Department for Integrative Evolutionary Biology, Max Planck Institute for Biology Tübingen, Tübingen, 72076, Germany.
School of Biological Sciences, The University of Utah, Salt Lake City, UT, USA.
Nat Commun. 2023 Apr 13;14(1):2095. doi: 10.1038/s41467-023-37734-z.
Development can be altered to match phenotypes with the environment, and the genetic mechanisms that direct such alternative phenotypes are beginning to be elucidated. Yet, the rules that govern environmental sensitivity vs. invariant development, and potential epigenetic memory, remain unknown. Here, we show that plasticity of nematode mouth forms is determined by histone 4 lysine 5 and 12 acetylation (H4K5/12ac). Acetylation in early larval stages provides a permissive chromatin state, which is susceptible to induction during the critical window of environmental sensitivity. As development proceeds deacetylation shuts off switch gene expression to end the critical period. Inhibiting deacetylase enzymes leads to fixation of prior developmental trajectories, demonstrating that histone modifications in juveniles can carry environmental information to adults. Finally, we provide evidence that this regulation was derived from an ancient mechanism of licensing developmental speed. Altogether, our results show that H4K5/12ac enables epigenetic regulation of developmental plasticity that can be stored and erased by acetylation and deacetylation, respectively.
发育可以被改变以匹配表型与环境，并且指导这种替代表型的遗传机制开始被阐明。然而，控制环境敏感性与不变发育以及潜在的表观遗传记忆的规则仍然未知。在这里，我们表明线虫口型的可塑性由组蛋白 4 赖氨酸 5 和 12 乙酰化（H4K5/12ac）决定。早期幼虫阶段的乙酰化提供了一种允许的染色质状态，这种状态容易在环境敏感性的关键窗口期间被诱导。随着发育的进行，去乙酰化关闭了开关基因的表达，从而结束了关键时期。抑制去乙酰化酶会导致先前发育轨迹的固定，这表明幼体中的组蛋白修饰可以将环境信息传递给成虫。最后，我们提供的证据表明，这种调节源自于一种古老的许可发育速度的机制。总的来说，我们的结果表明，H4K5/12ac 能够对发育可塑性进行表观遗传调控，这种调控可以分别通过乙酰化和去乙酰化来存储和擦除。
