EPOP 通过直接调节酶复合物的二聚化限制 PRC2.1 靶向染色质

Lihu Gong, Xiuli Liu, Xin Yang, Ze Yu, Siming Chen, Chao Xing, Xin Liu
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摘要

多聚胞抑制复合体 2(PRC2)作为两类全复合体(PRC2.1 和 PRC2.2)介导发育基因抑制。EPOP 是 PRC2.1 的特异性附属亚基,它还包含 PCL 蛋白。与其他共同促进 PRC2 靶向的附属亚基不同,EPOP 与其互作物 Elongin BC 一起被认为具有神秘的抑制作用。我们报告了一种不寻常的分子机制,即 EPOP 通过直接调节 PRC2.1 的寡聚状态来对其进行调控。EPOP 破坏了 PRC2.1 的二聚体,削弱了其与染色质的结合,这可能是由于二聚体复合物所产生的渴求效应失效了。与此相一致的是,特异性 PRC2 结合缺陷的 EPOP 突变体增强了小鼠上胚层类细胞中 MTF2 和 H3K27me3 的全基因组富集。Elongin BC在很大程度上不需要EPOP介导的PRC2.1抑制作用。EPOP定义了PRC2.1的一个独特亚类,它通过防止早期分化连续过程中关键基因调控因子的过度抑制来独特地维持表观遗传程序。
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EPOP Restricts PRC2.1 Targeting to Chromatin by Directly Modulating Enzyme Complex Dimerization
Polycomb repressive complex 2 (PRC2) mediates developmental gene repression as two classes of holocomplexes, PRC2.1 and PRC2.2. EPOP is an accessory subunit specific to PRC2.1, which also contains PCL proteins. Unlike other accessory subunits that collectively facilitate PRC2 targeting, EPOP was implicated in an enigmatic inhibitory role, together with its interactor Elongin BC. We report an unusual molecular mechanism whereby EPOP regulates PRC2.1 by directly modulating its oligomerization state. EPOP disrupts the PRC2.1 dimer and weakens its chromatin association, likely by disabling the avidity effect conferred by the dimeric complex. Congruently, an EPOP mutant specifically defective in PRC2 binding enhances genome-wide enrichments of MTF2 and H3K27me3 in mouse epiblast-like cells. Elongin BC is largely dispensable for the EPOP-mediated inhibition of PRC2.1. EPOP defines a distinct subclass of PRC2.1, which uniquely maintains an epigenetic program by preventing the over-repression of key gene regulators along the continuum of early differentiation.
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