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Mad2 prevents aneuploidy and premature proteolysis of cyclin B and securin during meiosis I in mouse oocytes

Lookup NU author(s): Dr Hayden Homer, Dr Mark Levasseur, Professor Alison Murdoch, Professor Mary Herbert

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Abstract

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.

Publication metadata

Author(s): Homer HA, McDougall A, Levasseur M, Yallop K, Murdoch AP, Herbert M

Publication type: Article

Publication status: Published

Journal: Genes and Development

Year: 2005

Volume: 19

Issue: 2

Pages: 202-207

ISSN (print): 0890-9369

ISSN (electronic): 1549-5477

Publisher: Cold Spring Harbor Laboratory Press

URL: http://dx.doi.org/10.1101/gad.328105

DOI: 10.1101/gad.328105

PubMed id: 15655110

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