Genomic and phenotypic consequences of asexuality

Sexual reproduction is expected to facilitate the removal of deleterious mutations from populations because biparental inheritance (i.e., segregation) and recombination during meiosis break down linkage disequilibria (LD), allowing mutations to be selected independently from their genetic background. Accordingly, the absence of recombination and segregation is expected to increase selective interference between loci, translating into reduced efficacy of natural selection. While there now exist multiple lines of evidence demonstrating that asexual lineages do experience accelerated accumulation of putatively harmful mutations, whether these mutations influence phenotype in a manner that could contribute to the maintenance of sex remains almost entirely unevaluated. Here, I use the New Zealand freshwater snail, Potamopyrgus antipodarum, to address these questions. In particular, I take advantage of the fact that the mitochondrial genome is expected to suffer from these mutational effects and interacts extensively with the nuclear genome to evaluate potential harmful effects of mutation accumulation in asexuals on a genome-wide scale. I present evidence that harmful mutations remain extant longer in asexual populations than in sexual populations, that the degree of functional constraint determines the extent of mutation accumulation in asexuals, that there is genetic variation for mitochondrial function in asexual lineages of P. antipodarum, and that phenotypic variation for mitochondrial function is mediated by both genetic and environmental variation. Together, these analyses provide strong evidence that asexual lineages are accumulating deleterious mutations, and that there is genetic variation, structured by lake, for mitochondrial function.