The mitochondria are central to Eukaryotic metabolism and drive cellular responses to environmental conditions. Mitochondrial dysfunction is implicated in diverse disease states such as diabetes, neurodegeneration and infertility, however only 15 % of dysfunction is brought about by genetic mutations in mitochondrial DNA. Accounting for the remaining causes of functional variation in the mitochondria remains a fertile area of research. An exciting avenue within this area is that of epigenetic modification of the mitochondrial DNA (MEM). MEM occurs in response to environmental stressors and disease but there are no studies linking environmental stress, MEM and mitochondrial function. I will bridge this gap in our knowledge using an avian model to characterize the influence of developmental temperature and oxygen stress in driving MEM (detected using Nanopore seq).