have been trimethylated at H3K27 by C. elegans MES-2 [E(Z)] to transcriptionally repress the Hox genes. Our results establish interplay of the H3K27me3 binding proteins, HP1/HPLs and H1/HIS-24 in the regulation of positional identity in the C. elegans males. |
| GSM840594_CVD109_N2_R1 | N2 exposed to CVD109, biological rep1 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840595_CVD109_N2_R2 | N2 exposed to CVD109, biological rep2 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840596_CVD109_N2_R3 | N2 exposed to CVD109, biological rep3 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840597_CVD110_N2_R1 | N2 exposed to CVD110, biological rep1 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840598_CVD110_N2_R2 | N2 exposed to CVD110, biological rep2 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840599_CVD110_N2_R3 | N2 exposed to CVD110, biological rep3 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840600_Del_hly_N2_R1 | N2 exposed to hemolysin mutant of E7946, biological rep1 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840601_Del_hly_N2_R2 | N2 exposed to hemolysin mutant of E7946, biological rep2 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840602_Del_hly_N2_R3 | N2 exposed to hemolysin mutant of E7946, biological rep3 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840603_E7946_N2_R1 | N2 exposed to E7946, biological rep1 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840604_E7946_N2_R2 | N2 exposed to E7946, biological rep2 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840605_E7946_N2_R3 | N2 exposed to E7946, biological rep3 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840606_OP50_N2_R1 | N2 exposed to OP50(E.coli), biological rep1 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840607_OP50_N2_R2 | N2 exposed to OP50(E.coli), biological rep2 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM840608_OP50_N2_R3 | N2 exposed to OP50(E.coli), biological rep3 (GSE34026: Expression data from C. elegans) | We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. |
| GSM842065 | wild-type 1 (GSE34113: Expression Profiling of Caenorabditis elegans tdp-1 loss-of-function mutant) | Transactive response DNA-binding protein of 43 kDa (TDP-43), a heterogeneous nuclear ribonucleoprotein (hnRNP) with diverse activities, is a common denominator in several neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Orthologs of TDP-43 exist from mammals to invertebrates, but their functions in lower organisms remain poorly understood. Here we systematically studied mutant Caenorhabditis elegans lacking the nematode TDP-43 ortholog, TDP-1. To understand the global gene expression regulation induced by the loss of tdp-1, the C. elegans transcriptomes were compared between the N2 WT animals and the tdp-1(ok803lf) mutant. Transcriptional profiling demonstrated that the loss of TDP-1 altered expression of genes functioning in RNA processing and protein folding. These results suggest that the C. elegans TDP-1 as an RNA-processing protein may have a role in the regulation of protein homeostasis and aging. Global gene expression profiling was performed to compare the transcriptome of wild-type (N2) Caenorabditis elegans and that of tdp-1(ok803) loss-of-function mutant. |
| GSM842066 | wild-type 2 (GSE34113: Expression Profiling of Caenorabditis elegans tdp-1 loss-of-function mutant) | Transactive response DNA-binding protein of 43 kDa (TDP-43), a heterogeneous nuclear ribonucleoprotein (hnRNP) with diverse activities, is a common denominator in several neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Orthologs of TDP-43 exist from mammals to invertebrates, but their functions in lower organisms remain poorly understood. Here we systematically studied mutant Caenorhabditis elegans lacking the nematode TDP-43 ortholog, TDP-1. To understand the global gene expression regulation induced by the loss of tdp-1, the C. elegans transcriptomes were compared between the N2 WT animals and the tdp-1(ok803lf) mutant. Transcriptional profiling demonstrated that the loss of TDP-1 altered expression of genes functioning in RNA processing and protein folding. These results suggest that the C. elegans TDP-1 as an RNA-processing protein may have a role in the regulation of protein homeostasis and aging. Global gene expression profiling was performed to compare the transcriptome of wild-type (N2) Caenorabditis elegans and that of tdp-1(ok803) loss-of-function mutant. |
| GSM842067 | wild-type 3 (GSE34113: Expression Profiling of Caenorabditis elegans tdp-1 loss-of-function mutant) | Transactive response DNA-binding protein of 43 kDa (TDP-43), a heterogeneous nuclear ribonucleoprotein (hnRNP) with diverse activities, is a common denominator in several neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Orthologs of TDP-43 exist from mammals to invertebrates, but their functions in lower organisms remain poorly understood. Here we systematically studied mutant Caenorhabditis elegans lacking the nematode TDP-43 ortholog, TDP-1. To understand the global gene expression regulation induced by the loss of tdp-1, the C. elegans transcriptomes were compared between the N2 WT animals and the tdp-1(ok803lf) mutant. Transcriptional profiling demonstrated that the loss of TDP-1 altered expression of genes functioning in RNA processing and protein folding. These results suggest that the C. elegans TDP-1 as an RNA-processing protein may have a role in the regulation of protein homeostasis and aging. Global gene expression profiling was performed to compare the transcriptome of wild-type (N2) Caenorabditis elegans and that of tdp-1(ok803) loss-of-function mutant. |
| GSM842068 | tdp-1(ok803) (GSE34113: Expression Profiling of Caenorabditis elegans tdp-1 loss-of-function mutant) | Transactive response DNA-binding protein of 43 kDa (TDP-43), a heterogeneous nuclear ribonucleoprotein (hnRNP) with diverse activities, is a common denominator in several neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Orthologs of TDP-43 exist from mammals to invertebrates, but their functions in lower organisms remain poorly understood. Here we systematically studied mutant Caenorhabditis elegans lacking the nematode TDP-43 ortholog, TDP-1. To understand the global gene expression regulation induced by the loss of tdp-1, the C. elegans transcriptomes were compared between the N2 WT animals and the tdp-1(ok803lf) mutant. Transcriptional profiling demonstrated that the loss of TDP-1 altered expression of genes functioning in RNA processing and protein folding. These results suggest that the C. elegans TDP-1 as an RNA-processing protein may have a role in the regulation of protein homeostasis and aging. Global gene expression profiling was performed to compare the transcriptome of wild-type (N2) Caenorabditis elegans and that of tdp-1(ok803) loss-of-function mutant. |
| GSM842069 | tdp-1(ok803) 2 (GSE34113: Expression Profiling of Caenorabditis elegans tdp-1 loss-of-function mutant) | Transactive response DNA-binding protein of 43 kDa (TDP-43), a heterogeneous nuclear ribonucleoprotein (hnRNP) with diverse activities, is a common denominator in several neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Orthologs of TDP-43 exist from mammals to invertebrates, but their functions in lower organisms remain poorly understood. Here we systematically studied mutant Caenorhabditis elegans lacking the nematode TDP-43 ortholog, TDP-1. To understand the global gene expression regulation induced by the loss of tdp-1, the C. elegans transcriptomes were compared between the N2 WT animals and the tdp-1(ok803lf) mutant. Transcriptional profiling demonstrated that the loss of TDP-1 altered expression of genes functioning in RNA processing and protein folding. These results suggest that the C. elegans TDP-1 as an RNA-processing protein may have a role in the regulation of protein homeostasis and aging. Global gene expression profiling was performed to compare the transcriptome of wild-type (N2) Caenorabditis elegans and that of tdp-1(ok803) loss-of-function mutant. |
