Effects of mitochondrial genomic variation on life history trait expression in Drosophila melanogaster

The mitochondria are essential for life in eukaryotes, taking centre-stage in the process of cellular respiration. This process is regulated via a series of finely coordinated interactions encoded by two obligate genomes – nuclear and mitochondrial. Both genomes are required for the production of cellular energy, and thus their harmonious interaction is vital for the maintenance of mitochondrial integrity and the viability of eukaryote life. Recently many studies have shown an abundance of phenotype-changing genetic variation segregating within the mtDNA genome – and these results run counter to the traditional paradigm in which mitochondrial genetic variation was expected to be evolving neutrally. It remains unclear how this variation is accumulating – either adaptively under selection, or non-adaptively under mutation-selection balance. Furthermore, maternal inheritance of the mitochondrial genome predisposes this genome to accumulation of mutations that have male biased effect, and the existence of these male-harming mutations has recently been empirically substantiated. The aim of my thesis is to explore and elucidate the nature of the evolutionary processes that shape the molecular composition of the mitochondrial genome. My goal was to understand how much of the genetic variance accumulating within the genome is sex-specific, and in particular male-biased. This would support the idea that mitochondrial variation consisted largely of deleterious mutation loads that accumulate under maternal transmission. Secondly I was interested in understanding how much genetic variation is adaptive – occurring in both sexes, and exhibiting phenotypic responses to thermal stresses that concord with expected predictions based on where the mtDNA haplotypes have evolved. Finally, I aimed to elucidate the molecular mechanisms that bridge the link between mitochondrial genotype and phenotype.