Mitosis is controlled by reversible protein phosphorylation involving specific kinases and phosphatases. A handful of major mitotic protein kinases, such as the cyclin B–CDK1 complex, the Aurora kinases, and Polo-like kinase 1 (PLK1), cooperatively regulate distinct mitotic processes. Research has identified proteins and mechanisms that integrate these kinases into signaling cascades that guide essential mitotic events. These findings have important implications for our understanding of the mechanisms of mitotic regulation and may advance the development of novel antimitotic drugs. We review collected evidence that in vertebrates, the Aurora kinases serve as catalytic subunits of distinct complexes formed with the four scaffold proteins Bora, CEP192, INCENP, and TPX2, which we deem “core” Aurora cofactors. These complexes and the Aurora-PLK1 cascades organized by Bora, CEP192, and INCENP control crucial aspects of mitosis and all pathways of spindle assembly. We compare the mechanisms of Aurora activation in relation to the different spindle assembly pathways and draw a functional analogy between the CEP192 complex and the chromosomal passenger complex that may reflect the coevolution of centrosomes, kinetochores, and the actomyosin cleavage apparatus. We also analyze the roles and mechanisms of Aurora-PLK1 signaling in the cell and centrosome cycles and in the DNA damage response.

有丝分裂由涉及特定激酶和磷酸酶的可逆蛋白质磷酸化控制。一些主要的有丝分裂蛋白激酶，例如细胞周期蛋白 B-CDK1 复合物、Aurora 激酶和 Polo 样激酶 1 (PLK1)，协同调节不同的有丝分裂过程。研究已经确定了将这些激酶整合到指导重要有丝分裂事件的信号级联中的蛋白质和机制。这些发现对于我们理解有丝分裂调节机制具有重要意义，并可能促进新型抗有丝分裂药物的开发。我们回顾了收集的证据，表明在脊椎动物中，Aurora 激酶充当与四种支架蛋白 Bora、CEP192、INCENP 和 TPX2 形成的不同复合物的催化亚基，我们将其视为“核心”Aurora 辅助因子。这些复合物以及由 Bora、CEP192 和 INCENP 组织的 Aurora-PLK1 级联控制着有丝分裂的关键方面和纺锤体组装的所有途径。我们比较了与不同纺锤体组装途径相关的 Aurora 激活机制，并在 CEP192 复合体和染色体过客复合体之间进行了功能类比，这可能反映了中心体、动粒和肌动球蛋白裂解装置的共同进化。我们还分析了 Aurora-PLK1 信号在细胞和中心体周期以及 DNA 损伤反应中的作用和机制。