Phenotypic differences between the sexes evolve largely because selection favours a different complement of traits in either sex. Theory suggests that, despite its frequency, sexual dimorphism should be generally constrained from evolving because the sexes share much of their genome. While selection can lead to adaptation in one sex, correlated responses to selection can be maladaptive in the other. In this thesis I use Drosophila to examine the extent to which the shared genome constrains the evolution of sexual dimorphism and whether the sex chromosomes might play a special role in resolving intralocus sexual conflict. Gene expression data shows that intersexual genetic correlations are generally high, suggesting that genes often affect both sexes. The intersexual genetic correlation is negatively associated with sex-bias in expression in D. melanogaster, and the rate of change in sex-bias between D. melanogaster and six closely related species, showing that a sex-specific genetic architecture is a prerequisite for the evolution of sex difference. In further studies I find that genetic variance affecting lifespan is found in the male-limited Y chromosome within a population, which could offer a route to the evolution of further sexual dimorphism in lifespan, though the amount of variance was small suggesting adaptive potential from standing genetic variance is limited. Genetic variance on the X chromosome is also expected to be depleted once the sex chromosomes evolve, but here I find no evidence of depletion in either sex. Dosage compensation does not appear to double the male X-linked genetic variance, but this effect may be complex to detect. Finally, the X chromosome appears to be enriched for sex-specific genetic variance, and the consequences of this are explored using a variety of analytical methods to test biologically meaningful aspects of G-matrix structure. In summary, this thesis suggests that the evolution of sexual dimorphism is generally constrained by the shared genome, but intralocus sexual conflict could be resolved by novel mutations on the Y chromosomes, and by standing sex-specific genetic variance on the X chromosome. It highlights a special role for the X chromosome in the evolution of sexual dimorphism.

Chez les espèces sexuées, une sélection sexuellement antagoniste (SA) peut agir si les deux sexes ont des optimums en fitness différents pour un même trait. De plus, si l'architecture génétique de ce trait est partagée entre les sexes, un conflit sexuel intralocus (IASC) peut se produire, menant à l'évolution d'un dimorphisme sexuel. Un modèle de génétique des populations classique prédit que le chromosome X offre un environnement plus favorable à l'accumulation de locus sous sélection SA en comparaison aux autosomes. Nous nous sommes dans un premier temps intéressée à la détection d'une signature d'IASC dans le génome humain, c'est-à-dire des différences de fréquences alléliques entre les sexes. En effectuant un balayage du génome, nous avons mis en évidence un enrichissement en locus montrant une signature d'IASC sur le chromosome X en comparaison aux autosomes. Un mécanisme possible à l'origine des différences de fréquences alléliques entre les sexes dans une population est une distorsion de transmission sexe-spécifique. Dans un second temps, nous avons donc mis au point une méthode de détection de locus pour lesquels les parents transmettent préférentiellement un allèle à leurs fils, et un autre allèle à leurs filles, en utilisant une base de données de séquençage de trios parents-enfant. Nos résultats indiquent que des processus de distorsion de transmission sexe-spécifique seraient à l'origine d'une grande partie des différences de fréquences alléliques entre les sexes observées chez les enfants. Cela suggère que des processus sexuellement antagonistes agissant sur la survie pourraient avoir lieu entre la production des gamètes et la naissance chez l'Homme. / Sexually Antagonistic (SA) selection can occur when, within a species, the two sexes have different fitness optima for a trait. If a trait under SA selection is encoded by the same set of genes in the two sexes, an Intralocus Sexual Conflict (IASC) can arise, leading to the evolution of sexual dimorphism. A classical theoretical model predicts that the X chromosome should be a hotspot for the accumulation of loci under IASC, as compared to the autosomes. In this dissertation, we first aimed at detecting differences in allelic frequencies between males and females, a signature of IASC, in the human genome using a genome scan. We show that loci exhibiting signatures of ongoing IASC are preferentially located on the X chromosome as compared to autosomes. Moreover, they are enriched in genes involved in the determination of traits known to be sexually dimorphic in humans, including reproduction, metabolism and immune system, supporting an implication of sexually antagonistic selection in the evolution of sexual dimorphisms in humans. One possible mechanism leading to differences in allelic frequencies between the sexes is a sex-specific transmission distortion. Therefore, we aimed at detecting loci for which parents preferentially transmit one allele to their sons and another allele to their daughters in a sequencing dataset containing trios (parents-child). We found that sex-specific transmission distortions are at the origin of a large proportion of the differences in allelic frequencies between the sexes observed in children. This suggests that sexually antagonistic processes on survival may occur between the production of gametes and birth in humans.