Abstract
Epigenetic mechanisms contribute to generate heritable phenotypic variability. The most studied of these mechanisms is DNA methylation on cytosine residues. Methylation is predominantly (but not exclusively) located in CpG dinucleotides context. Surprisingly, DNA methylation has not been exhaustively studied in many species. During my PhD, I developed a new Galaxy-integrated software to predict DNA methylation based on mutation rates of methylated and unmethylated CpG regions. DNA methylation analysis from several data bases for 150 species have identified 4 typical profiles for methylation distribution all the long gene bodies. These methylation profiles are not congruent with kingdom classification. These results suggest evolutionary convergence under environmental or functional constraints and universality of the DNA methylation code. Our results contribute to pave the way for generating conceptual links between DNA methylation, genes function and environment for a large range of phylogenetic clades.To evaluate the significance of epigenetic program on the phenotypic plasticity, I focused also on the parasitic success of Schistosoma face to its intermediate host, the Biomphalaria glabrata snail. Indeed, the interaction between this trematode parasite causing of the second human disease after malaria and the mollusk is based on a compatibility polymorphism. On the side of the parasite, the main molecular marker of this compatibility is supported by expression profile of polymorphic mucins called SmPoMucs. We demonstrate that epimutator compounds induce chromatin structural modification on mucin promoters. These modifications are directly involved on the phenotypic plasticity since the infectivity rate is enhanced. In this work, we conclude that epigenetic modifications are key elements on adaptive and developmental plasticity for S. mansoni, as essential as the genetic component.