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RESEARCH COMMUNICATION
1 Newcastle Fertility Centre at Life, Centre for Life, Newcastle upon Tyne NE1 4EP, United Kingdom; 2 School of Cell and Molecular Biosciences and 3 School of Surgical and Reproductive Sciences, The Medical School, University of Newcastle, Newcastle upon Tyne NE2 4HH, United Kingdom
In mitosis, the spindle checkpoint protein Mad2 averts aneuploidy by delaying anaphase onset until chromosomes align. Here we show that depletion of Mad2 in meiosis I mouse oocytes induced an increased incidence of aneuploidy. Proteolysis of cyclin B and securin commenced earlier in Mad2-depleted oocytes, resulting in a shortened duration of meiosis I. Furthermore, overexpression of Mad2 inhibited homolog disjunction. We conclude that Mad2 delays the onset of cyclin B and securin degradation and averts aneuploidy during meiosis I in mammalian oocytes. The data suggest a link between trisomies such as Down syndrome and defective oocyte spindle checkpoint function.
[Keywords: Aneuploidy; Mad2; spindle checkpoint; mouse oocytes; cyclin B; securin]
Received April 16, 2004; revised version accepted October 14, 2004.
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.328105.
4 Present address: UMR 7009 CNRS/Université Pierre et Marie Curie (Paris VI), Observetoire Océanologique, 06230 Villefranche-sur-Mer, France.
5 E-MAIL h.a.homer{at}ncl.ac.uk; FAX 44-191-219-4747.
6 E-MAIL mary.herbert{at}ncl.ac.uk; FAX 44-191-219-4747.
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