| GSM842070 | tdp-1(ok803) 3 (GSE34113: Expression Profiling of Caenorabditis elegans tdp-1 loss-of-function mutant) | Transactive response DNA-binding protein of 43 kDa (TDP-43), a heterogeneous nuclear ribonucleoprotein (hnRNP) with diverse activities, is a common denominator in several neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Orthologs of TDP-43 exist from mammals to invertebrates, but their functions in lower organisms remain poorly understood. Here we systematically studied mutant Caenorhabditis elegans lacking the nematode TDP-43 ortholog, TDP-1. To understand the global gene expression regulation induced by the loss of tdp-1, the C. elegans transcriptomes were compared between the N2 WT animals and the tdp-1(ok803lf) mutant. Transcriptional profiling demonstrated that the loss of TDP-1 altered expression of genes functioning in RNA processing and protein folding. These results suggest that the C. elegans TDP-1 as an RNA-processing protein may have a role in the regulation of protein homeostasis and aging. Global gene expression profiling was performed to compare the transcriptome of wild-type (N2) Caenorabditis elegans and that of tdp-1(ok803) loss-of-function mutant. |
| GSM84278 | L2 (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84279 | N2 mixed stage (red, channel 2) vs. L4(repeat #1) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84280 | N2 mixed stage (red, channel 2) vs. L4 (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84281 | wt/hermaphrodite (red, channel 2) vs. him-8/male (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84282 | N2 mixed stage (red, channel 2) vs. L1(repeat #1) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84283 | N2 mixed stage (red, channel 2) vs. young adult (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84284 | N2 mixed stage (red, channel 2) vs. egg (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84285 | N2 mixed stage (red, channel 2) vs. L3(repeat #1) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84286 | N2 mixed stage (red, channel 2) vs. young adult(repeat #1) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84287 | N2 mixed stage (red, channel 2) vs. L1 (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84288 | N2 mixed stage (red, channel 2) vs. egg (repeat #1) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84289 | him-8m (green) vs. N2h (red) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84290 | N2h (red, channel 2) vs. him-8m (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84291 | N2 (red, channel 2) vs. him-5 male (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84292 | N2 mixed stage (red, channel 2) vs. L3 (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84293 | male/hermaphrodite (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84294 | N2 mixed stage (red, channel 2) vs. L2 (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84295 | N2 mixed stage (red, channel 2) vs. L4(repeat #3) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84296 | L3 (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84297 | N2 mixed stage (red, channel 2) vs. egg(repeat #2) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84298 | L4 (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84299 | N2 mixed stage (red, channel 2) vs. L2(repeat #2) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84300 | N2 mixed stage (red, channel 2) vs. egg(repeat #3) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84301 | L1 (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84302 | N2 mixed stage (red, channel 2) vs. L1(repeat #2) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84303 | N2 mixed stage (red, channel 2) vs. L2(repeat #3) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84304 | N2 mixed stage (red, channel 2) vs. L2(repeat #1) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84305 | adult (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84306 | N2 mixed stage (red, channel 2) vs. young adult(repeat #2) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84307 | N2 mixed stage (red, channel 2) vs. L3(repeat #2) (green, channel 1) (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM84308 | Egg (GSE3633: Genome-wide analysis of developmental and sex-regulated gene expression profiles in C. elegans) | We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM849809_09_30_11_MKrause1_IH_Celegans_1_4uM_Con_1 | 4uM-Con-1 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849810_09_30_11_MKrause2_IH_Celegans_2_4uM_Con_2 | 4uM-Con-2 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849811_09_30_11_MKrause3_IH_Celegans_3_4uM_Con_3 | 4uM-Con-3 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849812_09_30_11_MKrause4_IH_Celegans_4_20uM_Con_1 | 20uM-Con-1 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849813_09_30_11_MKrause5_IH_Celegans_5_20uM_Con_2 | 20uM-Con-2 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849814_09_30_11_MKrause6_IH_Celegans_6_20uM_Con_3 | 20uM-Con-3 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849815_09_30_11_MKrause7_IH_Celegans_7_4uM_Exp1 | 4uM-Exp1 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849816_09_30_11_MKrause8_IH_Celegans_8_4uM_Exp2 | 4uM-Exp2 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849817_09_30_11_MKrause9_IH_Celegans_9_4uM_Exp3 | 4uM-Exp3 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849818_09_30_11_MKrause10_IH_Celegans_10_20uM_Exp1 | 20uM-Exp1 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849819_09_30_11_MKrause11_IH_Celegans_11_20uM_Exp2 | 20uM-Exp2 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM849820_09_30_11_MKrause12_IH_Celegans_12_20uM_Exp3 | 20uM-Exp3 (GSE34471: Heme utilization in the Caenorhabditis elegans hypodermal cells is facilitated by HRG-2) | The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. |
| GSM85233 | skn-1 (red, channel 2) vs. par-1 (green, channel 1) (repeat #2) (GSE3681: PHA-4 organogenesis) | The pha-4 locus encodes a forkhead box A (FoxA/HNF3) transcription factor homolog that specifies organ identity for Caenorhabditis elegans pharyngeal cells. We used microarrays to identify pharyngeal genes and analyzed those genes to determine which were direct PHA-4 targets. Our data suggest that PHA-4 directly activates most or all pharyngeal genes. Furthermore, the relative affinity of PHA-4 for different TRTTKRY (R = A/G, K = T/G, Y = T/C) elements modulates the onset of gene expression, providing a mechanism to activate pharyngeal genes at different developmental stages. We suggest that direct transcriptional regulation of entire gene networks may be a common feature of organ identity genes. A genotyping experiment design type classifies an individual or group of individuals on the basis of alleles, haplotypes, SNP's. Keywords: genotyping_design |
| GSM85234 | par-1 strain kk822 (gree, channel 1) vs. skn-1 (zu67)/Dnt1[unc?; let?] strain EU1 (red, channel 2) (GSE3681: PHA-4 organogenesis) | The pha-4 locus encodes a forkhead box A (FoxA/HNF3) transcription factor homolog that specifies organ identity for Caenorhabditis elegans pharyngeal cells. We used microarrays to identify pharyngeal genes and analyzed those genes to determine which were direct PHA-4 targets. Our data suggest that PHA-4 directly activates most or all pharyngeal genes. Furthermore, the relative affinity of PHA-4 for different TRTTKRY (R = A/G, K = T/G, Y = T/C) elements modulates the onset of gene expression, providing a mechanism to activate pharyngeal genes at different developmental stages. We suggest that direct transcriptional regulation of entire gene networks may be a common feature of organ identity genes. A genotyping experiment design type classifies an individual or group of individuals on the basis of alleles, haplotypes, SNP's. Keywords: genotyping_design |
| GSM85235 | skn-1 (zu67)/Dnt1[unc?; let?] strain EU1 (red, channel 2) vs. par-1 strain kk822 (green, channel 1) (GSE3681: PHA-4 organogenesis) | The pha-4 locus encodes a forkhead box A (FoxA/HNF3) transcription factor homolog that specifies organ identity for Caenorhabditis elegans pharyngeal cells. We used microarrays to identify pharyngeal genes and analyzed those genes to determine which were direct PHA-4 targets. Our data suggest that PHA-4 directly activates most or all pharyngeal genes. Furthermore, the relative affinity of PHA-4 for different TRTTKRY (R = A/G, K = T/G, Y = T/C) elements modulates the onset of gene expression, providing a mechanism to activate pharyngeal genes at different developmental stages. We suggest that direct transcriptional regulation of entire gene networks may be a common feature of organ identity genes. A genotyping experiment design type classifies an individual or group of individuals on the basis of alleles, haplotypes, SNP's. Keywords: genotyping_design |
