Errors in mitotic chromosome segregation can lead to DNA damage and aneuploidy, both hallmarks of cancer. To achieve synchronous error-free segregation, mitotic chromosomes must align at the metaphase plate with stable amphitelic attachments to microtubules emanating from opposing spindle poles. The astrin–kinastrin (astrin is also known as SPAG5 and kinastrin as SKAP) complex, also containing DYNLL1 and MYCBP, is a spindle and kinetochore protein complex with important roles in bipolar spindle formation, chromosome alignment and microtubule–kinetochore attachment. However, the molecular mechanisms by which astrin–kinastrin fulfils these diverse roles are not fully understood. Here, we characterise a direct interaction between astrin and the mitotic kinase Plk1. We identify the Plk1-binding site on astrin as well as four Plk1 phosphorylation sites on astrin. Regulation of astrin by Plk1 is dispensable for bipolar spindle formation and bulk chromosome congression, but promotes stable microtubule–kinetochore attachments and metaphase plate maintenance. It is known that Plk1 activity is required for effective microtubule–kinetochore attachment formation, and we suggest that astrin phosphorylation by Plk1 contributes to this process.

有丝分裂染色体分离的错误会导致 DNA 损伤和非整倍性，这都是癌症的标志。为了实现同步无差错分离，有丝分裂染色体必须在中期板处对齐，并与从相反纺锤极发出的微管形成稳定的两性附着。astrin-kinastrin（astrin 也称为 SPAG5，kinastrin 称为 SKAP）复合物，也包含 DYNLL1 和 MYCBP，是一种纺锤体和着丝粒蛋白复合物，在双极纺锤体形成、染色体排列和微管-着丝粒附着中发挥重要作用。然而，阿斯汀-激肽发挥这些不同作用的分子机制尚不完全清楚。在这里，我们描述了 astrin 和有丝分裂激酶 Plk1 之间的直接相互作用。我们鉴定了 astrin 上的 Plk1 结合位点以及 astrin 上的四个 Plk1 磷酸化位点。Plk1 对 astrin 的调节对于双极纺锤体的形成和大量染色体的聚集是可有可无的，但可以促进稳定的微管-着丝粒附着和中期板的维持。众所周知，Plk1 活性是有效微管-着丝粒附着形成所必需的，我们认为 Plk1 引起的 astrin 磷酸化有助于这一过程。