Open AccessThe Caenorhabditis elegans JNK Signaling Pathway Activates Expression of Stress Response Genes by Derepressing the Fos/HDAC Repressor Complex
Author(s) -
Ayuna Hattori,
Tomoaki Mizuno,
Mayuko Akamatsu,
Naoki Hisamoto,
Kunihiro Matsumoto
Publication year - 2013
Publication title -
plos genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.587
H-Index - 233
eISSN - 1553-7404
pISSN - 1553-7390
DOI - 10.1371/journal.pgen.1003315
Subject(s) - derepression , repressor , biology , caenorhabditis elegans , transcription factor , histone deacetylase , phosphorylation , transcriptional regulation , microbiology and biotechnology , signal transduction , promoter , regulation of gene expression , psychological repression , histone , gene , gene expression , genetics
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 .