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|Title:||Non-canonical function of spindle assembly checkpoint proteins after APC activation reduces aneuploidy in mouse oocytes|
|Citation:||Nature Communications, 2014; 5(1):3444-1-3444-9|
|Simon I.R. Lane and Keith T. Jones|
|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.|
|Description:||Published 18 Mar 2014|
|Rights:||© 2014 Macmillan Publishers Limited. All rights reserved.|
|Appears in Collections:||Molecular and Biomedical Science publications|
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