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XB-ART-5185
Dev Cell. June 1, 2003; 4 (6): 813-26.

Prophase destruction of Emi1 by the SCF(betaTrCP/Slimb) ubiquitin ligase activates the anaphase promoting complex to allow progression beyond prometaphase.

Margottin-Goguet F , Hsu JY , Loktev A , Hsieh HM , Reimann JD , Jackson PK .


Abstract
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 SCF(betaTrCP/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.

PubMed ID: 12791267
Article link: Dev Cell.
Grant support: CA09302 NCI NIH HHS , CA09302 NCI NIH HHS , CA09302 NCI NIH HHS , CA09302 NCI NIH HHS , CA09302 NCI NIH HHS , CA09302 NCI NIH HHS , GM07365 NIGMS NIH HHS , GM54811 NIGMS NIH HHS , GM60439 NIGMS NIH HHS

Genes referenced: btrc ccnb1.2 cdk1 fbxo5 pold1
Antibodies referenced:
Morpholinos referenced:

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