Department of Biology, Aging Mind and Brain Initiative, Iowa City, United States.
Department of Biology, Iowa City, United States.
Elife. 2020 Apr 23;9:e55246. doi: 10.7554/eLife.55246.
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 , 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 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 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.
生殖细胞对压力很敏感。因此,生物体如何在环境波动的情况下保护其未来的后代免受伤害,是生物学中的一个基本问题。我们发现,在 中,母体神经元在压力下释放的血清素确保了未来后代的生存能力和抗压能力。血清素通过一个在 和哺乳动物细胞之间保守的信号转导途径发挥作用,使转录因子 HSF1 通过招募组蛋白伴侣 FACT 来改变即将受精的生殖细胞中的染色质,取代组蛋白,并启动保护性基因表达。如果没有母体神经元释放的血清素,HSF1 就不能在生殖细胞中招募 FACT,转录虽然会发生,但会延迟,而且压力下的 母亲的后代无法完成发育。这些研究揭示了一种新的机制,即神经元的压力感应与生殖细胞的转录反应时间相耦合,以保护未来的后代。