Abstract
The majority of parthenogenetic species are often thought to be clonal. Clonality is costly in the long term, as it can result in accumulation of deleterious mutations and lower adaptability. However, cases reporting non-clonal asexuals are accumulating. Non-clonal asexuality has very different genomic and fitness consequences compared to clonality, and may be a key intermediate step in the transition from sex to asexuality. Additionally, asexuality may be often non-obligate, with events of cryptic sex. These events may also shape the genome and evolution of asexual lineages. In this PhD, I investigated the reproductive mode of Artemia parthenogenetica and its role in the transition from sex to asexuality and the evolution of asexual lineages. Specifically, I used the capacity of asexually produced males (“rare males”) to cross with sexual females and transmit asexuality to their offspring (contagious asexuality), to experimentally generate new lineages. I showed that diploid asexual Artemia have a non-clonal reproductive mode, in which recombination results in loss of heterozygosity (LOH) in the offspring. LOH is costly as it can reveal recessive deleterious mutations. Perhaps due to selection caused by the deleterious consequences of LOH, the recombination rate in these asexuals was lower than in a closely related sexual species. I also found that sex-asex hybrids had a mixed sexual and asexual reproduction, and that asexual females from natural populations were capable of rare sex. This means that rare events of sex in asexual Artemia could occur between a rare male and an asexual female reproducing sexually. In a review of how asexual reproductive modes were identified in the literature, I found that there was a bias in the identification and general perception of asexuals toward clonality, as an important part of the asexual species reviewed were in fact non-clonal, and evidence for clonality was often missing. Furthermore, the maj ority of non-clonal asexuals had reproductive modes that resulted in low LOH. This suggests that non-clonal asexuals often evolve secondarily toward a more clonal-like reproduction, so that even clonal species may not have been clonal throughout their evolutionary history. Finally, using genomics on contagion-generated lineages, I found that in Artemia, rare males are produced asexually through recombination and thus LOH on the ZW sex chromosomes. We know that contagious asexuality, and possibly between-lineages crosses, occurred in the evolutionary history of A. parthenogenetica. Perhaps, contagious asexuality and/or within asexual sex events provide opportunities for the gene(s) controlling asexuality to escape declining lineages into new ones. In this case, contagious asexuality through rare males may be the reason why recombination persists in asexual Artemia. Whether non-clonal asexuality and sex events occur in many parthenogenetic species is still unclear, and requires thorou gh investigation. Theoretically, there is a strong need for models taking into account the genomic consequences of non-clonal and non-obligate asexuality, and their role in the transition from sex to asexuality and the maintenance of sex.