The field of mitochondrial medicine has developed rapidly following the description in the late 1980s of the first mitochondrial mutations that led to human disease. However, through the late 1990s, in vivo animal models were extremely rare and limited to characterizations of spontaneous mutations. My research interests relate to the technical hurdles associated with creating transmitochondrial research animals (i.e., animals harboring engineered mutations in the mitochondrial genome) and gene therapy approaches for correcting human diseases of the mtDNA. Though the mitochondrial genome is small (~16.6kb in vertebrates), transfection of mtDNA or entire mitochondrial genomes into mitochondria is not possible by conventional transgenic technologies. Furthermore, recombination within mitochondria is a rare event, such that harnessing the mitochondrial recombination machinery is not feasible. Ongoing research seeks to explore new strategies for introducing mtDNA into cells via liposome encapsulation and subsequent fusion of liposome vesicles with the outer and inner mitochondrial membranes. Going forward, development of strategies for increasing mtDNA recombination frequency would enable techniques for introducing specific point mutations, allowing for the creation of mouse models for a variety of human diseases of the mtDNA. Another area of research involves testing unique synthetic antioxidant compounds designed to alleviate oxidative damage caused by mitochondrial dysfunction. In addition to my own research, interactive studies in animal transgenesis through the Auburn University Transgenic Facility are envisioned across a broad spectrum of interests in the life sciences at Auburn University.