Polycomb complexes act redundantly to repress genomic repeats and genes

被引:264
作者
Leeb, Martin [1 ]
Pasini, Diego [2 ,3 ]
Novatchkova, Maria [1 ]
Jaritz, Markus [1 ]
Helin, Kristian [2 ,3 ]
Wutz, Anton [1 ]
机构
[1] Res Inst Mol Pathol, A-1030 Vienna, Austria
[2] Univ Copenhagen, BRIC, DK-2200 Copenhagen, Denmark
[3] Univ Copenhagen, Ctr Epigenet, DK-2200 Copenhagen, Denmark
基金
英国惠康基金; 奥地利科学基金会;
关键词
Polycomb; histone modification; chromatin; embryonic stem cells; tumor; retrovirus; EMBRYONIC STEM-CELLS; HISTONE METHYLTRANSFERASE ACTIVITY; GROUP PROTEINS RING1A/B; X-INACTIVATION; RESPONSE ELEMENTS; CHROMATIN; H3; METHYLATION; H2A; PLURIPOTENCY;
D O I
10.1101/gad.544410
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:265 / 276
页数:12
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