Journal
JOURNAL OF CELL BIOLOGY
Volume 199, Issue 1, Pages 27-37Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201205170
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Funding
- American Institute for Cancer Research
- Cancer Research UK [C6946/A14492]
- Wellcome Trust [092096]
- Cancer Research UK [13959] Funding Source: researchfish
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The spindle assembly checkpoint (SAC) is essential to ensure proper chromosome segregation and thereby maintain genomic stability. The SAC monitors chromosome attachment, and any unattached chromosomes generate a wait anaphase signal that blocks chromosome segregation. The target of the SAC is Cdc20, which activates the anaphase-promoting complex/cyclosome (APC/C) that triggers anaphase and mitotic exit by ubiq-uitylating securin and cyclin B1. The inhibitory complex formed by the SAC has recently been shown to inhibit Cdc20 by acting as a pseudosubstrate inhibitor, but in this paper, we show that Mad2 also inhibits Cdc20 by binding directly to a site required to bind the APC/C. Mad2 and the APC/C competed for Cdc20 in vitro, and a Cdc20 mutant that does not bind stably to Mad2 abrogated the SAC in vivo. Thus, we provide insights into how Cdc20 binds the APC/C and uncover a second mechanism by which the SAC inhibits the APC/C.
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