Serotonin signaling by maternal neurons upon stress ensures progeny survival

eLife

Veena Prahlad¹  Srijit Das²  Felicia K Ooi²  Johnny Cruz Corchado²  Joshua A Weiner³  Leah C Fuller³ 

[1] Iowa Neuroscience Institute, Iowa City, United States;Department of Biology, Aging Mind and Brain Initiative, Iowa City, United States;Department of Biology, Iowa City, United States;

关键词: HSF1;    serotonin;    cell non-autonomous;    neuronal signaling;    histone chaperone;    epigenetic;   

DOI  :  10.7554/eLife.55246

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown