Methylation of PLK1 by SET7/9 ensures accurate kinetochore–microtubule dynamics

• DOI: 10.1093/jmcb/mjz107
• Publication Date: 2019-12-02T15:41:34Z
• Authors: Ruoying Yu; Huihui Wu; Hazrat Ismail; Shihao Du; Jun Cao; Jianyu Wang; Tarsha Ward; Fengrui Yang; Ping Gui; Mahboob Ali; Lingluo Chu; Fei Mo; Qi Wang; Youjun Chu; Jianye Zang; Yun Zhao; Mingliang Ye; Guowei Fang; Peng R Chen; Zhen Dou; Xinjiao Gao; Wenwen Wang; Xing Liu; Xuebiao Yao
• Keywords: PLK1; Spindle checkpoint

Faithful segregation of mitotic chromosomes requires bi-orientation sister chromatids, which relies on the sensing correct attachments between spindle microtubules and kinetochores. Although mechanisms underlying PLK1 activation have been extensively studied, regulatory that couple activity to accurate chromosome are not well understood. In particular, is implicated in stabilizing kinetochore-microtubule attachments, but how kinetochore regulated avoid hyperstabilized kinetochore-microtubules mitosis remains elusive. Here, we show kinase modulated by SET7/9 via lysine methylation during early mitosis. The SET7/9-elicited dimethylation occurs at Lys191 PLK1, tunes down its limiting ATP utilization. Overexpression non-methylatable mutant or chemical inhibition methyltransferase resulted arrest due destabilized attachments. These data suggest essential for stable promotes dynamic error correction. Our findings define a novel homeostatic regulation integrates protein phosphorylation with maintenance genomic stability.