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Spindle checkpoint silencing requires association of PP1 to both Spc7 and kinesin-8 motors

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Meadows, John C., Shepperd, Lindsey A., Vanoosthuyse, Vincent, Lancaster, Theresa C., Sochaj, Alicja M., Buttrick, Graham J., Hardwick, K. G. and Millar, Jonathan B. A. (2011) Spindle checkpoint silencing requires association of PP1 to both Spc7 and kinesin-8 motors. Developmental Cell, Vol.20 (No.6). pp. 739-750. doi:10.1016/j.devcel.2011.05.008 ISSN 1534-5807.

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Official URL: http://dx.doi.org/10.1016/j.devcel.2011.05.008

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Abstract

The spindle checkpoint is the prime cell-cycle control mechanism that ensures sister chromatids are bioriented before anaphase takes place. Aurora B kinase, the catalytic subunit of the chromosome passenger complex, both destabilizes kinetochore attachments that do not generate tension and simultaneously maintains the spindle checkpoint signal. However, it is unclear how the checkpoint is silenced following chromosome biorientation. We demonstrate. that association of type 1 phosphatase (PP1(Dis2)) with both the N terminus of Spc7 and the nonmotor domains of the Klp5-Klp6 (kinesin-8) complex is necessary to counteract Aurora B kinase to efficiently silence the spindle checkpoint. The role of Klp5 and Klp6 in checkpoint silencing is specific to this class of kinesin and independent of their motor activities. These data demonstrate that at least two distinct pools of PP1, one kinetochore associated and the other motor associated, are needed to silence the spindle checkpoint.

Item Type: Journal Article
Subjects: Q Science > QH Natural history > QH301 Biology
Q Science > QP Physiology
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Cell & Developmental Biology
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
Library of Congress Subject Headings (LCSH): Cell cycle -- Regulation, Kinesin
Journal or Publication Title: Developmental Cell
Publisher: Cell Press
ISSN: 1534-5807
Official Date: 14 June 2011
Dates:
DateEvent
14 June 2011Published
Volume: Vol.20
Number: No.6
Page Range: pp. 739-750
DOI: 10.1016/j.devcel.2011.05.008
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access
Funder: Medical Research Council (Great Britain) (MRC), Wellcome Trust (London, England)

Data sourced from Thomson Reuters' Web of Knowledge

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