| GSM85967 | 6HR-7 (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM85968 | 6HR-5 (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM85969 | 6HR-3 (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM85970 | 15MIN-2 (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM85971 | 15MIN-1 (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM85972 | 30MIN (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM85973 | 6HR-4 (GSE3727: Ethanol-response genes and their regulation) | The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM866671 | Q control_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866672 | Q control_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866673 | Q control_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866674 | Q50_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866675 | Q50_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866676 | Q50_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866677 | Q100_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866678 | Q100_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866679 | Q100_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866680 | Q200_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866681 | Q200_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866682 | Q200_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866683 | TA Control_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866684 | TA Control_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866685 | TA Control_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866686 | TA100_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866687 | TA100_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866695 | TA100_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866696 | TA200_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866697 | TA200_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866698 | TA200_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866720 | TA300_rep1 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866721 | TA300_rep2 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866722 | TA300_rep3 (GSE35354: Meta-analysis of global transcriptomics of Quercetin and Tannic acid exposed C. elegans) | Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic. |
| GSM866728 | HF 3d control_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866729 | HF 3d control_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866730 | HF 3d control_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866731 | HF 3d_0.2_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866732 | HF 3d_0.2_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866733 | HF 3d_0.2_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866734 | HF 3d_2.0_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866735 | HF 3d_2.0_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866736 | HF 3d_2.0_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866737 | HF 11d control_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866750 | HF 11d control_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866751 | HF 11d control_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866752 | HF 11d_0.2_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866753 | HF 11d_0.2_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866754 | HF 11d_0.2_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866755 | HF 11d_2.0_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866756 | HF 11d_2.0_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866757 | HF 11d_2.0_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866758 | HFHQ 3d control_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866759 | HFHQ 3d control_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866760 | HFHQ 3d control_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866761 | HFHQ 3d_0.2_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866762 | HFHQ 3d_0.2_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866763 | HFHQ 3d_0.2_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866764 | HFHQ 3d_2.0_rep1 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866765 | HFHQ 3d_2.0_rep2 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM866766 | HFHQ 3d_2.0_rep3 (GSE35360: The complex interplay of genetic pathways in C.elegans following the treatment with humic substances) | Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. |
| GSM889558_G030040_01 | Ground Control (operation site) (GSE36358: Expression Data from International C.elegans Experiment 1st) | The effect of microgravity on gene expression in C.elegans was comprehensively analysed by DNA microarray. This is the first DNA microarray analysis for C.elegans grown under microgravity. Hyper gravity and clinorotation experiments were performed as reference against the flight experiment. |
| GSM889559_G030040_02 | Ground Control (Tsukuba space center) (GSE36358: Expression Data from International C.elegans Experiment 1st) | The effect of microgravity on gene expression in C.elegans was comprehensively analysed by DNA microarray. This is the first DNA microarray analysis for C.elegans grown under microgravity. Hyper gravity and clinorotation experiments were performed as reference against the flight experiment. |
| GSM889560_G030040_03 | Space Flight (GSE36358: Expression Data from International C.elegans Experiment 1st) | The effect of microgravity on gene expression in C.elegans was comprehensively analysed by DNA microarray. This is the first DNA microarray analysis for C.elegans grown under microgravity. Hyper gravity and clinorotation experiments were performed as reference against the flight experiment. |
| GSM889561_G030040_04 | Clino Rotation (GSE36358: Expression Data from International C.elegans Experiment 1st) | The effect of microgravity on gene expression in C.elegans was comprehensively analysed by DNA microarray. This is the first DNA microarray analysis for C.elegans grown under microgravity. Hyper gravity and clinorotation experiments were performed as reference against the flight experiment. |
| GSM889562_G030040_05 | Hyper Gravity (GSE36358: Expression Data from International C.elegans Experiment 1st) | The effect of microgravity on gene expression in C.elegans was comprehensively analysed by DNA microarray. This is the first DNA microarray analysis for C.elegans grown under microgravity. Hyper gravity and clinorotation experiments were performed as reference against the flight experiment. |
| GSM893037 | Asynch-Intestine-Rep1 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893038 | Asynch-Intestine-Rep2 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893039 | Asynch-Intestine-Rep3 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893040 | Asynch-Intestine-Rep4 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893041 | Asynch-Muscle-Rep1 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893042 | Asynch-Muscle-Rep2 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893043 | Asynch-Muscle-Rep3 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893044 | Asynch-Muscle-Rep4 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893045 | L4-Intestine-Rep1 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893046 | L4-Intestine-Rep2 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893047 | L4-Intestine-Rep3 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893048 | L4-Intestine-Rep4 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893049 | L4-Intestine-Rep5 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893050 | GFP-Rep1 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM893051 | GFP-Rep2 (GSE36419: Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response) | Gene regulation by microRNAs (miRNAs) under specific physiological conditions often involves complex interactions between multiple miRNAs and a large number of their targets, as well as coordination with other regulatory mechanisms, limiting the effectiveness of classical genetic methods to identify miRNA functions. We took a systematic approach to analyze the miRNA-induced silencing complex (miRISC) in individual tissues of C. elegans and found that mRNAs encoded by pathogen-responsive genes were dramatically over-represented in the intestinal miRISC, and that multiple miRNAs accumulated in the intestinal miRISCs upon infection. Inactivation of the miRISC or ablation of miRNAs from different families, resulted in over-expression of several pathogen-responsive genes under basal conditions and, surprisingly, enhanced worm survival on pathogenic Pseudomonas aeruginosa. These results indicate that much of the miRNA activity in the gut is dedicated to attenuating the activity of the pathogen response system, uncovering a novel and complex physiological function of the miRNA network. |
