The evolutionary feedback between genetic conflict and genome architecture

The advent of separate sexes set the stage for dramatic evolutionary innovation across a wide range of taxa. Much of this innovation is attributable to divergent evolutionary interests between now distinct sub-populations of males and females. Trade-offs inherent to these divergent life histories, coupled with a common genome, conspire to limit natural selection's ability to simultaneously maximize the fitness of both sexes. Such conflict between the sexes has therefore largely shaped the history of the genomes of sexual taxa. However, various aspects of the genomic environment---including genes' spatial distributions, abilities to regulate their expression, and rates of recombination---also feed back to influence future sex-specific evolutionary trajectories. Using various genomic resources and transcriptome sequences for the lab mouse, I test several theoretical predictions regarding this feedback between genetic conflict and features of genomic organization.;I begin first by testing recent predictions regarding the clustering of loci experiencing sexual antagonism. Using methods from spatial ecology, I show that autosomal, but not X-linked, sex-biased genes form numerous clusters of limited spatial extent. This spatial organization likely facilitates the invasion of new sexually antagonistic alleles, yet may counterintuitively accelerate sex-specific adaptation as well. Then, I test common intuition on the role of hormones in promoting sex-biased expression. Contrary to expectations, I find that the canonical model of hormone-mediated transcriptional control has little explanatory power, suggesting more of a role for trans -acting genes in providing genes direct information on their sexual environment. These results also suggest that the resolution of sexual antagonism may proceed more slowly than one might expect from the rate at which sex-biased expression evolves. Finally, I also test recent predictions on the relationship between sex-biased recombination rates and genomic imprinting. Consistent with theory, I find imprinted genes are associated with greater sex differences in recombination while controlling for other molecular features of the genome. I then discuss how such associations can couple the future trajectories of genes experiencing sexual and parental antagonism despite the independent ecological origins of such selection pressures.