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The histone- and PRMT5-associated protein COPR5 is required for myogenic differentiation

机译：组蛋白和PRMT5相关蛋白COPR5是成肌分化所必需的

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摘要

Myogenic differentiation requires the coordination between permanent cell cycle withdrawal, mediated by members of the cyclin-dependent kinase inhibitor (CKI) family, and activation of a cascade of myogenic transcription factors, particularly MYOGENIN (MYOG). Recently, it has been reported that the Protein aRginine Methyl Transferase PRMT5 modulates the early phase of induction of MYOG expression. Here, we show that the histone- and PRMT5-associated protein COPR5 (cooperator of PRMT5) is required for myogenic differentiation. C2C12 cells, in which COPR5 had been silenced, could not irreversibly exit the cell cycle and differentiate into muscle cells. This phenotype might be explained by the finding that, in cells in which COPR5 was downregulated, p21 and MYOG induction was strongly reduced and PRMT5 recruitment to the promoters of these genes was also altered. Moreover, we suggest that COPR5 interaction with the Runt-related transcription factor 1 (RUNX1)-core binding factor-β (CBFβ) complex contributes to targeting the COPR5-PRMT5 complex to these promoters. Finally, we present evidence that COPR5 depletion delayed the in vivo regeneration of cardiotoxin-injured mouse skeletal muscles. Altogether, these data extend the role of COPR5 from an adaptor protein required for nuclear functions of PRMT5 to an essential coordinator of myogenic differentiation.
机译：肌源性分化需要细胞周期蛋白依赖性激酶抑制剂（CKI）家族成员介导的永久性细胞周期停药与级联的肌源性转录因子，尤其是肌生成素（MYOGENIN）（MYOG）的激活之间的协调。近来，已经报道蛋白精氨酸甲基转移酶PRMT5调节诱导MYOG表达的早期。在这里，我们显示组蛋白和PRMT5相关蛋白COPR5（PRMT5的合作者）是成肌分化所必需的。 COPR5被沉默的C2C12细胞无法不可逆转地退出细胞周期并分化为肌肉细胞。这种表型可以通过以下发现来解释：在COPR5被下调的细胞中，p21和MYOG的诱导被大大降低，PRMT5募集到这些基因的启动子也被改变。此外，我们建议COPR5与Runt相关转录因子1（RUNX1）-核心结合因子-β（CBFβ）复合物的相互作用有助于将COPR5-PRMT5复合物靶向这些启动子。最后，我们提供了证据，表明COPR5耗竭延迟了心脏毒素损伤的小鼠骨骼肌的体内再生。总而言之，这些数据将COPR5的作用从PRMT5的核功能所需的衔接子蛋白扩展到了成肌分化的重要协调者。

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