MST1 Limits the Kinase Activity of Aurora B to Promote Stable Kinetochore-Microtubule Attachment
- Authors
- Oh, Hyun Jung; Kim, Mi Ju; Song, Su Jung; Kim, Tackhoon; Lee, Dongjun; Kwon, Seung-Hae; Choi, Eui-Ju; Lim, Dae-Sik
- Issue Date
- 9-3월-2010
- Publisher
- CELL PRESS
- Keywords
- CELLBIO
- Citation
- CURRENT BIOLOGY, v.20, no.5, pp.416 - 422
- Indexed
- SCIE
SCOPUS
- Journal Title
- CURRENT BIOLOGY
- Volume
- 20
- Number
- 5
- Start Page
- 416
- End Page
- 422
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/116815
- DOI
- 10.1016/j.cub.2009.12.054
- ISSN
- 0960-9822
- Abstract
- The establishment and maintenance of proper attachment of kinetochores to microtubules are required to prevent chromosome missegregation and consequent chromosomal instability and tumorigenesis. Although MST1 (mammalian sterile 20-like kinase 1) has been implicated in many aspects of cell cycle regulation and tumor suppression [1], its precise mechanism of action has remained largely unknown. We now show that MST1 promotes accurate kinetochore-microtubule attachment by modulating the kinase activity of Aurora B. HeLa cells depleted of MST1 failed to develop stable end-on kinetochore-microtubule attachment, giving rise to unaligned mitotic chromosomes. The misaligned chromosomes activated the Mad2- and BubR1-dependent spindle checkpoint response, resulting in a delay in anaphase onset. The kinase activity of Aurora B, which promotes destabilization of kinetochore-microtubule attachment [2-4], was increased in cells depleted of MST1 or NDR1, a downstream kinase of MST1. MST1 and NDR1 associated with Aurora B. Moreover, MST1 directly phosphorylated Aurora B and inhibited its kinase activity in vitro. Depletion of Aurora B restored the stability of kinetochore-microtubule attachment in cells depleted of MST1 or NDR1. MST1 is thus a key regulator of Aurora B activity that ensures mitotic chromosome congression and accurate chromosome segregation.
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