Meeting Abstract
The hypothesis that the strictly maternal transmission of mitochondrial DNA (mtDNA) affords an opportunity for the accumulation and fixation of mitochondrial variants that harm males but not females (i.e., the Mother’s Curse) is tantalizing. Yet, direct evidence that mutations in the mitochondria exhibit such sexually-antagonistic fitness effects is sparse. Male-specific mutational effects may seem unlikely, given that the physiological function of the mitochondria is largely shared between the sexes. Nevertheless, male-specific effects could potentially occur if sex-specific cell types or tissues have energy requirements that are differentially impacted by mutations in energy metabolism. Indeed, patterns of gene duplication and evolution suggest the resolution of potentially sexually-antagonistic effects of the mtDNA via the evolution of male-specific expression of nuclear-encoded mitochondrial gene duplicates. Here we employ a model of mitochondrial-nuclear incompatibility in the fruit fly Drosophila to test whether there are sex-specific mechanisms underlying temperature-sensitive sterility in males and females. We compare the effects of this mitochondrial-nuclear incompatibility to generate sterility in males and females exposed to ecologically relevant high temperatures at different stages of development, as well as the cellular etiology of sterility in both sexes. We discuss the potential for Mother’s Curse in this system in the context of the recent literature supporting or refuting the evolutionary potential for sexually-antagonistic effects of mitochondrial mutations.