| GSM895821 | C. elegans: S. aureus vs. E. coli OP50 exposure; 4hours, Biological Replicate 1 (GSE36493: C. elegans immune response to Staphylococcus aureus, 4 hour exposure) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Staphylococcus aureus for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Staphylococcus aureus, Serratia marcescens, Xenorhabdus nematophila. Keywords: Expression profiling by array |
| GSM895822 | C. elegans: S. aureus vs. E. coli OP50 exposure; 4hours, Biological Replicate 2 (GSE36493: C. elegans immune response to Staphylococcus aureus, 4 hour exposure) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Staphylococcus aureus for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Staphylococcus aureus, Serratia marcescens, Xenorhabdus nematophila. Keywords: Expression profiling by array |
| GSM895823 | C. elegans: S. aureus vs. E. coli OP50 exposure; 4hours, Biological Replicate 3 (Dye-swap) (GSE36493: C. elegans immune response to Staphylococcus aureus, 4 hour exposure) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Staphylococcus aureus for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Staphylococcus aureus, Serratia marcescens, Xenorhabdus nematophila. Keywords: Expression profiling by array |
| GSM895824 | C. elegans: S. aureus vs. E. coli OP50 exposure; 4hours, Biological Replicate 4 (Dye-swap) (GSE36493: C. elegans immune response to Staphylococcus aureus, 4 hour exposure) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Staphylococcus aureus for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Staphylococcus aureus, Serratia marcescens, Xenorhabdus nematophila. Keywords: Expression profiling by array |
| GSM895879 | C. elegans: S. marcescens vs. E. coli OP50 exposure; 4hours, Biological Replicate 1 (Dye-swap) (GSE36499: C. elegans young adults: Exposed to Serratia marcescens versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Serratia marcescens for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Xenorhabdus nematophila. |
| GSM895880 | C. elegans: S. marcescens vs. E. coli OP50 exposure; 4hours, Biological Replicate 2 (Dye-swap) (GSE36499: C. elegans young adults: Exposed to Serratia marcescens versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Serratia marcescens for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Xenorhabdus nematophila. |
| GSM895881 | C. elegans: S. marcescens vs. E. coli OP50 exposure; 4hours, Biological Replicate 3 (GSE36499: C. elegans young adults: Exposed to Serratia marcescens versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Serratia marcescens for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Xenorhabdus nematophila. |
| GSM895882 | C. elegans: S. marcescens vs. E. coli OP50 exposure; 4hours, Biological Replicate 4 (GSE36499: C. elegans young adults: Exposed to Serratia marcescens versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Serratia marcescens for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Xenorhabdus nematophila. |
| GSM895904 | C. elegans: X. nematophila vs. E. coli OP50 exposure; 4hours, Biological Replicate 1 (GSE36501: C. elegans young adults: Exposed to Xenorhabdus nematophila versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Xenorhabdus nematophila for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Serratia marcescens. |
| GSM895905 | C. elegans: X. nematophila vs. E. coli OP50 exposure; 4hours, Biological Replicate 2 (GSE36501: C. elegans young adults: Exposed to Xenorhabdus nematophila versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Xenorhabdus nematophila for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Serratia marcescens. |
| GSM895906 | C. elegans: X. nematophila vs. E. coli OP50 exposure; 4hours, Biological Replicate 3 (Dye swap) (GSE36501: C. elegans young adults: Exposed to Xenorhabdus nematophila versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Xenorhabdus nematophila for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Serratia marcescens. |
| GSM895907 | C. elegans: X. nematophila vs. E. coli OP50 exposure; 4hours, Biological Replicate 4 (Dye swap) (GSE36501: C. elegans young adults: Exposed to Xenorhabdus nematophila versus exposed to E. coli OP50 : 4 hours) | Transcriptional profiling of C. elegans young adult worms exposed to pathogen Xenorhabdus nematophila for 4 hours versus age-matched worms exposed to control lab food E. coli OP50. The goal was to identify genes regulated in response to pathogen. The broader goal of study was to study evolution of pathogen response by comparing this expression profile to that obtained by exposing the nematode Pristionchus pacificus to the same pathogen. Other experiments which are a part of this study include expression profiling of C. elegans and P. pacificus on other pathogens including Bacillus thuringiensis, Staphylococcus aureus, and Serratia marcescens. |
| GSM899880 | C. elegans cultured on : Bacillus strain 67 vs. E. coli OP50 exposure; Biological Replicate 1 (GSE36733: C. elegans young adults cultured on Bacillus subtilis strain 67 vs cultured on E. coli OP50) | Transcriptional profiling of C. elegans young adult worms cultured on non-pathogenic Bacillus subtilis strain 67 versus age-matched worms cultured on the control lab food E. coli OP50. The goal was to identify genes regulated in response to differences in diet, which potentially confer immunity to later exposures to pathogenic Bacillus thuringiensis DB27. |
| GSM899881 | C. elegans cultured on : Bacillus strain 67 vs. E. coli OP50 exposure; Biological Replicate 2 (GSE36733: C. elegans young adults cultured on Bacillus subtilis strain 67 vs cultured on E. coli OP50) | Transcriptional profiling of C. elegans young adult worms cultured on non-pathogenic Bacillus subtilis strain 67 versus age-matched worms cultured on the control lab food E. coli OP50. The goal was to identify genes regulated in response to differences in diet, which potentially confer immunity to later exposures to pathogenic Bacillus thuringiensis DB27. |
| GSM899882 | C. elegans cultured on : Bacillus strain 67 vs. E. coli OP50 exposure; Biological Replicate 3. Dye-swap-1 (GSE36733: C. elegans young adults cultured on Bacillus subtilis strain 67 vs cultured on E. coli OP50) | Transcriptional profiling of C. elegans young adult worms cultured on non-pathogenic Bacillus subtilis strain 67 versus age-matched worms cultured on the control lab food E. coli OP50. The goal was to identify genes regulated in response to differences in diet, which potentially confer immunity to later exposures to pathogenic Bacillus thuringiensis DB27. |
| GSM899883 | C. elegans cultured on : Bacillus strain 67 vs. E. coli OP50 exposure; Biological Replicate 4. Dye-swap-2 (GSE36733: C. elegans young adults cultured on Bacillus subtilis strain 67 vs cultured on E. coli OP50) | Transcriptional profiling of C. elegans young adult worms cultured on non-pathogenic Bacillus subtilis strain 67 versus age-matched worms cultured on the control lab food E. coli OP50. The goal was to identify genes regulated in response to differences in diet, which potentially confer immunity to later exposures to pathogenic Bacillus thuringiensis DB27. |
| GSM90746 | EM673(lin-22) (red) vs. EM672(hlh-2; lin-32) (repeat #2) (green) (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM90747 | EM673(dpy-28;lin-22;him-5) (red) vs. EM672(hlh-2;dpy-28;him-5;lin-32) (green) (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM90748 | EM673(lin-22) (red) vs. EM672(hlh-2; lin-32) (repeat #3) (green) (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM90749 | hlh-2; dpy-28; him-5; lin-32 adult males vs. dpy-28; lin-22; him-5 adult males #1 (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM90750 | hlh-2; dpy-28; him-5; lin-32 adult males vs. dpy-28; lin-22; him-5 adult males #2 (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM90751 | EM673(dpy-28;lin-22;him-5)(red, channel 2) vs. EM672(hlh-2;dpy-28;him-5;lin-32)(green, channel 1) (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM90752 | EM673(dpy-28;lin-22;him-5)(red) vs. EM672(hlh-2;dpy-28;him-5;lin-32)(green) (repeat #1) (GSE3979: Sensory ray genes) | These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Keywords: time_series_design |
