Untangling the contribution of Haspin and Bub1 to Aurora B function during mitosis.

Autor:	Hadders MA; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Hindriksen S; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Truong MA; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Mhaskar AN; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Wopken JP; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Vromans MJM; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Lens SMA; Oncode Institute and Center for Molecular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Jazyk:	angličtina
Zdroj:	The Journal of cell biology [J Cell Biol] 2020 Mar 02; Vol. 219 (3).
DOI:	10.1083/jcb.201907087
Abstrakt:	Aurora B kinase is essential for faithful chromosome segregation during mitosis. During (pro)metaphase, Aurora B is concentrated at the inner centromere by the kinases Haspin and Bub1. However, how Haspin and Bub1 collaborate to control Aurora B activity at centromeres remains unclear. Here, we show that either Haspin or Bub1 activity is sufficient to recruit Aurora B to a distinct chromosomal locus. Moreover, we identified a small, Bub1 kinase-dependent Aurora B pool that supported faithful chromosome segregation in otherwise unchallenged cells. Joined inhibition of Haspin and Bub1 activities fully abolished Aurora B accumulation at centromeres. While this impaired the correction of erroneous KT-MT attachments, it did not compromise the mitotic checkpoint, nor the phosphorylation of the Aurora B kinetochore substrates Hec1, Dsn1, and Knl1. This suggests that Aurora B substrates at the kinetochore are not phosphorylated by centromere-localized pools of Aurora B, and calls for a reevaluation of the current spatial models for how tension affects Aurora B-dependent kinetochore phosphorylation. (© 2020 Hadders et al.)
Databáze:	MEDLINE
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