RYBP-PRC1 Complexes Mediate H2A Ubiquitylation at Polycomb Target Sites Independently of PRC2 and H3K27me3
RYBP-PRC1 Complexes Mediate H2A Ubiquitylation at Polycomb Target Sites Independently of PRC2 and H3K27me3
复制标题
RYBP-PRC1 复合物独立于 PRC2 和 H3K27me3 介导 Polycomb 靶位点的 H2A 泛素化
DOI：
10.1016/j.cell.2012.06.011
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发表时间：
2012-06-22
期刊：
影响因子：
64.5
通讯作者：
Brockdorff N
中科院分区：
文献类型：
--
作者：
Tavares L;Dimitrova E;Oxley D;Webster J;Poot R;Demmers J;Bezstarosti K;Taylor S;Ura H;Koide H;Wutz A;Vidal M;Elderkin S;Brockdorff N
多梳抑制复合物1（PRC 1）在分化和发育过程中调节遗传性基因沉默中起着重要作用。PRC 1募集通常归因于核心蛋白Polycomb的染色体结构域与三甲基组蛋白H3 K27（H3 K27 me 3）的相互作用，由第二复合物PRC 2催化。出乎意料的是，我们发现RING 1B，PRC 1的催化亚基，以及相关的组蛋白H2 A的单泛素化被靶向到野生型和PRC 2缺陷小鼠胚胎干细胞（mESC）中的紧密重叠位点，证明了PRC 1活性募集的H3 K27 me 3独立途径。我们表明，这一途径是介导的RYBP-PRC 1，一个复杂的催化亚基PRC 1和蛋白质RYBP。RYBP-PRC 1被募集到mESC中的靶位点，并且还参与Xist RNA介导的沉默，后者表明在Polycomb沉默中具有更广泛的作用。我们讨论了这些研究结果的意义，了解招聘和功能的Polycomb抑制剂。
Polycomb-repressive complex 1 (PRC1) has a central role in the regulation of heritable gene silencing during differentiation and development. PRC1 recruitment is generally attributed to interaction of the chromodomain of the core protein Polycomb with trimethyl histone H3K27 (H3K27me3), catalyzed by a second complex, PRC2. Unexpectedly we find that RING1B, the catalytic subunit of PRC1, and associated monoubiquitylation of histone H2A are targeted to closely overlapping sites in wild-type and PRC2-deficient mouse embryonic stem cells (mESCs), demonstrating an H3K27me3-independent pathway for recruitment of PRC1 activity. We show that this pathway is mediated by RYBP-PRC1, a complex comprising catalytic subunits of PRC1 and the protein RYBP. RYBP-PRC1 is recruited to target loci in mESCs and is also involved in Xist RNA-mediated silencing, the latter suggesting a wider role in Polycomb silencing. We discuss the implications of these findings for understanding recruitment and function of Polycomb repressors.
影响因子：
64.5
作者：
Tavares L;Dimitrova E;Oxley D;Webster J;Poot R;Demmers J;Bezstarosti K;Taylor S;Ura H;Koide H;Wutz A;Vidal M;Elderkin S;Brockdorff N
通讯作者：
Brockdorff N