生物
母子转换
组蛋白H4
组蛋白
细胞生物学
基因表达调控
遗传学
乙酰化
合子
基因
胚胎
胚胎发生
作者
Maria Samata,Anastasios Alexiadis,Gautier Richard,Plamen Georgiev,Johannes Nuebler,Tanvi Kulkarni,Gina Renschler,M. Felicia Basilicata,Fides Zenk,Maria Shvedunova,Giuseppe Semplicio,Leonid A. Mirny,Nicola Iovino,Asifa Akhtar
出处
期刊:Cell
[Elsevier]
日期:2020-07-01
卷期号:182 (1): 127-144.e23
被引量:57
标识
DOI:10.1016/j.cell.2020.05.026
摘要
Summary
Before zygotic genome activation (ZGA), the quiescent genome undergoes reprogramming to transition into the transcriptionally active state. However, the mechanisms underlying euchromatin establishment during early embryogenesis remain poorly understood. Here, we show that histone H4 lysine 16 acetylation (H4K16ac) is maintained from oocytes to fertilized embryos in Drosophila and mammals. H4K16ac forms large domains that control nucleosome accessibility of promoters prior to ZGA in flies. Maternal depletion of MOF acetyltransferase leading to H4K16ac loss causes aberrant RNA Pol II recruitment, compromises the 3D organization of the active genomic compartments during ZGA, and causes downregulation of post-zygotically expressed genes. Germline depletion of histone deacetylases revealed that other acetyl marks cannot compensate for H4K16ac loss in the oocyte. Moreover, zygotic re-expression of MOF was neither able to restore embryonic viability nor onset of X chromosome dosage compensation. Thus, maternal H4K16ac provides an instructive function to the offspring, priming future gene activation.
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