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首页> 外文期刊>Current Biology: CB >Ska3 Phosphorylated by Cdk1 Binds Ndc80 and Recruits Ska to Kinetochores to Promote Mitotic Progression
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Ska3 Phosphorylated by Cdk1 Binds Ndc80 and Recruits Ska to Kinetochores to Promote Mitotic Progression

机译：CDK1磷酸化的SKA3绑定NDC80，并招募SKA到Kinetochores以促进有丝分裂进展

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摘要

The spindle and kinetochore-associated (Ska) protein complex is required for accurate chromosome segregation during mitosis [1-6] and consists of two copies each of Ska1, Ska2, and Ska3 proteins [4, 7]. The Ska complex contains multiple microtubule-binding elements and promotes kinetochore-microtubule attachment [8-11]. The Ska1 C-terminal domain (CTD) recruits protein phosphatase 1 (PP1) to kinetochores to promote timely anaphase onset [12]. The Ska complex regulates, and is regulated by, Aurora B [13]. Aurora B phosphorylates both Ska1 and Ska3 to inhibit the kinetochore localization of the Ska complex [14]. Despite its multitude of functions at kinetochores, how the Ska complex itself is recruited to kinetochores is unclear. It is unknown whether any mitotic kinases positively regulate the localization of the Ska complex to kinetochores. Here, we show that Cdk1 phosphorylates Ska3 to promote its direct binding to the Ndc80 complex (Ndc80C), a core outer kinetochore component. We also show that this phosphorylation occurs specifically during mitosis and is required for the kinetochore localization of the Ska complex. Ska3 mutants deficient in Cdk1 phosphorylation are defective in kinetochore localization but retain microtubule localization. These mutants support chromosome alignment but delay anaphase onset. We propose that Ska3 phosphorylated by Cdk1 in mitosis binds to Ndc80C and recruits the Ska complex to kinetochores where Ska1 can bind both PP1 and microtubules to promote anaphase onset.
机译：纺织和运动学相关（SKA）蛋白质复合物是在丝分裂期间精确染色体隔离所需的[1-6]，并且由SKA1，SKA2和SKA3蛋白中的两个拷贝组成[4,7]。 SKA络合物含有多种微管粘合元素，并促进KINETOCHORE-MICROTUMULE附件[8-11]。 SKA1 C-末端域（CTD）促进蛋白磷酸酶1（PP1）至KINetochores以促进及时的神服发作[12]。 SKA复合物调节，并由极光（Aurora B）调节[13]。 Aurora B借助SKA1和SKA3，以抑制SKA复合体的Kinetochore本地化[14]。尽管在KINETOCHIORE众多函数中，SKA Complex本身是如何招募到Kinetochores的。尚不清楚是否有丝分裂激酶是否积极调节SKA复合物的定位到Kinetochores。在这里，我们表明CDK1磷酸化SKA3以促进其直接结合NDC80复合物（NDC80C），核心外核熵组分。我们还表明，这种磷酸化在有丝分裂期间特别发生，并且是SKA复合物的Kinetochore定位所必需的。 CDK1磷酸化缺乏的SKA3突变体在Kinetochore定位中有缺陷，但保持微管定位。这些突变体支持染色体取向，但延迟后源性发作。我们提出通过CDK1磷酸化的SKA3在有丝分裂中结合NDC80C，并促进SKA1可以结合PP1和微管率以促进脱脑发作的KINETOCHORE促进SKA复合物。

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