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Spindle assembly checkpoint: the third decade
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DOI：10.1098/rstb.2011.0072.png)
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The spindle assembly checkpoint controls cell cycle progression during mitosis, synchronizing it with the attachment of chromosomes to spindle microtubules. After the discovery of the mitotic arrest deficient (MAD) and budding uninhibited by benzymidazole (BUB) genes as crucial checkpoint components in 1991, the second decade of checkpoint studies (2001-2010) witnessed crucial advances in the elucidation of the mechanism through which the checkpoint effector, the mitotic checkpoint complex, targets the anaphase-promoting complex (APC/C) to prevent progression into anaphase. Concomitantly, the discovery that the Ndc80 complex and other components of the microtubule-binding interface of kinetochores are essential for the checkpoint response finally asserted that kinetochores are crucial for the checkpoint response. Nevertheless, the relationship between kinetochores and checkpoint control remains poorly understood. Crucial advances in this area in the third decade of checkpoint studies (2011-2020) are likely to be brought about by the characterization of the mechanism of kinetochore recruitment, activation and inactivation of checkpoint proteins, which remains elusive for the majority of checkpoint components. Here, we take a molecular view on the main challenges hampering this task.
Keyword:
spindle assembly checkpoint
kinetochore
cell cycle
Aurora B
KMN network
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分享收藏The human mitotic checkpoint protein BubR1 regulates chromosome-spindle attachments.png)
NATURE CELL BIOLOGY
NATURE CELL BIOLOGYIF19.1
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分享收藏Checkpoint inhibition of the APC/C in HeLa cells is mediated by a complex of BUBR1, BUB3, CDC20, and MAD2HeLa细胞中APC/C的检查点抑制由BUBR1，BUB3，CDC20和MAD2的复合物介导OAAI
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