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Open Access Dissertation

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First Advisor

Carol A. Brenner


Assisted Reproduction Technologies (ART) have been used to treat infertility since 1790. In the centuries following, dramatic advances have been made in the field of infertility research through the employment of a variety of species. Despite these advances, determination of oocyte and embryo quality remains largely subjective. Ascertainment of methods to measure oocyte and embryo quality to improve selection in ART clinics and increase pregnancy success rates is imperative. These methods are only possible with a more comprehensive understanding of the cellular and molecular properties of oocytes and preimplantation embryos. A key component of all cells, including oocytes and embryos, is the mitochondrion, which produces energy and maintains its own DNA for encoding proteins necessary for energy production. Defects in either the proteins responsible for energy production, the mitochondrial DNA (mtDNA) genome, or other contributing factors can lead to loss of oocyte competence and embryo quality. Human oocytes and embryos would be the optimal material to use for performing studies on preimplantation development. However, practical and ethical constraints prevent the use of human material for intensive, potentially terminal studies; thus, compelling researchers to find and use suitable animal models instead. The non-human primate (NHP) is the most befitting animal model for human reproduction due to evolutionary closeness and the dramatic similarities in reproductive function and preimplantation development. Furthermore, because studies in human preimplantation development are restricted to the use of discarded oocytes from infertility clinics, the use of the NHP has established the rhesus macaque as an excellent research model for human reproduction due to the availability of normal, viable oocytes and embryos from fertile animals. Therefore, the overall goals of this study were to evaluate mitochondria in NHP oocytes and embryos and to determine how mtDNA mutations and mitochondrial function affect oocyte and embryo quality.

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