Mitochondrial Inheritance and Natural Phenotypic Variation Among \u3ci\u3eCaenorhabditis briggsae\u3c/i\u3e Populations

Mutations affecting the mitochondrial electron transport chain cause numerous neurodegenerative disorders in humans and affect longevity in other organisms. A natural model system to study the relationship between mitochondrial function and aging within an evolutionary or population genetic context has been lacking. Natural populations of Caenorhabditis briggsae nematodes were recently found to harbor mitochondrial genetic variation with likely functional consequences for aging. Specifically, C. briggsae isolates containing high frequencies of a deletion mutation affecting the mitochondrial NADH dehydrogenase 5 (ND5) gene were found to have reduced reproductive fitness and lifespan and elevated levels of mutagenic superoxide. Here, rates of growth and aging and aerobic respiratory capacity were evaluated in several isolates spanning the range of mitochondrial genetic variation in this species. There is considerable variation among isolates for all measured traits, although the observed relationships between isolate-specific trait means and ND5 deletion frequency did not always conform to my expectations. In an effort to determine whether the among-isolate phenotypic variation is due to mitochondrial rather than to nuclear genetic variation, inter-population hybrids of C. briggsae were created and compared to the progenitor isolates. Surprisingly, evidence for paternal mitochondrial inheritance was detected in many of these hybrid lines. Where mitochondrial genomes were maternally inherited as expected, intergenomic epistasis appears to contribute to fitness, longevity, and aging in this species