By increasing genomic size, whole-genome duplication (WGD) is considered a major source of evolutionary innovation and speciation. We examined sequence evolution and expression divergence following WGD in a tetraploid African clawed frog (\textit{Silurana}). We hypothesized that the redundancy generated by WGD might allow for sex-specific and/or tissue-specific divergence, contributing to sexual dimorphism in this frog, and that such changes could be detected at both the expression and sequence levels. We investigated this hypothesis with a transcriptome-based approach, comparing both sexes across brain, heart and liver. We compared molecular evolution and expression divergence of duplicate gene homeologs to singleton genes and to an extant diploid relative, and identified genes with evidence for sex-biased expression. In doing so, we provide evidence for an allopolyploid mechanism of WGD and speciation in \textit{Silurana}. Additionally, we find that female-biased gene expression is more prevalent among duplicate genes than male-biased expression, particularly in brain where expression levels are highest. We similarly identified antagonistically sex-biased homeologs with indication of positive selection. Our results indicate that divergent evolution at both the sequence and expression levels following WGD favors the co-option of female-biased gene expression and may help resolve sexually antagonistic selection in this frog, thereby facilitating the evolution of sexual dimorphism. / Thesis / Master of Science (MSc) / Whole-genome duplication (WGD) is considered a major source of evolutionary innovation and a driver of speciation. By increasing genetic content and introducing redundancy, selective pressures are reduced and paralogous pairs diverge. We investigate how sex and tissue type contribute to duplicate gene divergence following WGD in a tetraploid African clawed frog. We find evidence for sex-dependent variation in sex-biased expression patterns of duplicate genes in brain, heart and liver, and evaluate how molecular evolution of duplicate genes accounts for expression divergence between sexes. This thesis provides a general framework for investigating sex-biased duplicate gene evolution in an amphibious tetrapod.

Parmi plus de 20000 espèces de trématodes hermaphrodites, les Schistosomatidae ont un statut particulier car ils sont gonochoriques (i.e. deux sexes séparés). Le gonochorisme chez ces espèces, et leur dimorphisme sexuel, seraient en fait une stratégie d’adaptation à leur habitat : le système veineux des vertébrés à sang chaud, dont l’Homme. Malgré un mode chromosomique de déterminisme du sexe (i.e. hétérogamétie femelle ZW), les individus mâles et femelles demeurent phénotypiquement identiques durant tous les stades larvaires de leur cycle de vie hétéroxène. La différenciation sexuelle n’a lieu qu’après l’infestation de leur hôte définitif. Dans ce travail, nous nous sommes intéressés aux facteurs moléculaires déclenchant cette différenciation chez Schistosoma mansoni. Nous avons établi le profil d’expression sexe-dépendant de gènes conservés de la cascade de détermination/différenciation chez les animaux : les DMRT (Double-sex and Male-abnormal-3 Related Transcription Factors). Nous avons par ailleurs généré un transcriptome comparatif mâle/femelle (RNA-seq) sur 5 stades de développement in vivo, dont 3 stades « schistosomules » inédits. Cela nous a permis d’identifier de potentiels gènes « clés » de la différenciation sexuelle et de souligner l’importance de l’interaction hôte-parasite. Enfin, par la combinaison de cette approche transcriptomique et d’une analyse épigénomique (ChIP-seq), nous avons montré une dynamique de la compensation de dose génique au cours du cycle de vie chez les femelles ainsi que la mise en place d’une stratégie transcriptionnelle particulière chez les mâles, optimisant leur développement dans l’hôte et ainsi, leur succès reproducteur. / Parasitic flatworms include more than 20.000 species that are mainly hermaphrodites. Among them, the hundred species of Schistosomatidae are intriguing because they are gonochoric. The acquisition of gonochorism in these species is supposed to provide genetic and functional advantages to adapt to their hosts: warm-blooded animals. Sex of schistosomes is genetically determined at the time of fertilization (i.e. ZW female heterogametic system). However, there is no phenotypic dimorphism through all the larval stages of its complex lifecycle: sexual dimorphism appears only in the definitive host. The molecular mechanisms triggering this late sexual differentiation remain unclear, and this is precisely the topic of our present work. We performed transcriptomic (RNA-Sequencing and quantitative-PCRs) and structural (ChIP-Sequencing) analyses at different stages of Schistosoma mansoni development. Here, we present data suggesting that the sexual differentiation relies on a combination of genetic and epigenetic factors. In a genetic point of view, we show a sex-associated expression of the DMRT genes (Double-sex and Mab-3 Related Transcription Factors) that are known to be involved in sex determination/differentiation through all the animal kingdom. In addition, we propose new potential sex-determining key genes and a pivotal role of host-pathogen interaction at the time of development. In a structural point of view, we highlight a dynamic status of dosage compensation in females and chromatin modifications in males. This intense remodeling reveals a specific transcriptomic strategy which optimizes male development and beyond that, schistosomes reproductive success.