Sexual differences are dramatic and widespread across taxa. However, a common genome between males and females should hinder phenotypic divergence. In this thesis I have used experimental, genomic, and theoretical approaches to study processes that can facilitate and maintain differences between males and females. I studied two mechanisms for the evolution of sexual dimorphism - condition-dependence and gene duplication. If sex-specific traits are costly, then individuals should only express such traits when they possess enough resources to do so. I experimentally manipulated adult condition and found that the sex-biased gene expression depends on condition. Second, duplication events can permit different gene copies to adopt sex-specific expression. I showed that half of all duplicate families have paralogs with different sex-biased expression patterns between members. I investigated how current sexual dimorphism may support novel dimorphism. With regards gene duplication, I found that related duplicates did not always have different expression patterns. However, duplicating a pre-existing sex-biased gene effectively increases organismal sexual dimorphism overall. From a theoretical perspective, I investigated how sexually dimorphic recombination rates allow novel sexually antagonistic variation to invade. Male and female recombination rates separately affect invasion probabilities of new alleles. Finally, I examined the assumption that a common genetic architecture impedes the evolution of sexual dimorphism. First, I conducted a literature review to test whether additive genetic variances in shared traits were different between the sexes. There were few significant statistical differences. However, extreme male-biased variances were more common than extreme female-biased variances. Sexual dimorphism is expected to evolve easily in such traits. Second, I compared these results to findings from the multivariate literature. In contrast to single trait studies, almost all multivariate studies of sexual dimorphism have found variance differences, both in magnitude and orientation, between males and females. Overall, this thesis concludes that sexual dimorphism can evolve by processes that generate novel sexual dimorphism or that take advantage of pre-existing dimorphism. Furthermore, a common genome is not necessarily a strong barrier if genetic variances differ between the sexes. It will be an exciting challenge to understand how mutation and selection work together to allow organisms differ in their ability evolve sexual dimorphism.

Sexual differences are dramatic and widespread across taxa. However, a common genome between males and females should hinder phenotypic divergence. In this thesis I have used experimental, genomic, and theoretical approaches to study processes that can facilitate and maintain differences between males and females. I studied two mechanisms for the evolution of sexual dimorphism - condition-dependence and gene duplication. If sex-specific traits are costly, then individuals should only express such traits when they possess enough resources to do so. I experimentally manipulated adult condition and found that the sex-biased gene expression depends on condition. Second, duplication events can permit different gene copies to adopt sex-specific expression. I showed that half of all duplicate families have paralogs with different sex-biased expression patterns between members. I investigated how current sexual dimorphism may support novel dimorphism. With regards gene duplication, I found that related duplicates did not always have different expression patterns. However, duplicating a pre-existing sex-biased gene effectively increases organismal sexual dimorphism overall. From a theoretical perspective, I investigated how sexually dimorphic recombination rates allow novel sexually antagonistic variation to invade. Male and female recombination rates separately affect invasion probabilities of new alleles. Finally, I examined the assumption that a common genetic architecture impedes the evolution of sexual dimorphism. First, I conducted a literature review to test whether additive genetic variances in shared traits were different between the sexes. There were few significant statistical differences. However, extreme male-biased variances were more common than extreme female-biased variances. Sexual dimorphism is expected to evolve easily in such traits. Second, I compared these results to findings from the multivariate literature. In contrast to single trait studies, almost all multivariate studies of sexual dimorphism have found variance differences, both in magnitude and orientation, between males and females. Overall, this thesis concludes that sexual dimorphism can evolve by processes that generate novel sexual dimorphism or that take advantage of pre-existing dimorphism. Furthermore, a common genome is not necessarily a strong barrier if genetic variances differ between the sexes. It will be an exciting challenge to understand how mutation and selection work together to allow organisms differ in their ability evolve sexual dimorphism.