Mitochondria are well known for housing the oxidative phosphorylation pathway, a complex structure essential for ATP production. Mitochondrial malfunction can result from versions of OXPHOS protein complexes that consist of incompatible nuclear and mitochondrial DNA. In this ongoing study, we aim to determine the manifestations of genetic incompatibilities on the physiological output of mitochondria. We utilize Nasonia spp. crosses, all containing varying combinations of nuclear alleles and mtDNA, to measure ATP in F2 hybrids. An introgression strain will be used to repair allelic incompatibilities at a locus housing genes involved with OXPHOS pathway protein complexes. Mitochondria will be isolated via homogenization in an isolation buffer from 100 Nasonia larvae of various allelic combinations and subsequently quantified using a luminescent cell viability assay. We expect that hybrids crossed with the introgression strain will have increased ATP production compared to non-introgression strains, indicating that resolving genetic incompatibilities recovers physiological activity of mitochondria.
