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

Simon I.R. Lane () and Keith T. Jones ()
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Simon I.R. Lane: Centre for Biological Sciences, Faculty and Natural and Environmental Sciences, University of Southampton
Keith T. Jones: Centre for Biological Sciences, Faculty and Natural and Environmental Sciences, University of Southampton

Nature Communications, 2014, vol. 5, issue 1, 1-9

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms4444

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