Abstract
Phenotypic variability is defined as the capacity of a given population to produce phenotypic variants under theinfluence of the environment. Some of the phenotypic variants are heritable. It is generally assumed that thegenetic variations are the sole source of heritable phenotypic variants. However, recent studies have shown thatepigenetic variations can provide alternative source for phenotypic variants without change in DNA sequence. Inhost / parasite interactions, parasites impose selective pressures on their hosts and vice versa, leading to a genuinearms race between both partners. Such interaction leads to rapid adaptation where each partner has to evolve thecapacity to express new phenotypic variants. We propose that epigenetic variations play an important role in thegenesis of phenotypic variability. Schistosoma mansoni is a human parasite that causes intestinal schistosomiasis.During the PhD project, I was interested in the interaction of S. mansoni with its intermediate host Biomphalariaglabrata. The two main goals of this PhD project were: (i) To determine the relative weight of epigenetics andgenetics in the expression of phenotypic variants in the parasite. (ii) To initiate the investigation of epigeneticmechanisms in the host.The results show that histone modifications i.e. changes in the epigenetic information are indeed a source ofphenotypic variants in S. mansoni. These phenotypic variants confer a higher fitness to the parasite, by increasingits compatibility towards the mollusk. Finally, studying the heritability of epigenetic changes showed a nonmendeliansegregation. For B. glabrata, I was the first to show the DNA methylation in the snail. 2% of totalcytosines are methylated in his genome.