The uniparental inheritance of mtDNA is an evolutionary conserved feature in mammals. One of the key drivers of uniparental inheritance is to prevent the coexistence of two different mtDNA haplotypes within offspring, or heteroplasmy, a state that can compromise overall organismal fitness. As such, safeguarding uniparental inheritance involves a biased transmission towards maternal mitochondria and the selective elimination of paternal mitochondria. The mechanisms surrounding the elimination of paternal mitochondria comprises mtDNA elimination during spermatogenesis, followed by selective removal of paternal mitochondria during early embryo development. However, the underlying molecular mechanisms that govern uniparental inheritance, and more importantly how paternal mitochondria are eliminated remains unclear. To investigate these questions, we use a combination of molecular biology and imaging techniques. We show in mice that mtDNA gradually decreases between the spermatocyte and round spermatid stages of spermatogenesis. As a consequence, mature spermatozoa isolated from the epididymis harbour mitochondria lacking intact mtDNA. Consistent with recent findings, the decline in mtDNA correlates with the loss of a major mtDNA-binding protein, mitochondrial transcription factor A (TFAM) from the mitochondria. After fertilisation, sperm mitochondria are gradually degraded throughout early embryo development and are largely undetectable by blastocyst stage. We show that this process is regulated by mitochondrial fission factor, Dynamin-related protein 1 (Drp1), as evident by a delay in the degradation of sperm mitochondria in Drp1 knockout oocytes. Further studies are in progress to understand how mtDNA are degraded during spermatogenesis, and whether the selective elimination of sperm paternal mitochondria during embryo development is of physiological significance.