Journal
DEVELOPMENTAL CELL
Volume 20, Issue 6, Pages 739-750Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2011.05.008
Keywords
-
Categories
Funding
- MAC
- SULSA
- University of Edinburgh
- MRC
- Wellcome Trust
- MRC [G0601118] Funding Source: UKRI
- Medical Research Council [G0601118] Funding Source: researchfish
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available