Center of Regenerative Medicine in Barcelona, Aiguader 88, E-08003 Barcelona, Spain.
Nat Cell Biol. 2013 Apr;15(4):348-50. doi: 10.1038/ncb2723.
The recruitment of the silencing complex Polycomb group (PcG) to its target sites in mammalian cells has remained elusive. A prevalent model proposes that the PRC1 component is recruited through recognition of methylated H3K27 found at target sites occupied by the PRC2 component. However, mounting evidence suggests that PRC2-independent mechanisms of PRC1 recruitment exist. Three studies describe that the histone demethylase Kdm2b binds to unmethylated CpG islands and recruits a subset of PRC1 complexes to chromatin in pluripotent stem cells.
招募沉默复合物多梳组 (PcG) 到哺乳动物细胞的靶位点仍然难以捉摸。一个流行的模型提出,PRC1 成分是通过识别 PRC2 成分占据的靶位点上发现的甲基化 H3K27 来募集的。然而,越来越多的证据表明,PRC1 的募集存在与 PRC2 无关的机制。三项研究表明,组蛋白去甲基酶 Kdm2b 结合到未甲基化的 CpG 岛上,并将一部分 PRC1 复合物募集到多能干细胞的染色质上。