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Mol. Hum. Reprod. Advance Access published online on December 22, 2005
Molecular Human Reproduction, doi:10.1093/molehr/gah227
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© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received June 13, 2005
Revised July 29, 2005
Accepted August 18, 2005

Article

Mitochondrial DNA deletions in rhesus macaque oocytes and embryos

T.C. Gibson 1, H.M. Kubisch 2, and C.A. Brenner 1 *

1 Department of Biological Sciences, University of New Orleans, New Orleans
2 Tulane National Primate Research Center, Covington, LA, USA

* To whom correspondence should be addressed.
C.A. Brenner, E-mail: cbrenner{at}uno.edu


  Abstract

Mitochondria are the most abundant organelles in mammalian oocytes and early embryos. Mitochondrial DNA (mtDNA) mutations, including the common deletion, have been found in skeletal muscle fibres from aged rhesus macaques. The specific aims of this study were to determine whether the mitochondrial common deletion is present in rhesus oocytes after hormonal stimulation and in embryos generated by in vitro production, or whether this deletion is already present in the immature oocyte. Using a nested primer PCR strategy, we found a significant increase in the proportion of mtDNA deletions in stimulated oocytes and embryos from rhesus macaques, compared with mtDNA deletions in immature, unstimulated oocytes derived from necropsied ovaries of age-matched monkeys. The common deletion is larger in the rhesus (5704 bp) than in humans (4977 bp). Accumulation of mtDNA deletions in oocytes may contribute to mitochondrial dysfunction and impaired ATP production. We propose the rhesus to be an excellent model to assess the quality of gametes and embryos and their developmental competence in primates, including humans.

Keywords: embryos/mitochondrial deletions/oocyte maturation/ovarian stimulation/rhesus monkeys.
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