The Caenorhabditis elegans JNK signaling pathway activates expression of stress response genes by derepressing the Fos/HDAC repressor complex

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-...

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Bibliographic Details
Published in:PLoS genetics 2013-02, Vol.9 (2), p.e1003315-e1003315
Main Authors: Hattori, Ayuna, Mizuno, Tomoaki, Akamatsu, Mayuko, Hisamoto, Naoki, Matsumoto, Kunihiro
Format: Article
Language:English
Subjects:
Animals
Biology
Caenorhabditis elegans
Caenorhabditis elegans - genetics
Caenorhabditis elegans - physiology
Caenorhabditis elegans Proteins - genetics
Caenorhabditis elegans Proteins - metabolism
Caenorhabditis elegans Proteins - physiology
Gene expression
Genetic aspects
Genetic transcription
Genetics
Health aspects
Histone Deacetylases - genetics
Histone Deacetylases - metabolism
JNK Mitogen-Activated Protein Kinases - genetics
JNK Mitogen-Activated Protein Kinases - physiology
Kinases
MAP Kinase Signaling System - genetics
MAP Kinase Signaling System - physiology
Mitogen-activated protein kinases
Nematodes
Phosphorylation
Physiological aspects
Promoter Regions, Genetic
Proto-Oncogene Proteins c-fos - metabolism
Proto-Oncogene Proteins c-fos - physiology
Stress, Physiological - genetics
Transcriptional Activation
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Summary: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.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1003315