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Reevaluating the roles of histone-modifying enzymes and their associated chromatin modifications in transcriptional regulation.重新评估组蛋白修饰酶及其相关染色质修饰在转录调控中的作用。
Nat Genet. 2020 Dec;52(12):1271-1281. doi: 10.1038/s41588-020-00736-4. Epub 2020 Nov 30.
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Hansel, Gretel, and the Consequences of Failing to Remove Histone Methylation Breadcrumbs.汉塞尔、格蕾特和未能清除组蛋白甲基化面包屑的后果。
Trends Genet. 2020 Mar;36(3):160-176. doi: 10.1016/j.tig.2019.12.004. Epub 2020 Jan 29.
3
Roles and regulation of histone methylation in animal development.组蛋白甲基化在动物发育中的作用和调控。
Nat Rev Mol Cell Biol. 2019 Oct;20(10):625-641. doi: 10.1038/s41580-019-0151-1. Epub 2019 Jul 2.
4
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5
Sperm-inherited H3K27me3 impacts offspring transcription and development in C. elegans.精子遗传的 H3K27me3 影响秀丽隐杆线虫后代的转录和发育。
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Caenorhabditis elegans sperm carry a histone-based epigenetic memory of both spermatogenesis and oogenesis.秀丽隐杆线虫的精子携带了由组蛋白为基础的表观遗传记忆,这种记忆来自于精子发生和卵子发生过程。
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FastQ Screen: A tool for multi-genome mapping and quality control.FastQ Screen:一种用于多基因组比对和质量控制的工具。
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Distinct Roles of Two Histone Methyltransferases in Transmitting H3K36me3-Based Epigenetic Memory Across Generations in .两种组蛋白甲基转移酶在. 中跨代传递基于 H3K36me3 的表观遗传记忆中的独特作用
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9
Histone Lysine Methylation and Neurodevelopmental Disorders.组蛋白赖氨酸甲基化与神经发育障碍
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通过平衡遗传的组蛋白甲基化来建立生殖细胞与体细胞。

establishes germline versus soma by balancing inherited histone methylation.

机构信息

Department of Cell Biology, Emory University School of Medicine, Atlanta GA 30322, USA.

Johns Hopkins University School of Medicine, Baltimore MD 21205, USA.

出版信息

Development. 2021 Feb 10;148(3):dev196600. doi: 10.1242/dev.196600.

DOI:10.1242/dev.196600
PMID:33462111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7888751/
Abstract

Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In , this reprogramming is mediated by the H3K4me2 demethylase SPR-5 and the H3K9 methyltransferase, MET-2. In contrast, the H3K36 methyltransferase MES-4 maintains H3K36me2/3 at germline genes between generations to facilitate re-establishment of the germline. To determine whether the MES-4 germline inheritance pathway antagonizes reprogramming, we examined the interaction between these two pathways. We found that the developmental delay of mutant progeny is associated with ectopic H3K36me3 and the ectopic expression of MES-4-targeted germline genes in somatic tissues. Furthermore, the developmental delay is dependent upon MES-4 and the H3K4 methyltransferase, SET-2. We propose that MES-4 prevents crucial germline genes from being repressed by antagonizing maternal reprogramming. Thus, the balance of inherited histone modifications is necessary to distinguish germline versus soma and prevent developmental delay.This article has an associated 'The people behind the papers' interview.

摘要

受精卵的形成伴随着广泛的表观遗传重编程,以确保组蛋白甲基化的适当遗传,并防止发育迟缓。在这一过程中,H3K4me2 去甲基酶 SPR-5 和 H3K9 甲基转移酶 MET-2 介导了这一重编程。相比之下,H3K36 甲基转移酶 MES-4 在世代之间维持生殖系基因的 H3K36me2/3,以促进生殖系的重新建立。为了确定 MES-4 生殖系遗传途径是否拮抗重编程,我们研究了这两条途径之间的相互作用。我们发现, 突变体后代的发育迟缓与体细胞组织中 H3K36me3 的异位和 MES-4 靶向生殖系基因的异位表达有关。此外,这种发育迟缓依赖于 MES-4 和 H3K4 甲基转移酶 SET-2。我们提出,MES-4 通过拮抗母体重编程来防止关键的生殖系基因受到抑制。因此,遗传组蛋白修饰的平衡对于区分生殖系和体细胞以及防止发育迟缓是必要的。本文有一个相关的“论文背后的人物”采访。