期刊
DEVELOPMENTAL CELL
卷 4, 期 6, 页码 813-826出版社
CELL PRESS
DOI: 10.1016/S1534-5807(03)00153-9
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资金
- NCI NIH HHS [CA09302] Funding Source: Medline
- NIGMS NIH HHS [GM07365, GM54811, GM60439] Funding Source: Medline
Progression through mitosis occurs because cyclin B/Cdc2 activation induces the anaphase promoting complex (APC) to cause cyclin B destruction and mitotic exit. To ensure that cyclin B/Cdc2 does not prematurely activate the APC in early mitosis, there must be a mechanism delaying APC activation. Emi1 is a protein capable of inhibiting the APC in S and G2. We show here that Emi1 is phosphorylated by Cdc2, and on a DSGxxS consensus site, is subsequently recognized by the SCFbetaTrCP/Slimb ubiquitin ligase and destroyed, thus providing a delay for APC activation. Failure of betaTrCP-dependent Emi1 destruction stabilizes APC substrates and results in mitotic catastrophe including centrosome overduplication, potentially explaining mitotic deficiencies in Drosophila Slimb/betaTrCP mutants. We hypothesize that Emi1 destruction relieves a late prophase checkpoint for APC activation.
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