FN Archimer Export Format
PT J
TI Epigenetic origin of adaptive phenotypic variants in the human blood fluke Schistosoma mansoni
BT 
AF FNEICH, Sara
   THERON, Andre
   COSSEAU, Celine
   ROGNON, Anne
   ALIAGA, Benoit
   BUARD, Jerome
   DUVAL, David
   ARANCIBIA, Nathalie
   BOISSIER, Jerome
   ROQUIS, David
   MITTA, Guillaume
   GRUNAU, Christoph
AS 1:1,2,5;2:1,2;3:1,2;4:1,2;5:1,2;6:3;7:1,2;8:1,2;9:1,2;10:1,2,4;11:1,2;12:1,2;
FF 1:;2:;3:;4:;5:;6:;7:;8:;9:;10:;11:;12:;
C1 UPVD, IHPE, 52 Ave Paul Alduy, F-66860 Perpignan, France.
   IHPE, CNRS, UMR 5244, F-66860 Perpignan, France.
   IGH, CNRS, UPR1142, F-34396 Montpellier, France.
   TUM, Liesel Beckmann Str 2, D-85354 Freising Weihenstephan, Germany.
   Univ Paris Saclay, UMR BDR, INRA, ENVA, F-78350 Jouy En Josas, France.
C2 UNIV PERPIGNAN, FRANCE
   CNRS, FRANCE
   CNRS, FRANCE
   TUM, GERMANY
   UNIV PARIS SACLAY, FRANCE
UM IHPE
IN DOAJ
IF 5.189
TC 12
UR https://archimer.ifremer.fr/doc/00615/72708/71730.pdf
   https://archimer.ifremer.fr/doc/00615/72708/71731.pdf
   https://archimer.ifremer.fr/doc/00615/72708/71732.xlsx
   https://archimer.ifremer.fr/doc/00615/72708/71733.pdf
   https://archimer.ifremer.fr/doc/00615/72708/71734.pdf
LA English
DT Article
DE ;Epigenetics;Adaptive evolution;Compatibility polymorphism;Schistosoma mansoni
AB 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. 
PY 2016
PD JUN
SO Epigenetics & Chromatin
SN 1756-8935
PU Biomed Central Ltd
VL 9
IS 27
UT 000379259600001
DI 10.1186/s13072-016-0076-2
ID 72708
ER

EF