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2篇 您的检索式:作者名="Lingluo Chu"
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1LRIF1 interacts with HPla to coordinate accurate chromosome segregation during mitosis显示文摘Heterochromatin protein 1α (HP1α)regulates chromatin specification and plasticity during cell fate decision.Different structural determinants account for HP1α Localization and function during cell division cycle.Our earlier study showed that centromeric Localization of HP1α depends on the epigenetic mark H3K9me3 in interphase,while its centromeric location in mitosis relies on uncharacterized PXVXL-containing factors.Here,we identified a PXVXL-containing protein,Ligand-dependent nuclear receptorinteracting factor 1 (LRIF1),which recruits HPla to the centromere of mitotic chromosomes and its interaction with HP1α is essential for accurate chromosome segregation during mitosis.LRIF1 interacts directly with HPla chromoshadow domain via an evolutionariLy conserved PXVXL motif within its C-terminus.Importantly,the LRIF1-HPla interaction is critical for Aurora B activity in the inner centromere.Mutation of PXVXL motif of LRIF1 Leads to defects in HPla centromere targeting and aberrant chromosome segregation.These findings reveal a previously unrecognized direct Link between LRIF1 and HP1α in centromere plasticity control and illustrate the critical role of LRIF1-HP1α interaction in orchestrating accurate cell division.Saima Akram Fengrui Yang Junying Li Gregory Adams Yingying Liu Xiaoxuan Zhuang Lingluo Chu Xu Liu Nerimah Emmett Winston Thompson McKay Mullen Saravana Muthusamy Wenwen Wang Fei Mo Xing Liu 2018Journal of Molecular Cell Biology2018,10,6:5
2Methylation of PLK1 by SET7/9 ensures accurate kinetochore–microtubule dynamics显示文摘Faithful segregation of mitotic chromosomes requires bi-orientation of sister chromatids, which relies on the sensing of correct attachments between spindle microtubules and kinetochores. Although the mechanisms underlying PLK1 activation have been extensively studied, the regulatory mechanisms that couple PLK1 activity to accurate chromosome segregation are not well understood. In particular, PLK1 is implicated in stabilizing kinetochore–microtubule attachments, but how kinetochore PLK1 activity is regulated to avoid hyperstabilized kinetochore–microtubules in mitosis remains elusive. Here, we show that kinetochore PLK1 kinase activity is modulated by SET7/9 via lysine methylation during early mitosis. The SET7/9-elicited dimethylation occurs at the Lys191 of PLK1, which tunes down its activity by limiting ATP utilization. Overexpression of the non-methylatable PLK1 mutant or chemical inhibition of SET7/9 methyltransferase activity resulted in mitotic arrest due to destabilized kinetochore–microtubule attachments. These data suggest that kinetochore PLK1 is essential for stable kinetochore–microtubule attachments and methylation by SET7/9 promotes dynamic kinetochore–microtubule attachments for accurate error correction. Our findings define a novel homeostatic regulation at the kinetochore that integrates protein phosphorylation and methylation with accurate chromosome segregation for maintenance of genomic stability.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 RChen Zhen Dou Xinjiao Gao Wenwen Wang Xing Liu Xuebiao Yao 2020Journal of Molecular Cell Biology2020,12,6:0
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