Histone H1 binding is inhibited by histone variant H3.3
Histone H1 binding is inhibited by histone variant H3.3
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DOI：
10.1038/emboj.2009.301
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发表时间：
2009-12-02
期刊：
影响因子：
11.4
通讯作者：
van Steensel, Bas
中科院分区：
文献类型：
--
作者：
Braunschweig, Ulrich;Hogan, Greg J.;van Steensel, Bas
接头组蛋白参与了高阶染色质结构的形成和特定基因的调节，但仍不清楚其主要结合决定因素是什么。我们使用DAMID生成了果蝇细胞中接头H1的全基因组高分辨率结合图。 H1在经典的斑塑素和异染色质中以相似水平的相似水平结合。令人惊讶的是，在活性基因和许多遥远的顺式调节位点，在转录起始位点周围有明显的H1占用率降低。 H1下降并不是由于缺乏核小体。相反，所有具有低结合H1的区域均显示组蛋白变体H3.3的富集。 H3.3的敲低导致H1水平在这些位点增加，核小体重复长度随之增加。这些变化与转录变化无关。我们的结果表明，H3.3蛋白抵消H1的关联，提供了一种将多种基因组位点保持开放式染色质构象的机制。 EMBO Journal（2009）28，3635-3645。 doi：10.1038/emboj.2009.301; 2009年10月15日在线发布
Linker histones are involved in the formation of higher-order chromatin structure and the regulation of specific genes, yet it remains unclear what their principal binding determinants are. We generated a genome-wide high-resolution binding map for linker histone H1 in Drosophila cells, using DamID. H1 binds at similar levels across much of the genome, both in classic euchromatin and heterochromatin. Strikingly, there are pronounced dips of low H1 occupancy around transcription start sites for active genes and at many distant cis-regulatory sites. H1 dips are not due to lack of nucleosomes; rather, all regions with low binding of H1 show enrichment of the histone variant H3.3. Knockdown of H3.3 causes H1 levels to increase at these sites, with a concomitant increase in nucleosome repeat length. These changes are independent of transcriptional changes. Our results show that the H3.3 protein counteracts association of H1, providing a mechanism to keep diverse genomic sites in an open chromatin conformation. The EMBO Journal (2009) 28, 3635-3645. doi: 10.1038/emboj.2009.301; Published online 15 October 2009