Epigenetic origin of adaptive phenotypic variants in the human blood fluke Schistosoma mansoni
|Author(s)||Fneich Sara1, 2, 5, Theron Andre1, 2, Cosseau Celine1, 2, Rognon Anne1, 2, Aliaga Benoit1, 2, Buard Jerome3, Duval David1, 2, Arancibia Nathalie1, 2, Boissier Jerome1, 2, Roquis David1, 2, 4, Mitta Guillaume1, 2, Grunau Christoph1, 2|
|Affiliation(s)||1 : UPVD, IHPE, 52 Ave Paul Alduy, F-66860 Perpignan, France.
2 : IHPE, CNRS, UMR 5244, F-66860 Perpignan, France.
3 : IGH, CNRS, UPR1142, F-34396 Montpellier, France.
4 : TUM, Liesel Beckmann Str 2, D-85354 Freising Weihenstephan, Germany.
5 : Univ Paris Saclay, UMR BDR, INRA, ENVA, F-78350 Jouy En Josas, France.
|Source||Epigenetics & Chromatin (1756-8935) (Biomed Central Ltd), 2016-07 , Vol. 9 , N. 27 , P. 13p.|
|WOS© Times Cited||11|
|Keyword(s)||Epigenetics, Adaptive evolution, Compatibility polymorphism, Schistosoma mansoni|
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 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. 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.