Meeting Abstract
The parasitoid wasp genus Nasonia serves as an emerging model for mitochondrial disease due to an incompatibility between nuclear and mitochondrial genomes between sister taxa. Male hybrids of Nasonia vitripennis and Nasonia giraulti experience mortality during the larval stage of development as compared to parent strains. Previous research has shown that 98% of F2 males with an incompatible allele on chromosome 5 combined with N. giraulti maternity die. This region of interest on chromosome 5 encodes a gene suspected to be involved in the NADH pathway, possibly explaining the energetic shortfall preventing the organism from reaching adulthood. The goal of this research is to further explore what genetic basis underlies the mortality seen in N. vitripennis and N. giraulti hybrids and the energetic effects of a given genotype. To better understand how this mitochondrial incompatibility affects individuals, progeny counts will be taken of each life stage to determine fecundity of backcrossed F2 females and parent crosses. Larvae and pupae will be collected at arrested stages to determine genotype, as diapause can be an indicator of lesser metabolic capability. Offspring and parents of each cross will be genotyped to determine allele ratios. Rate of oxygen consumption will be measured in backcrossed F2 female mitochondria to test energy metabolism and deduce what energetic consequence each genotype has across strains. Once we can describe the relationships between genotype and metabolic phenotype in Nasonia, we can begin to explore what other combinations of factors lead to lethality during hybrid development.