| GSM91446 | N2 ref. JL1 vs. fer-15 day 9 (8/12/00) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91447 | N2 ref. JL1 vs. spe-9;fer-15 day 3 (1E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91448 | N2 ref. JL1 vs. spe-9;fer-15 day 16 (49E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91449 | N2 ref. JL1 vs. fer-15 day 3 (8/6/00) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91450 | N2 ref. JL1 vs. fer-15 day 6 (5/12/00) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91451 | N2 ref. JL1 vs. spe-9;fer-15 day 4 (6E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91452 | N2 ref. JL1 vs. spe-9;emb-27 day 3 (40E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91453 | N2 ref. JL1 vs. spe-9;fer-15 day 9 (3E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91454 | N2 ref. JL1 vs. spe-9;fer-15 day 3 (2E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91455 | N2 ref. JL1 vs. spe-9;fer-15 day 6 (31E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91456 | N2 ref. JL1 vs. spe-9;fer-15 day 13 (48E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91457 | N2 ref. JL1 vs. spe-9;fer-15 day 10 (53E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91458 | N2 ref. JL1 vs. spe-9;fer-15 day 19 (50E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91459 | N2 ref. JL1 vs. spe-9;fer-15 day 16 (54E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91460 | N2 ref. JL1 vs. spe-9;emb-27 day 12 (43E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91461 | N2 ref. JL1 vs. spe-9;fer-15 day 3 (21C) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91462 | N2 ref. JL1 vs. spe-9;fer-15 day 9 (4E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91463 | N2 ref. JL1 vs. spe-9;fer-15 day 10 (47E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91464 | N2 ref. JL1 vs. spe-9;fer-15 day 4 (51E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91465 | N2 ref. JL1 vs. spe-9;fer-15 day 4 (45E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91466 | N2 ref. JL1 vs. spe-9;emb-27 day 6 (41E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91467 | N2 ref. JL1 vs. spe-9;fer-15 day 7 (46E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91468 | N2 ref. JL1 vs. fer-15 day 12 (8/15/00) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91469 | N2 ref. JL1 vs. spe-9;emb-27 day 14 (44E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91470 | N2 ref. JL1 vs. spe-9;fer-15 day 11 (33E) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM91471 | N2 ref. JL1 vs. fer-15 day 3 (5/30/00) (GSE4005: Aging time course) | Transcriptional Profile of Aging in C. elegans Whole-genome analysis of gene expression during chronological aging of the worm provides a rich database of age-specific changes in gene expression and represents one way to distinguish among these models. Using a rigorous statistical model with multiple replicates, we find that a relatively small number of genes (only 164) show statistically significant changes in transcript levels as aging occurs (<1% of the genome). Expression of heat shock proteins decreases, while expression of certain transposases increases in older worms, and these findings are consistent with a higher mortality risk due to a failure in homeostenosis and destabilization of the genome in older animals. Finally, a specific subset of genes is coordinately altered both during chronological aging and in the transition from the reproductive form to the dauer, demonstrating a mechanistic overlap in aging between these two processes. Groups of assays that are related as part of a time series. Age: Age of organism Keywords: time_series_design |
| GSM915201_DMSO_G | DMSO G (GSE37266: Stimulation of Host Immune Defenses by a Small Molecule Protects C. elegans from Bacterial Infection) | The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24. |
| GSM915202_DMSO_H | DMSO H (GSE37266: Stimulation of Host Immune Defenses by a Small Molecule Protects C. elegans from Bacterial Infection) | The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24. |
| GSM915203_DMSO_I | DMSO I (GSE37266: Stimulation of Host Immune Defenses by a Small Molecule Protects C. elegans from Bacterial Infection) | The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24. |
| GSM915204_RPW_24_G | RPW-24 G (GSE37266: Stimulation of Host Immune Defenses by a Small Molecule Protects C. elegans from Bacterial Infection) | The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24. |
| GSM915205_RPW_24_H | RPW-24 H (GSE37266: Stimulation of Host Immune Defenses by a Small Molecule Protects C. elegans from Bacterial Infection) | The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24. |
| GSM915206_RPW_24_I | RPW-24 I (GSE37266: Stimulation of Host Immune Defenses by a Small Molecule Protects C. elegans from Bacterial Infection) | The nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24. |
| GSM919250_EM3742_Celegans_030407 | N2 rep1 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919251_EM3745_Celegans_030407 | N2 rep2 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919252_EM3748_Celegans_030407 | N2 rep3 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919253_EM3743_Celegans_030407 | piwi n4357 n4358 rep1 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919254_EM3744_Celegans_030407 | piwi n4357 n4358 rep2 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919255_EM3746_Celegans_030407 | piwi n4357 n4358 rep3 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919256_EM3747_Celegans_030407 | piwi n4503 nDf57 rep1 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919257_EM3749_Celegans_030407 | piwi n4503 nDf57 rep2 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM919258_EM3750_Celegans_030407 | piwi n4503 nDf57 rep3 (GSE37433: Function, targets and evolution of Caenorhabditis elegans piRNAs) | This SuperSeries is composed of the SubSeries listed below. |
| GSM936472_AN_1_Celegans | wild-type-control, biological rep1 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936473_AN_2_Celegans | wild-type-treated, biological rep1 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936474_AN_3_Celegans | atfs-1(tm4525)-control, biological rep1 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936475_AN_4_Celegans | atfs-1(tm4525)-treated, biological rep1 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936476_AN_5_Celegans | wild-type-control, biological rep2 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936477_AN_6_Celegans | wild-type-treated, biological rep2 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936478_AN_7_Celegans | atfs-1(tm4525)-control, biological rep2 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936479_AN_8_Celegans | atfs-1(tm4525)-treated, biological rep2 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936480_AN_9_Celegans | wild-type-control, biological rep3 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936481_AN_10_Celegans | wild-type-treated, biological rep3 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936482_AN_11_Celegans | atfs-1(tm4525)-control, biological rep3 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM936483_AN_12_Celegans | atfs-1(tm4525)-treated, biological rep3 (GSE38196: ATFS-1 mediates a protective transcription program during mitochondrial stress) | ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress |
| GSM93684 | dDf-16 D (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93685 | daf-16 A (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93686 | dBf-16 B (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93687 | dCf-16 C (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93688 | C7 vs R7 (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93689 | C8 vs R8 (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93690 | C12 vs R12 (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93691 | C10 vs R10 (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93692 | sir2.1(1.8.1.2) (prep.2) vs. unc-119 (prep.2) (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93693 | sir2.1(1.8.1.2) (prep.3) vs. unc-119 (prep.3) (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93694 | sir2.1(1.8.1.2) (prep.4) vs. unc-119 (prep.4) (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93695 | sir2.1(1.8.1.2) (prep.1) vs. unc-119 (prep.1) (GSE4402: A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span) | Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below. |
