4.7 Article

Spindle Checkpoint Silencing Requires Association of PP1 to Both Spc7 and Kinesin-8 Motors

Journal

DEVELOPMENTAL CELL
Volume 20, Issue 6, Pages 739-750

Publisher

CELL PRESS
DOI: 10.1016/j.devcel.2011.05.008

Keywords

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Funding

  1. MAC
  2. SULSA
  3. University of Edinburgh
  4. MRC
  5. Wellcome Trust
  6. MRC [G0601118] Funding Source: UKRI
  7. Medical Research Council [G0601118] Funding Source: researchfish

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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.

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