Abstract
BackgroundAdaptive evolution is not possible without the generation of phenotypic variants. The origin of these variations has been a central topic in evolutionary biology. Up to now, it was commonly accepted that standing genetic variation is the only cause of phenotypic variants. However, epigenetic information is emerging as a complementary source of heritable phenotypic variation that contributes to evolution. The relative importance of genetics and epigenetics in generating heritable phenotypic variation is nevertheless a matter of debate.ResultsWe used a host–parasite system to address this question. The human blood fluke Schistosoma mansoni can adapt rapidly to new intermediate snail hosts. The interaction between parasite and mollusk is characterized by a compatibility polymorphism illustrating the evolutionary dynamics in this system. The principal molecular marker for compatibility (infection success) is the expression pattern of a group of polymorphic mucins (SmPoMuc) in the parasite. We show here that chromatin structure changes as the SmPoMuc promoters are the cause for SmPoMuc transcription polymorphism leading to phenotypic novelty and increase in infection success, i.e., fitness.ConclusionWe establish that epigenetic changes can be the major if not only cause of adaptive phenotypic variants in Schistosoma mansoni, suggesting that epimutations can provide material for adaptive evolution in the absence of genetic variation in other systems. In addition, our results indicate that epidrugs can be used to control parasite development but also parasite evolution.Electronic supplementary materialThe online version of this article (doi:10.1186/s13072-016-0076-2) contains supplementary material, which is available to authorized users.
Highlights
Adaptive evolution is not possible without the generation of phenotypic variants
Inbred S. mansoni strains used in the study are pure lines Our laboratory maintains the life cycle of currently five inbred strains of Schistosoma mansoni and their corresponding sympatric Biomphalaria glabrata host strains
We focused our analysis on histone modifications in the promoter regions by native chromatin immunoprecipitation (N-Chromatin immunoprecipitation (ChIP)) using two different antibodies that recognize histone H3 acetylated on lysine 9 (H3K9ac) and histone H3 tri-methylated on lysine 9 (H3K9me3)
Summary
Adaptive evolution is not possible without the generation of phenotypic variants. The origin of these variations has been a central topic in evolutionary biology. Adaptive evolution relies on the generation of heritable phenotypic variants on which selection can act. There is a relative broad consensus that genotype environment interactions represent the major, if not exclusive, source of phenotypic novelty. This view has been challenged by theoretical. None of them is adaptive in the sense that the phenotype provides a fitness gain and is favored by selection under ecologically realistic conditions. It remains an open question whether epigenetic inheritance contributes significantly to adaptive evolution. To the best of our knowledge, for the first time experimental evidence for an epigenetically encoded adaptive phenotype
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