期刊
JOURNAL OF CELL BIOLOGY
卷 203, 期 6, 页码 957-969出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201306054
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资金
- National Institutes of Health [R01 GM088371]
- Pew Scholars Program in the Biomedical Sciences
Aurora B kinase phosphorylates kinetochore proteins during early mitosis, increasing kinetochore- microtubule (MT) turnover and preventing premature stabilization of kinetochore-MT attachments. Phosphorylation of kinetochore proteins during late mitosis is low, promoting attachment stabilization, which is required for anaphase onset. The kinetochore protein KNL1 recruits Aurora B-counteracting phosphatases and the Aurora B-targeting factor Bub1, yet the consequences of KNL1 depletion on Aurora B phospho-regulation remain unknown. Here, we demonstrate that the KNL1 N terminus is essential for Aurora B activity at kinetochores. This region of KNL1 is also required for Bub1 kinase activity at kinetochores, suggesting that KNL1 promotes Aurora B activity through Bub1-mediated Aurora B targeting. However, ectopic targeting of Aurora B to kinetochores does not fully rescue Aurora B activity in KNL1-depleted cells, suggesting KNL1 influences Aurora B activity through an additional pathway. Our findings establish KNL1 as a requirement for Aurora B activity at kinetochores and for wild-type kinetochore-MT attachment dynamics.
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