| GSM93986 | R087 (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93987 | R112 (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93988 | R113 (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93989 | R088 (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93990 | 3.1a vs 3.1b (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93991 | 1.1a vs 1.1b (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93992 | 5.1a vs 5.1b (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93993 | 5.2a vs 5.2b (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93994 | 1.2a vs 1.2b (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM93995 | 2.1a vs 2.1b (GSE4111: Expression profiling of five different xenobiotics using a C. elegans microarray) | Using a C. elegans whole genome DNA microarray in this study, the effects of five different xenobiotics on the gene expression of the nematode were investigated. The exposure time for the following five applied compounds beta-NF (5 mg/l), Fla (0.5 mg/l), atrazine (25 mg/l), clofibrate (10 mg/l) and DES (0.5 mg/l) was 48+/-5 h. The analysis of the data showed a clear induction of 203 genes belonging to different families like the cytochromes P450, UDP-glucoronosyltransferases (UDPGT), glutathione S-transferases (GST), carboxylesterases, collagenes, C-type lectins and others. Under the applied conditions, fluoranthene was able to induce most of the induceable genes, followed by clofibrate, atrazine, beta-naphthoflavone and diethylstilbestrol. A decreased expression could be shown for 153 genes with atrazine having the strongest effect followed by fluoranthene, diethylstilbestrol, beta-naphthoflavone and clofibrate. For upregulated genes a change ranging from approximately 2.1- till 42.3-fold and for downregulated genes from approximately 2.1 till 6.6-fold of gene expression could be affected through the applied xenobiotics. Sample Treatments (by exptids) Clofibrate: 14317, 16443, 16505 Fluoranthene: 33664, 33667, 33669, 23484 beta-Naphthoflavone: 6844, 14320, 14316 Atrazin: 33672, 33674, 23487, 23486 DES: 33671, 23485 A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design |
| GSM94427 | N2 II (starting line) (red, channel 2) vs. MA96 II (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94428 | N2-I (starting line) (red,channel 2)vs PB306-I (with selection) (green,channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94429 | N2-III (starting line) (red, channel 2) vs. MA59-III (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94430 | N2-II (starting line) (red, channel 2) vs MA59-II (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94431 | MA41-4 (A) (no selection) (red, channel 2) vs. MA24-4 (B) (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94432 | MA41-3 (A) (no selection) (red, channel 2) vs. MA24-3 (B) (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94433 | CB4856-3(A) (red, channel 2) vs. AB1-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94434 | CB4856-4(A) (red, channel 2) vs. AB1-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94435 | N2 I (starting line) (red, channel 2) vs. MA96 I (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94436 | MA24 vs N2 - 1 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94437 | MA24 vs N2 - 2 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94438 | MA24 vs N2 - 3 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94439 | MA99 vs N2 - 1 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94440 | MA24-3(A) (red, channel 2) vs. N2-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94441 | N2-II (starting line) (red, channel 2) vs. PB306-II (with selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94442 | N2-III (starting line) (red, channel 2) vs. PB306-III (with selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94443 | MA24-2 (B) (no selection) (red, channel 2) vs. MA41-2 (A) (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94444 | MA24-1 (B) (no selection) (red, channel 2) vs. MA41-1 (A) (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94445 | N2-I (starting line) (red, channel 2) vs. MA59-I (no selection) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94446 | PB303-3(A) (red, channel 2) vs. N2-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94447 | AB1-3(A) (red, channel 2) vs. PB306-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94448 | MA83-2(B) (red, channel 2) vs. MA99-2(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94449 | AB1-1(B) (red, channel 2) vs. CB4856-1(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94450 | MA83-1(B) (red, channel 2) vs. MA99-1(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94451 | CB4856-2(B) (red, channel 2) vs. N2-2(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94452 | MA99-4(A) (red, channel 2) vs. MA83-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94453 | MA99-3(A) (red, channel 2) vs. MA83-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94454 | N2-3(A) (red, channel 2) vs. CB4856-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94455 | PB303-4(A) (red, channel 2) vs. N2-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94456 | MA99 vs N2 - 2 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94457 | MA41-1(B) (red, channel 2) vs. MA83-1(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94458 | N2-4(A) (red, channel 2) vs. CB4856-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94459 | PB303-1(B) (red, channel 2) vs. PB306-1(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94460 | N2 vs MA99 - 1 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94461 | MA83-4(A) (red, channel 2) vs. MA41-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94462 | AB1-2(B) (red, channel 2) vs. CB4856-2(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94463 | PB303-2(B) (red, channel 2) vs. PB306-2(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94464 | N2 vs MA99 - 2 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94465 | MA83-3(A) (red, channel 2) vs. MA41-3(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94466 | PB306-4(A) (red, channel 2) vs. PB303-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94467 | PB303 vs N2 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94468 | N2-1(B) (red, channel 2) vs. PB303-1(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94469 | PB306-1(B) (red, channel 2) vs. AB1-1(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94470 | PB306-1 vs AB1 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94471 | MA24-4(A) (red, channel 2) vs. N2-4(B) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94472 | PB306-2(B) (red, channel 2) vs. AB1-2(A) (green, channel 1) (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94473 | PB306-2 vs PB303 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94474 | N2 vs CB4856 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94475 | MA83 vs MA41 (GSE4123: The transcriptional consequences of mutation and natural selection in Caenorhabditis elegans) | This set of arrays contains all microarray experiments done involving comparisons among C. elegans natural isolates and mutation-accumulation lines. Abstract: The evolutionary importance of gene-expression divergence is unclear: some studies suggest that it is an important mechanism for evolution by natural selection, whereas others claim that most between-species regulatory changes are neutral or nearly neutral. We examined global transcriptional divergence patterns in a set of Caenorhabditis elegans mutation-accumulation lines and natural isolate lines to provide insights into the evolutionary importance of transcriptional variation and to discriminate between the forces of mutation and natural selection in shaping the evolution of gene expression. We detected the effects of selection on transcriptional divergence patterns and characterized them with respect to coexpressed gene sets, chromosomal clustering of expression changes and functional gene categories. We directly compared observed transcriptional variation patterns in the mutation-accumulation and natural isolate lines to a neutral model of transcriptome evolution to show that strong stabilizing selection dominates the evolution of transcriptional change for thousands of C. elegans expressed sequences. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs |
| GSM94883 | intestine mRNAtagging exp. 5 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94884 | intestine mRNAtagging exp. 4 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94885 | intestine mRNAtagging exp. 1 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94886 | intestine mRNAtagging exp. 6 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94887 | intestine mRNAtagging exp. 7 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94888 | intestine mRNAtagging exp. 2 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94889 | intestine mRNAtagging exp. 8 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM94890 | intestine mRNAtagging exp. 3 (GSE4150: mRNA tagging (intestine)) | For each experiment (as described in Pauli et al. 2006): Channel 1: whole worm lysate from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 Channel 2: mRNA immunoprecipitated from strain SD1084 carrying transgene Pges-1::FLAG::PAB-1 mRNA was amplified and hybridized to C. elegans DNA arrays from the Stuart Kim lab Set of arrays that are part of repeated experiments Keywords: Biological Replicate, mRNA tagging |
