Mol. Hum. Reprod. Advance Access originally published online on October 5, 2005
Molecular Human Reproduction 2005 11(9):623-630; doi:10.1093/molehr/gah231
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Post-ovulatory aging of mouse oocytes leads to decreased MAD2 transcripts and increased frequencies of premature centromere separation and anaphase
1Department of Biology, STECH 257, 9201 University City Boulevard, Charlotte, NC 28223, USA and 2Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center, P.O.Box 33932, 1501 Kings Hwy, Shreveport, LA 71130, USA
1 To whom correspondence should be addressed at: Department of Biology, STECH 257, 9201 University City Boulevard, Charlotte, NC 28223, USA. E-mail: nsteuerw{at}email.uncc.edu or nury.steuerwald{at}embryos.net
Numerous cytological and biochemical alterations occur as mammalian oocytes age post-ovulation. Some of these changes can predispose cells to aneuploidy. The objective of this study was to test the hypothesis that the level of MAD2 spindle assembly checkpoint (SAC) transcripts decrease as mouse oocytes age post-ovulation and that this decrease was associated with chromosome missegregation. Female Institute of Cancer Research (ICR) mice were superovulated and oocytes collected at 14 h, 19 h and 24 h post-HCG for cytogenetic and quantitative real-time rapid cycle fluorescent RT–PCR analyses. Premature centromere separation (PCS) is now generally recognized as a predisposition to aneuploidy. The data showed that the frequencies of PCS-incomplete (PCS-I) did not significantly (P > 0.05) increase with time post-ovulation; whereas the proportions of oocytes displaying PCS-complete (PCS-C) and premature anaphase (PA) were significantly (P < 0.01) greater at 19 h and 24 h post-HCG, respectively. The higher frequencies of PCS-C and PA found at 19 h and 24 h coincided with decreased levels of MAD2 transcripts at these same times. Although the decline in MAD 2 transcripts with oocyte aging represents only one of many potential mechanisms responsible for aneuploidy, a compromised SAC appears to have a role in the unfavourable reproductive outcome associated with post-ovulatory aged oocytes.
Key words: checkpoint genes/cytogenetics/gene expression/meiosis/oocyte
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