Polycomb complexes act redundantly to repress genomic repeats and genes
Polycomb complexes act redundantly to repress genomic repeats and genes
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DOI：
10.1101/gad.544410
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发表时间：
2010-02-01
影响因子：
10.5
通讯作者：
Wutz, Anton
中科院分区：
文献类型：
--
作者：
Leeb, Martin;Pasini, Diego;Wutz, Anton
多梳复合物建立染色质修饰以维持基因抑制，并且对小鼠胚胎发育至关重要。在这里，我们使用多能胚胎干（ES）细胞，以证明一个意想不到的冗余之间的Polycomb抑制复合物1（PRC1）和PRC2在分化细胞的形成。缺乏PRC1或PRC2功能的ES细胞可以分化成三个胚层的细胞，而PRC1和PRC2的同时缺失则会消除分化。在分子水平上，分化缺陷是由ES细胞中被PRC1和PRC2冗余抑制的一组基因的去抑制引起的。此外，我们发现基因组重复序列是Polycomb靶点，并表明在没有Polycomb复合物的情况下，内源性小鼠白血病病毒元件可以动员。这表明Polycomb组系统对防御寄生DNA的贡献，以及基因组重复序列在Polycomb介导的基因调控中的潜在作用。
Polycomb complexes establish chromatin modifications for maintaining gene repression and are essential for embryonic development in mice. Here we use pluripotent embryonic stem (ES) cells to demonstrate an unexpected redundancy between Polycomb-repressive complex 1 (PRC1) and PRC2 during the formation of differentiated cells. ES cells lacking the function of either PRC1 or PRC2 can differentiate into cells of the three germ layers, whereas simultaneous loss of PRC1 and PRC2 abrogates differentiation. On the molecular level, the differentiation defect is caused by the derepression of a set of genes that is redundantly repressed by PRC1 and PRC2 in ES cells. Furthermore, we find that genomic repeats are Polycomb targets and show that, in the absence of Polycomb complexes, endogenous murine leukemia virus elements can mobilize. This indicates a contribution of the Polycomb group system to the defense against parasitic DNA, and a potential role of genomic repeats in Polycomb-mediated gene regulation.