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Article Dans Une Revue Epigenetics and Chromatin Année : 2016

Epigenetic origin of adaptive phenotypic variants in the human blood-fluke Schistosoma mansoni

Anne Rognon
David Duval

Résumé

Background: Adaptive 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 comple‑ mentary 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. Results: We 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. Conclusion: We 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.
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Dates et versions

hal-01364014 , version 1 (12-09-2016)

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Sara Fneich, André Théron, Celine Cosseau, Anne Rognon, Benoit Aliaga, et al.. Epigenetic origin of adaptive phenotypic variants in the human blood-fluke Schistosoma mansoni. Epigenetics and Chromatin, 2016, 9, pp.227. ⟨10.1186/s13072-016-0076-2⟩. ⟨hal-01364014⟩
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