Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/115684
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Type: Journal article
Title: Reduced ability to recover from spindle disruption and loss of kinetochore spindle assembly checkpoint proteins in oocytes from aged mice
Author: Yun, Y.
Holt, J.
Lane, S.
McLaughlin, E.
Merriman, J.
Jones, K.
Citation: Cell Cycle, 2014; 13(12):1938-1947
Publisher: Taylor & Francis
Issue Date: 2014
ISSN: 1538-4101
1551-4005
Statement of
Responsibility: 
Yan Yun, Janet E Holt, Simon IR Lane, Eileen A McLaughlin, Julie A Merriman, and Keith T Jones
Abstract: Currently, maternal aging in women, based on mouse models, is thought to raise oocyte aneuploidy rates, because chromosome cohesion deteriorates during prophase arrest, and Sgo2, a protector of centromeric cohesion, is lost. Here we show that the most common mouse strain, C57Bl6/J, is resistant to maternal aging, showing little increase in aneuploidy or Sgo2 loss. Instead it demonstrates significant kinetochore-associated loss in the spindle assembly checkpoint protein Mad2 and phosphorylated Aurora C, which is involved in microtubule-kinetochore error correction. Their loss affects the fidelity of bivalent segregation but only when spindle organization is impaired during oocyte maturation. These findings have an impact clinically regarding the handling of human oocytes ex vivo during assisted reproductive techniques and suggest there is a genetic basis to aneuploidy susceptibility.
Keywords: Spindle assembly checkpoint; oocyte; aging; cell cycle; aneuploidy; error correction; meiosis
Description: Published online: 23 Apr 2014
Rights: © 2014 Landes Bioscience
RMID: 0030095275
DOI: 10.4161/cc.28897
Grant ID: http://purl.org/au-research/grants/arc/DP120100946
Appears in Collections:Molecular and Biomedical Science publications

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