Through the early 1990s, various early attempts to create transmitochondrial strains of mammalian species by introduction of foreign mitochondria into germ cells were largely unsuccessful. A number of constraints have been identified or postulated, from perturbations of biological pathways to mechanistic aspects of the specific protocols used. Since 1997, a number of laboratories have reported on methodologies used to create transmitochondrial animals. To date, methods for mitochondria isolation and interspecific transfer of mitochondria have been reported both in laboratory and domestic animal models.[3,10,11]

Interestingly, early reports on development of cloned animals by nuclear transfer resulted in conflicting consequences when retrospective studies on mitochondrial transmission were reported.[12-16] Indeed, dependent upon the specific methodology employed for nuclear transfer and cytoplasm/ooplasm transfer to rescue low-quality embryos, additional models of heteroplasmy may or may not have been characterized as a consequence of mitochondrial dysfunction. As such, research independent of targeted mitochondrial genomic modifications may also help unlock mechanisms underlying the dynamics related to persistence of foreign mitochondria and maintenance of heteroplasmy in various cloning protocols.

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