蛋白质精氨酸甲基转移酶5
生物
组蛋白
DNA修复
同源重组
甲基转移酶
甲基化
细胞生物学
乙酰化
DNA甲基化
表观遗传学
组蛋白乙酰转移酶
组蛋白甲基转移酶
遗传学
DNA
基因
基因表达
作者
Thomas L. Clarke,María Pilar Sánchez-Bailón,Kelly Chiang,John J. Reynolds,Joaquín Herrero‐Ruiz,Tiago M. Bandeiras,Pedro M. Matias,Sarah Maslen,Mark Skehel,Grant S. Stewart,Clare C. Davies
出处
期刊:Molecular Cell
[Elsevier BV]
日期:2017-02-23
卷期号:65 (5): 900-916.e7
被引量:167
标识
DOI:10.1016/j.molcel.2017.01.019
摘要
Protein post-translation modification plays an important role in regulating DNA repair; however, the role of arginine methylation in this process is poorly understood. Here we identify the arginine methyltransferase PRMT5 as a key regulator of homologous recombination (HR)-mediated double-strand break (DSB) repair, which is mediated through its ability to methylate RUVBL1, a cofactor of the TIP60 complex. We show that PRMT5 targets RUVBL1 for methylation at position R205, which facilitates TIP60-dependent mobilization of 53BP1 from DNA breaks, promoting HR. Mechanistically, we demonstrate that PRMT5-directed methylation of RUVBL1 is critically required for the acetyltransferase activity of TIP60, promoting histone H4K16 acetylation, which facilities 53BP1 displacement from DSBs. Interestingly, RUVBL1 methylation did not affect the ability of TIP60 to facilitate ATM activation. Taken together, our findings reveal the importance of PRMT5-mediated arginine methylation during DSB repair pathway choice through its ability to regulate acetylation-dependent control of 53BP1 localization.
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