Breakers and amplifiers in chromatin circuitry: acetylation and ubiquitination control the heterochromatin machinery.
Breakers and amplifiers in chromatin circuitry: acetylation and ubiquitination control the heterochromatin machinery.
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DOI：
10.1016/j.sbi.2021.06.012
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发表时间：
2021-12
影响因子：
6.8
通讯作者：
Schalch T
中科院分区：
文献类型：
--
作者：
Bailey LT;Northall SJ;Schalch T
真核生物的基因组被分为活性常染色质区室和抑制异染色质区室。基因调控网络、染色体结构和基因组完整性依赖于活性和沉默状态的及时和位点特异性建立，以保护基因组并为细胞分裂和细胞身份的规范提供基础。在这里，我们专注于在裂殖酵母中建立异染色质的机制和分子机制，并将其与酿酒酵母和哺乳动物polycomb系统进行比较。我们提出了最近的结构和机制的证据，这表明，组蛋白乙酰化通过破坏异染色质机制所使用的正反馈回路来保护主动转录，并且H2A和H3单泛素化积极驱动异染色质，而H2B单泛素化动员防御来淬灭异染色质。异染色质相关复合物被组蛋白标记吸引和排斥。特定赖氨酸残基的乙酰化保护常染色质免于沉默。组蛋白H3赖氨酸9和27的甲基化扩增异染色质。核小体遍在蛋白化许可并强制执行反馈回路。
Eukaryotic genomes are segregated into active euchromatic and repressed heterochromatic compartments. Gene regulatory networks, chromosomal structures, and genome integrity rely on the timely and locus-specific establishment of active and silent states to protect the genome and provide the basis for cell division and specification of cellular identity. Here, we focus on the mechanisms and molecular machinery that establish heterochromatin in Schizosaccharomyces pombe and compare it with Saccharomyces cerevisiae and the mammalian polycomb system. We present recent structural and mechanistic evidence, which suggests that histone acetylation protects active transcription by disrupting the positive feedback loops used by the heterochromatin machinery and that H2A and H3 monoubiquitination actively drives heterochromatin, whereas H2B monoubiquitination mobilizes the defenses to quench heterochromatin. Heterochromatin-associated complexes are attracted and repelled by histone marks. Acetylation of specific lysine residues protects euchromatin from silencing. Methylation of histone H3 lysine 9 and 27 amplifies heterochromatin. Nucleosome ubiquitination licences and enforces feedback loops.
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影响因子：
4.5
作者：
Buscaino A;White SA;Houston DR;Lejeune E;Simmer F;de Lima Alves F;Diyora PT;Urano T;Bayne EH;Rappsilber J;Allshire RC
通讯作者：
Allshire RC
影响因子：
16
作者：
Flury V;Georgescu PR;Iesmantavicius V;Shimada Y;Kuzdere T;Braun S;Bühler M
通讯作者：
Bühler M
影响因子：
16.6
作者：
Douse CH;Tchasovnikarova IA;Timms RT;Protasio AV;Seczynska M;Prigozhin DM;Albecka A;Wagstaff J;Williamson JC;Freund SMV;Lehner PJ;Modis Y
通讯作者：
Modis Y
影响因子：
11.4
作者：
Buscaino, Alessia;Lejeune, Erwan;Allshire, Robin C.
通讯作者：
Allshire, Robin C.
影响因子：
16.6
作者：
通讯作者：
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