Introduction of epigenetic variation contribute to resistance against the human parasite Schistosoma mansoni

Abstract

Background: Waddington-type kick-start of adaptive evolution is assumed to be possible based on epigenetic variation alone. We tested this hypothesis in the snail Biomphalaria glabrata, vector of Schistosoma mansoni, the causative agent of the human disease schistosomiasis. Epilines and epigenetic recombinant inbred lines (epiRILs) were used to propagate DNA methylation variants over 3 generations. Results: The fecundity and susceptibility to infection by S. mansoni were measured. Average parasite prevalence has a higher variance in epiRILs than in controls and decreased from 84 ± 5% in controls to 68 ± 21% in epiRILs. The increase in fertility in epiRILs was 12%, with an average heritability of 0.55. The introduction of 1% epimutant offspring snail into resident susceptible populations was simulated by a model. If genetic assimilation of the resistance occurred in 0.3% of the introduced epimutants, susceptibility would be replaced by resistance after less than one hundred generations. Conclusions: Environmental management can therefore be envisaged by introducing epigenetically modified organisms to prevent parasite infections from spreading to the intermediate host and, ultimately, the human population.