| GSM951324 | 15xG vs 1xG rep2 (GSE38877: Worms spun in centrifuge at elevated g values) | Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) |
| GSM951325 | 15xG vs 1xG rep1 (GSE38877: Worms spun in centrifuge at elevated g values) | Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) |
| GSM951327 | 5xG vs 1xG rep1 (GSE38877: Worms spun in centrifuge at elevated g values) | Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) |
| GSM951328 | 5XG vs 1xG rep2 (GSE38877: Worms spun in centrifuge at elevated g values) | Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) |
| GSM951329 | 15xG vs 1xG rep3 (GSE38877: Worms spun in centrifuge at elevated g values) | Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) |
| GSM951332 | 10xG vs 1xG rep3 (GSE38877: Worms spun in centrifuge at elevated g values) | Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) |
| GSM95245 | N2 (green, channel 1) vs daf-8 (red, channel 2) Trial #3 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95246 | N2 (green, channel 1) vs daf-7 (red, channel 2) Trial #4 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95247 | N2 (green, channel 1) vs daf-7 (red, channel 2) Trial #2 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95248 | N2 (green, channel 1) vs daf-8 (red, channel 2) Trial #2 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95249 | N2 (green, channel 1) vs daf-7 (red, channel 2) Trial #1 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95250 | N2 (green, channel 1) vs daf-14 (red, channel 2) Trial #2 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95251 | N2 (green, channel 1) vs daf-14 (red, channel 2) Trial #3 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95252 | N2 (green, channel 1) vs daf-8 (red, channel 2) Trial #4 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95253 | N2 (green, channel 1) vs daf-14 (red, channel 2) Trial #1 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM95254 | N2 (green, channel 1) vs daf-7 (red, channel 2) Trial #3 (GSE4164: Regulation of signaling genes by TGFbeta during entry into dauer diapause in C. elegans) | BACKGROUND: When resources are scant, C. elegans larvae arrest as long-lived dauers under the control of insulin/IGF- and TGFbeta-related signaling pathways. : We have identified genes that show different levels of expression in a comparison of wild-type L2 or L3 larvae (non-dauer) to TGFbeta mutants at similar developmental stages undergoing dauer formation. Many insulin/IGF pathway and other known dauer regulatory genes have changes in expression that suggest strong positive feedback by the TGFbeta pathway. In addition, many insulin-like ligand and novel genes with similarity to the extracellular domain of insulin/IGF receptors have altered expression. We have identified a large group of regulated genes with putative binding sites for the FOXO transcription factor, DAF-16. Genes with DAF-16 sites upstream of the transcription start site tend to be upregulated, whereas genes with DAF-16 sites downstream of the coding region tend to be downregulated. Finally, we also see strong regulation of many novel hedgehog- and patched-related genes, hormone biosynthetic genes, cell cycle genes, and other regulatory genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set |
| GSM953405_1540_3674_18638_1c48_Celegans | experiment 1 control samples at 48 h 1c48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953406_1540_3674_18639_1u48_Celegans | experiment 1 UVC-exposed samples at 48 h 1u48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953407_1540_3674_18640_1e48_Celegans | experiment 1 EtBr-exposed samples at 48 h 1e48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953408_1540_3674_18641_1eu48_Celegans | experiment 1 UVC- and EtBr-exposed samples at 48 h 1eu48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953409_1540_3674_18642_1c51_Celegans | experiment 1 control samples at 51 h 1c51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953410_1540_3674_18643_1u51_Celegans | experiment 1 UVC-exposed samples at 51 h 1u51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953411_1540_3674_18644_1e51_Celegans | experiment 1 EtBr-exposed samples at 51 h 1e51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953412_1540_3674_18645_1eu51_Celegans | experiment 1 UVC- and EtBr-exposed samples at 51 h 1eu51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953413_1540_3099_15305_2c51_Celegans | experiment 2 control samples at 51 h 2c51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953414_1540_3099_15307_2e51_Celegans | experiment 2 EtBr-exposed samples at 51 h 2e51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953415_1540_3099_15308_2eu51_Celegans | experiment 2 UVC- and EtBr-exposed samples at 51 h 2eu51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953416_1540_3674_18590_4c3_Celegans | experiment 4 control samples at 3 h 4c3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953417_1540_3674_18591_4u3_Celegans | experiment 4 UVC-exposed samples at 3 h 4u3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953418_1540_3674_18592_4e3_Celegans | experiment 4 EtBr-exposed samples at 3 h 4e3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953419_1540_3674_18593_4eu3_Celegans | experiment 4 UVC- and EtBr-exposed samples at 3 h 4eu3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953420_1540_3674_18594_4c24_Celegans | experiment 4 control samples at 24 h 4c24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953421_1540_3674_18595_4u24_Celegans | experiment 4 UVC-exposed samples at 24 h 4u24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953422_1540_3674_18596_4e24_Celegans | experiment 4 EtBr-exposed samples at 24 h 4e24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953423_1540_3674_18597_4eu24_Celegans | experiment 4 UVC- and EtBr-exposed samples at 24 h 4eu24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953424_1540_3674_18598_4c48_Celegans | experiment 4 control samples at 48 h 4c48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953425_1540_3674_18599_4u48_Celegans | experiment 4 UVC-exposed samples at 48 h 4u48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953426_1540_3674_18600_4e48_Celegans | experiment 4 EtBr-exposed samples at 48 h 4e48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953427_1540_3674_18601_4eu48_Celegans | experiment 4 UVC- and EtBr-exposed samples at 48 h 4eu48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953428_1540_3674_18602_4c51_Celegans | experiment 4 control samples at 51 h 4c51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953429_1540_3674_18603_4u51_Celegans | experiment 4 UVC-exposed samples at 51 h 4u51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953430_1540_3674_18604_4e51_Celegans | experiment 4 EtBr-exposed samples at 51 h 4e51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953431_1540_3674_18605_4eu51_Celegans | experiment 4 UVC- and EtBr-exposed samples at 51 h 4eu51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953432_1540_3674_18606_5c3_Celegans | experiment 5 control samples at 3 h 5c3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953433_1540_3674_18607_5u3_Celegans | experiment 5 UVC-exposed samples at3 h 5u3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953434_1540_3674_18608_5e3_Celegans | experiment 5 EtBr-exposed samples at 3 h 5e3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953435_1540_3674_18609_5eu3_Celegans | experiment 5 UVC- and EtBr-exposed samples at 3 h 5eu3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953436_1540_3674_18610_5c24_Celegans | experiment 5 control samples at 24 h 5c24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953437_1540_3674_18611_5u24_Celegans | experiment 5 UVC-exposed samples at 24 h 5u24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953438_1540_3674_18612_5e24_Celegans | experiment 5 EtBr-exposed samples at 24 h 5e24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953439_1540_3674_18613_5eu24_Celegans | experiment 5 UVC- and EtBr-exposed samples at 24 h 5eu24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953440_1540_3674_18614_5c48_Celegans | experiment 5 control samples at 48 h 5c48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953441_1540_3674_18615_5u48_Celegans | experiment 5 UVC-exposed samples at 48 h 5u48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953442_1540_3674_18617_5eu48_Celegans | experiment 5 UVC- and EtBr-exposed samples at 48 h 5Eu48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953443_1540_3674_18618_5c51_Celegans | experiment 5 control samples at 51 h 5c51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953444_1540_3674_18619_5u51_Celegans | experiment 5 UVC-exposed samples at 51 h 5u51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953445_1540_3674_18620_5e51_Celegans | experiment 5 EtBr-exposed samples at 51 h 5e51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953446_1540_3674_18621_5eu51_Celegans | experiment 5 UVC- and EtBr-exposed samples at 51 h 5Eu51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953447_1540_3674_18622_6c3_Celegans | experiment 6 control samples at 3 h 6c3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953448_1540_3674_18623_6u3_Celegans | experiment 6 UVC-exposed samples at 3 h 6u3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953449_1540_3674_18624_6e3_Celegans | experiment 6 EtBr-exposed samples at 3 h 6e3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953450_1540_3674_18625_6eu3_Celegans | experiment 6 UVC- and EtBr-exposed samples at 3 h 6Eu3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953451_1540_3674_18626_6c24_Celegans | experiment 6 control samples at 24 h 6c24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953452_1540_3674_18627_6u24_Celegans | experiment 6 UVC-exposed samples at 24 h 6u24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953453_1540_3674_18628_6e24_Celegans | experiment 6 EtBr-exposed samples at 24 h 6e24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953454_1540_3674_18629_6eu24_Celegans | experiment 6 UVC- and EtBr-exposed samples at 24 h 6Eu24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953455_1540_3674_18632_6e48_Celegans | experiment 6 EtBr-exposed samples at 48 h 6e48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953456_1540_3674_18633_6eu48_Celegans | experiment 6 UVC- and EtBr-exposed samples at 48 h 6Eu48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953457_1540_3674_18635_6e51_Celegans | experiment 6 EtBr-exposed samples at 51 h 6e51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953458_1540_3674_18637_6eu51_Celegans | experiment 6 UVC- and EtBr-exposed samples at 51 h 6Eu51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953459_1540_3099_15277r_7c3_Celegans | experiment 7 control samples at 3 h 7c3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953460_1540_3099_15278r_7u3_Celegans | experiment 7 UVC-exposed samples at 3 h 7u3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953461_1540_3099_15279_7e3_Celegans | experiment 7 EtBr-exposed samples at 3 h 7e3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953462_1540_3099_15280r_7eu3_Celegans | experiment 7 UVC- and EtBr-exposed samples at 3 h 7eu3 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953463_1540_3099_15281_7c24_Celegans | experiment 7 control samples at 24 h 7c24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953464_1540_3099_15282r_7u24_Celegans | experiment 7 UVC-exposed samples at 24 h 7u24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953465_1540_3099_15283_7e24_Celegans | experiment 7 EtBr-exposed samples at 24 h 7e24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953466_1540_3099_15284_7eu24_Celegans | experiment 7 UVC- and EtBr-exposed samples at 24 h 7eu24 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953467_1540_3099_15285r_7c48_Celegans | experiment 7 control samples at 48 h 7c48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953468_1540_3099_15286r_7u48_Celegans | experiment 7 UVC-exposed samples at 48 h 7u48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953469_1540_3099_15287_7e48_Celegans | experiment 7 EtBr-exposed samples at 48 h 7e48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953470_1540_3099_15288_7eu48_Celegans | experiment 7 UVC- and EtBr-exposed samples at 48 h 7eu48 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953471_1540_3099_15289r_7c51_Celegans | experiment 7 control samples at 51 h 7c51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953472_1540_3099_15290r_7u51_Celegans | experiment 7 UVC-exposed samples at 51 h 7u51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953473_1540_3099_15292_7eu51_Celegans | experiment 7 UVC- and EtBr-exposed samples at 51 h 7eu51 (GSE38997: Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation) | Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). |
| GSM953766_AS_0 | L3 stage worm AS_.003, biological replicate 1 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953767_AS_0 | L3 stage worm AS_.003, biological replicate 2 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953768_AS_0 | L3 stage worm AS_.003, biological replicate 3 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953769_AS_0 | L3 stage worm AS_.03, biological replicate 1 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953770_AS_0 | L3 stage worm AS_.03, biological replicate 2 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953771_AS_0 | L3 stage worm AS_.03, biological replicate 3 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953772_AS_Control_R1 | L3 stage worm AS_Control, biological replicate 1 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953773_AS_Control_R2 | L3 stage worm AS_Control, biological replicate 2 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM953774_AS_Control_R3 | L3 stage worm AS_Control, biological replicate 3 (GSE39012: Expression data from L3 stage Caernorhabditis elegans after arsenic exposure) | We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic |
| GSM956917 | ercc-1_I (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956918 | ercc-1_II (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956919 | ercc-1_III (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956920 | ercc-1_IV (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956921 | wild-type_N2_I (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956922 | wild-type_N2_II (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956923 | wild-type_N2_III (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM956924 | wild-type_N2_IV (GSE39145: Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.) | We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. |
| GSM958827 | N2_rep1 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958828 | N2_rep2 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958829 | N2_rep3 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958830 | N2_rep4 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958831 | N2_rep5 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958832 | xpa-1_rep1 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958833 | xpa-1_rep2 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958834 | xpa-1_rep3 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958835 | xpa-1_rep4 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM958836 | xpa-1_rep5 (GSE39252: Expression changes in Caenorhabditis elegans xpa-1 mutant) | Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant. |
| GSM986045 | MK_Celegans_Control_1 (GSE40127: GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.) | NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. |
| GSM986046 | 1E_MK_Celegans_E_1 (GSE40127: GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.) | NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. |
| GSM986047 | 2c_MK_Celegans_Control_2 (GSE40127: GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.) | NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. |
| GSM986048 | 2E_MK_Celegans_E_2 (GSE40127: GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.) | NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. |
| GSM986049 | 4c_MK_Celegans_Control_4 (GSE40127: GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.) | NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. |
| GSM986050 | 4E_MK_Celegans_E_4 (GSE40127: GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.) | NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. |
| intact | intact | intact |
| jaspar_celegans | jaspar_celegans | jaspar_celegans |
| mint | mint | mint |
| wb_gene_inter_corr | wb_gene_inter_corr | wb_gene_inter_corr |