Abstracts (first author)
Is predator-induced phenotypic plasticity regulated by DNA-methylation in tadpoles?
Phenotypic plasticity is the ability of a genotype to modify its phenotype in response to reliable environmental cues. The knowledge of the mechanisms involved in plasticity is the key to understand its ecological, developmental and evolutionary consequences. In the last decade, epigenetic changes have been pointed out as explanations for several phenotypically plastic changes. In particular, DNA methylation has been linked to phenotypic plasticity and evidence is quickly accumulating across different taxa. Here we tested if the predator-induced phenotype observed in many amphibian larvae was the consequence of changes in gene expression derived from changes in the pattern of DNA methylation. Tadpoles produce anti-predator phenotypes that include a conspicuous increase in relative tail depth and a reduction of activity rate. To test if these plastic responses are epigenetically regulated, we exposed Pelobates cultripes tadpoles to the presence or absence of chemical cues from predators, while previously treating or not tadpoles with 5-azacytidine, a DNA methylation inhibitor, in a 2x2 factorial experiment. Our experimental treatments were: control (clean water), predator cues (dragonfly nymphs, Anax imperator), 5-azacytidine, and 5-azacytidine plus predator cues. Tadpoles exposed to predator cues showed the expected antipredator morphology, whereas tadpoles exposed to predator cues but earlier treated with 5-azacytidine showed an intermediate phenotype between the control and predator exposed tadpoles. They also showed a substantial decrease in activity rate as compared to control tadpoles and even to predator-exposed tadpoles. We are currently undertaking a molecular analysis with methylation-sensitive amplified length polymorphism (MSAPs), to quantify the changes in epigenetic marks. In view of these results, it seems like epigenetic regulation of predator-induced phenotypic changes in Pelobates tadpoles may be at least partially driven by DNA-methylation.