Phosphorylation regulates the p31Comet – Mitotic Arrest Deficient 2 (Mad2) interaction to promote Spindle Assembly Checkpoint (SAC) activity [Cell Biology]

March 4th, 2014 by Date, D. A., Burrows, A. C., Summers, M. K.

The spindle assembly checkpoint (SAC) ensures the faithful segregation of the genome during mitosis by ensuring that sister chromosomes form bipolar attachments with microtubules of the mitotic spindle. p31Comet is an antagonist of the SAC effector Mad2 and promotes silencing of the SAC and mitotic progression. However, p31Comet interacts with Mad2 throughout the cell cycle. We show that p31Comet binds Mad2 solely in an inhibitory manner. We demonstrate that attenuating the affinity of p31Comet for Mad2 by phosphorylation promotes SAC activity in mitosis. Specifically, phosphorylation of S102 weakens p31Comet−Mad2 binding and enhances p31Comet−mediated bypass of the SAC. Our results provide the first evidence for regulation of p31Comet and demonstrate a previously unknown event controlling SAC activity.
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