Abstract
Aurora B, a member of the Aurora family of serine/threonine protein kinases, is a key player in chromosome segregation. As part of a macromolecular complex known as the chromosome passenger complex, Aurora B concentrates early during mitosis in the proximity of centromeres and kinetochores, the sites of attachment of chromosomes to spindle microtubules. There, it contributes to a number of processes that impart fidelity to cell division, including kinetochore stabilization, kinetochore–microtubule attachment, and the regulation of a surveillance mechanism named the spindle assembly checkpoint. In the regulation of these processes, Aurora B is the fulcrum of a remarkably complex network of interactions that feed back on its localization and activation state. In this review, we discuss the multiple roles of Aurora B during mitosis, focusing in particular on its role at centromeres and kinetochores. Many details of the network of interactions at these locations remain poorly understood, and we focus here on several crucial outstanding questions.
Highlights
GENERAL REMARKSCells executing mitosis are challenged in ways that can jeopardize their viability and survival [1]
Reviewed by: Deborah Stroka, University of Bern, Switzerland Marcos Malumbres, Spanish National Cancer Research Centre (CNIO), Spain Adrian Thomas Saurin, University of Dundee, UK
While it is clear that Aurora B substrates at centromeres and kinetochores undergo dynamic changes in their phosphorylation state during the relatively short time it takes kinetochores to attach to the spindle, it is uncertain to which extent these changes reflect the dynamic regulation of Aurora B activity by the intrinsic and extrinsic mechanisms discussed above [41]
Summary
Cells executing mitosis are challenged in ways that can jeopardize their viability and survival [1]. Two feedback mechanisms control the process of kinetochore– microtubule attachment during mitosis, and Aurora B contributes decisively to both of them These pathways are named error correction (EC) and spindle assembly checkpoint (SAC, known as mitotic checkpoint, metaphase checkpoint, or “wait anaphase signal”). Cyclin-dependent kinase 1 (Cdk1), Aurora B, monopolar spindle 1 (Mps1), and budding uninhibited by benzimidazoles 1 (Bub1), all mitotic protein kinases, are required to promote correct kinetochore–microtubule-binding configurations, as well as for the SAC response [59]. They are likely to regulate both phenomena at the same time and from the same place, the kinetochores. We focus on some of the molecular details that implicate Aurora B in these two pathways
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