Meeting Abstract
Intra-species hybridization can result in mitochondrial dysfunction due to recombination of epistatic mitochondrial-nuclear alleles that coevolved to maintain electron transport chain (ETC) function within each population. However, mitochondria also play many roles, such as apoptosis, in cellular functions not directly related to ATP production. Thus, outstanding questions include whether hybrid dysfunction phenotypes are related to ETC dysfunction, and what are the identities of the genetic variants that induce hybrid mitochondrial dysfunction. Cytoplasmic-nuclear hybrids (cybrids) of the nematode Caenorhabditis briggsae suffer from mitochondrial dysfunction. A fraction of F2 hybrids also experience a 25% delay in development rate compared to wild-type siblings. We inquired whether mitochondrial dysfunction underlies developmental delay. We analyzed developmental timing in C. briggsae, comparing parental, F2, and cybrid strains. F2 hybrids and cybrids exhibited developmental delay. F2 delayed hybrids differ in mitochondrial biochemistry from their wild-type F2 siblings. Genetic mapping using F2 hybrids, near-isogenic and advanced-intercross recombinant inbred lines identified a nuclear locus related to hybrid incompatibility. We also produced and genotyped cybrids at two temperatures and found temperature-dependent complex allele segregation patterns. This segregation distortion suggests both an interaction between environment and genotype on hybrid fitness and also that multiple nuclear alleles are involved in mitochondrial coevolution. A key implication of these results is establishing a connection between genotype, cellular biochemistry, an organismal phenotype, and individual fitness.
