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XB-ART-5185
Dev Cell 2003 Jun 01;46:813-26. doi: 10.1016/s1534-5807(03)00153-9.
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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 .


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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.

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Species referenced: Xenopus
Genes referenced: btrc fbxo5 pold1

References :
Peters, Emi1 proteolysis: how SCF(beta-Trcp1) helps to activate the anaphase-promoting complex. 2003, Pubmed, Xenbase