Transmission of Dysfunctional Mitochondrial DNA and Its Implications for Mammalian Reproduction.

摘要: Mitochondrial DNA (mtDNA) encodes proteins for the electron transport chain which produces vast majority of cellular energy. MtDNA has its own replication and transcription machinery that relies on nuclear-encoded factors. is inherited in a non-Mendelian fashion as maternal-only mtDNA passed onto next generation. Mutation to can cause mitochondrial dysfunction, affects energy production tissue organ function. In somatic cell nuclear transfer (SCNT), there an issue with mixing two populations mtDNA, namely from donor recipient oocyte. This review focuses transmission SCNT embryos offspring. The be prevented by depleting using depletion agents prior SCNT. As result, harbour oocyte-only mtDNA. Moreover, culturing derived depleted cells media supplemented reprograming agent increase levels expression genes related embryo development when compared non-depleted cell-derived embryos. Furthermore, we have reviewed how supplementation oocytes beneficial effects increasing copy number involved decreasing embryonic death. Notably, are over use terms regulating gene Taken together, manipulating and/or could enhance efficiency.