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首页> 外文期刊>Molecular cell >Gene silencing triggers polycomb repressive complex 2 recruitment to CpG Islands genome wide
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Gene silencing triggers polycomb repressive complex 2 recruitment to CpG Islands genome wide

机译：基因沉默触发多梳抑制复合物2招募到CpG Islands全基因组

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摘要

Polycomb group (PcG) proteins are required for normal differentiation and development and are frequently deregulated in cancer. PcG proteins are involved in gene silencing; however, their role in initiation and maintenance of transcriptional repression is not well defined. Here, we show that knockout of the Polycomb repressive complex 2 (PRC2) does not lead to significant gene expression changes in mouse embryonic stem cells (mESCs) and that it is dispensable for initiating silencing of target genes during differentiation. Transcriptional inhibition in mESCs is sufficient to induce genome-wide ectopic PRC2 recruitment to endogenous PcG target genes found in other tissues. PRC2 binding analysis shows that it is restricted to nucleosome-free CpG islands (CGIs) of untranscribed genes. Our results show that it is the transcriptional state that governs PRC2 binding, and we propose that it binds by default to nontranscribed CGI genes to maintain their silenced state and to protect cell identity.
机译：正常的分化和发育需要聚梳组（PcG）蛋白，并且在癌症中经常被放松调节。 PcG蛋白参与基因沉默。然而，它们在转录抑制的启动和维持中的作用尚不清楚。在这里，我们表明敲除Polycomb抑制复合物2（PRC2）不会导致小鼠胚胎干细胞（mESCs）中的基因表达发生显着变化，并且对于分化过程中启动目标基因的沉默是必不可少的。 mESCs中的转录抑制作用足以诱导全基因组异位PRC2募集到其他组织中发现的内源性PcG靶基因。 PRC2结合分析表明它仅限于未转录基因的无核小体的CpG岛（CGI）。我们的结果表明，控制PRC2结合的是转录状态，并且我们建议默认情况下它与未转录的CGI基因结合以维持其沉默状态并保护细胞身份。

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