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Nat Commun. 2014 Mar 18;5:3444. doi: 10.1038/ncomms4444.

Non-canonical function of spindle assembly checkpoint proteins after APC activation reduces aneuploidy in mouse oocytes.

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1
1] Centre for Biological Sciences, Faculty and Natural and Environmental Sciences, University of Southampton, Southampton SO17 1BJ, UK [2] School of Biomedical Sciences & Pharmacy, University of Newcastle, Callaghan, New South Wales 2308, Australia.

Abstract

The spindle assembly checkpoint (SAC) prevents aneuploidy by coupling anaphase onset, through anaphase-promoting complex (APC) activation, with chromosome attachment to spindle microtubules. Here, we examine APC activity in oocytes, noted for their susceptibility to chromosome mis-segregation during the first meiotic division (MI). We find that MI oocytes only contain sub-maximal APC activity, measured through cyclin B1-GFP degradation, because inhibition of SAC proteins when the APC is normally fully active increases cyclin B1 degradation twofold and reduces the length of this division by 2 h. In addition, inhibiting the SAC component Mps1 only when the APC is already active increases aneuploidy rates in the resulting egg by up to 30%. We therefore establish that the activities of SAC proteins and the APC co-exist in oocytes, and such concurrence has a vital role in reducing aneuploidy rates by extending MI, probably by allowing time for numerous erroneous microtubule attachments to be corrected.

PMID:
24637522
DOI:
10.1038/ncomms4444
[Indexed for MEDLINE]
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