| Citation | Hattori A, Mizuno T, Akamatsu M, Hisamoto N, Matsumoto K. The Caenorhabditis elegans JNK signaling pathway activates expression of stress response genes by derepressing the Fos/HDAC repressor complex. PLoS Genet, 2013. |
| PubMed ID | 23437011 |
| Short Description | The Caenorhabditis elegans JNK signaling pathway activates expression of stress response genes by derepressing the Fos/HDAC repressor complex. GEO Record: GSE42703 Platform: GPL200 Download gene-centric, log2 transformed data: WBPaper00042067.ce.mr.csv |
| # of Conditions | 4 |
Full Description
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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. In this study, we identified FOS-1, a bZIP transcription factor, as a target of KGB-1-mediated phosphorylation. We further identified two transcriptional targets of the KGB-1 pathway, kreg-1 and kreg-2/lys-3, which are required for the defense against heavy metal stress. FOS-1 plays a critical role in the transcriptional repression of the kreg-1 gene by recruiting histone deacetylase (HDAC) to its promoter. KGB-1 phosphorylation prevents FOS-1 dimerization and promoter binding, resulting in promoter derepression. Thus, HDAC behaves as a co-repressor modulating FOS-1-mediated transcriptional regulation. This study describes the direct link from JNK signaling, Fos phosphorylation, and regulation of kreg gene transcription, which modulates the stress response in C. elegans. Experimental Details: WBPaper00042067:WT_H2O_rep1 WBPaper00042067:WT_CopperSulfate_rep1 WBPaper00042067:kgb-1_H2O_rep1 WBPaper00042067:kgb-1_CopperSulfate_rep1. |
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