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bioRxiv · 10.1101/2021.02.22.432344

Germline activity of the heat shock factor HSF-1 programs the insulin-receptor daf-2 in C. elegans

Prahlad, V.·Das, S.·Min, S.
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Abstract

The mechanisms by which maternal stress alters offspring phenotypes remain poorly understood. Here we report that the heat shock transcription factor HSF-1, activated in the C. elegans maternal germline upon stress, epigenetically programs the insulin-like receptor daf-2 by increasing repressive H3K9me2 levels throughout the daf-2 gene. This increase occurs by the recruitment of the C. elegans SETDB1 homolog MET-2 by HSF-1. Increased H3K9me2 levels at daf-2 persist in offspring to downregulate daf-2, activate the C. elegans FOXO ortholog DAF-16 and enhance offspring stress resilience. Thus, HSF-1 activity in the mother promotes the early life programming of the insulin/IGF-1 signaling (IIS) pathway and determines the strategy of stress resilience in progeny. One Sentence SummaryHSF-1 recruits MET-2 to silence daf-2 and mediate early life programming of C. elegans upon stress

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Prahlad, V., Das, S., Min, S.. 2021-02-22. Germline activity of the heat shock factor HSF-1 programs the insulin-receptor daf-2 in C. elegans. https://doi.org/10.1101/2021.02.22.432344

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