Serotonin signaling by maternal neurons upon stress ensures progeny survival
Abstract
Germ cells are vulnerable to stress. Therefore, how organisms protect their future progeny from damage in a fluctuating environment is a fundamental question in biology. We show that in Caenorhabditis elegans, serotonin released by maternal neurons during stress ensures the viability and stress resilience of future offspring. Serotonin acts through a signal transduction pathway conserved between C. elegans and mammalian cells to enable the transcription factor HSF1 to alter chromatin in soon-to-be fertilized germ cells by recruiting the histone chaperone FACT, displacing histones, and initiating protective gene expression. Without serotonin release by maternal neurons, FACT is not recruited by HSF1 in germ cells, transcription occurs but is delayed, and progeny of stressed C. elegans mothers fail to complete development. These studies uncover a novel mechanism by which stress sensing by neurons is coupled to transcription response times of germ cells to protect future offspring.
Data availability
RNA-seq data have been deposited and available at https://www.ncbi.nlm.nih.gov/bioproject/PRJNA576016
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Transcriptome of C. elegans upon alteration of 5-HTNCBI:BioProject, PRJNA594152.
Article and author information
Author details
Funding
National Institutes of Health (AG 050653)
- Veena Prahlad
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Siu Sylvia Lee, Cornell University, United States
Version history
- Received: January 17, 2020
- Accepted: April 22, 2020
- Accepted Manuscript published: April 23, 2020 (version 1)
- Version of Record published: May 19, 2020 (version 2)
Copyright
© 2020, Das et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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