Haldane's rule, which states that the heterogametic sex is preferentially afflicted if one of hybrid sexes is sterile or inviable, is a general pattern in all animals that possess sex chromosomes. The hybrid sterility component of this rule is especially important because hybrid sterility is involved in the onset of postzygotic isolation. Accumulating evidence on the fast evolution of individual sex genes have stimulated us to hypothesize that the fast evolution of sex genes may be the force underlying the excess of hybrid heterogametic sterility. This study tests the evolutionary patterns of sex genes in comparison to non-sex genes, as a general group. The divergences between a group of 19 sex genes and 20 non-sex genes from X chromosome were compared between D. melanogaster, D. mauritiana, D. simulans, and D. sechellia using PCR-RFLP. Within species polymorphism data were also obtained for D. simulans and D. mauritiana. The results show a significantly higher divergence for sex genes than non-sex genes, while a comparable level of intraspecific polymorphism was revealed in both groups. Among the sex gene group, genes related to male reproduction appear to evolve faster than femalereproductive genes. The evolution of both sex and non-sex genes conforms to the neutral theory under Tajima's test and HKA test. The faster evolution of sex genes supports the fast-sex theory as an explanation for the hybrid sterility component of Haldane's rule. Localization of some examples of hybrid sterility genes is crucial to ultimately untangle the genetics of hybrid sterility. The car region of D. mauritiana, which has been shown to harbor genes that confer full effect of hybrid sterility in the D. simulans genetic background, was introgressed into the D. simulans genome by continuous backcrosses. Recombination mapping analysis, taking advantage of molecular markers, revealed that at least two regions are capable of causing hybrid sterility in this species group. The phenotypes of hybrid testes were examined during the backcross process. / Thesis / Master of Science (MSc)

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.