Aurora-A regulates MCRS1 function during mitosis.
Aurora-A regulates MCRS1 function during mitosis.
复制标题
DOI：
10.1080/15384101.2016.1187342
复制
发表时间：
2016-07-02
期刊：
影响因子：
--
通讯作者：
Vernos I
中科院分区：
文献类型：
--
作者：
Meunier S;Timón K;Vernos I
有丝分裂纺锤体是由微管（MT）通过不同的途径成核，涉及中心体，染色体或预先存在的MT的壁。MCRS 1是RanGTP靶点，其特异性地与染色体驱动的MT结合，保护它们免受MT解聚酶的侵害。MCRS 1还需要控制中期的动粒纤维（K-纤维）MT负末端动态。在这里，我们研究了MCRS 1活性在M期的调节。我们发现MCRS 1在有丝分裂中被Aurora-A激酶在Ser 35/36上磷酸化。虽然这种磷酸化对MCRS 1定位于染色体MT和K-纤维负端没有作用，但我们发现它调节MCRS 1在有丝分裂中的活性。我们的结论是极光-A活性是特别重要的K-纤维负端动力学在有丝分裂的调谐。
The mitotic spindle is made of microtubules (MTs) nucleated through different pathways involving the centrosomes, the chromosomes or the walls of pre-existing MTs. MCRS1 is a RanGTP target that specifically associates with the chromosome-driven MTs protecting them from MT depolymerases. MCRS1 is also needed for the control of kinetochore fiber (K-fiber) MT minus-ends dynamics in metaphase. Here, we investigated the regulation of MCRS1 activity in M-phase. We show that MCRS1 is phosphorylated by the Aurora-A kinase in mitosis on Ser35/36. Although this phosphorylation has no role on MCRS1 localization to chromosomal MTs and K-fiber minus-ends, we show that it regulates MCRS1 activity in mitosis. We conclude that Aurora-A activity is particularly important in the tuning of K-fiber minus-ends dynamics in mitosis.