Journal article
Gene bookmarking by the heat shock transcription factor programs the insulin-like signaling pathway
Molecular cell, Vol.81(23), pp.4843-4860.e8
10/2021
DOI: 10.1016/j.molcel.2021.09.022
PMID: 34648748
Abstract
Maternal stress can have long-lasting epigenetic effects on offspring. To examine how epigenetic changes are triggered by stress, we examined the effects of activating the universal stress-responsive heat shock transcription factor HSF-1 in the germline of Caenorhabditis elegans. We show that, when activated in germ cells, HSF-1 recruits MET-2, the putative histone 3 lysine 9 (H3K9) methyltransferase responsible for repressive H3K9me2 (H3K9 dimethyl) marks in chromatin, and negatively bookmarks the insulin receptor daf-2 and other HSF-1 target genes. Increased H3K9me2 at these genes persists in adult progeny and shifts their stress response strategy away from inducible chaperone expression as a mechanism to survive stress and instead rely on decreased insulin/insulin growth factor (IGF-1)-like signaling (IIS). Depending on the duration of maternal heat stress exposure, this epigenetic memory is inherited by the next generation. Thus, paradoxically, HSF-1 recruits the germline machinery normally responsible for erasing transcriptional memory but, instead, establishes a heritable epigenetic memory of prior stress exposure.
Details
- Title: Subtitle
- Gene bookmarking by the heat shock transcription factor programs the insulin-like signaling pathway
- Creators
- Srijit DasSehee MinVeena Prahlad
- Resource Type
- Journal article
- Publication Details
- Molecular cell, Vol.81(23), pp.4843-4860.e8
- DOI
- 10.1016/j.molcel.2021.09.022
- PMID
- 34648748
- ISSN
- 1097-2765
- eISSN
- 1097-4164
- Grant note
- DOI: 10.13039/100000002, name: National Institutes of Health, award: P40 OD010440, R01 AG 050653
- Language
- English
- Date published
- 10/2021
- Academic Unit
- Iowa Neuroscience Institute; Biology
- Record Identifier
- 9984187040302771
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