Abstracts (first author)

Talk 

Is predator-induced phenotypic plasticity regulated by DNA-methylation in tadpoles?

Author(s): Burraco P, Arribas Ramos R, Gomez-Mestre I

Summary:

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.


Video


Abstracts (coauthor)

Summary:

Chemical detection of predator cues is crucial for aquatic prey, because it allows predator avoidance and activation of plastic antipredatory defenses. This is the case of many larval amphibians that respond to water-borne cues from potential predators by strongly reducing activity levels. However, as a consequence of increasing anthropogenic activity, a variety of harmful contaminants are dumped in freshwater ecosystems, where they can create interferences in the cue recognition system of tadpoles. Here we analyze the potential effects of two contaminants (i. e., humic acid and ammonium nitrate) on the ability of tadpoles of the western spadefoot toad (Pelobates cultripes) to recognize chemical cues from a common predator, nymphs of the dragonfly Anax imperator. We compared swimming activity of tadpoles in presence and absence of water-borne chemical cues from dragonflies, at different concentrations of humic acid and ammonium nitrate. Changes in tadpole activity associated to toxicity were non-significant. In contrast, the interaction between predator cues and presence of contaminants was significant: tadpoles effectively responded to predator cues in the absence of pollutants by reducing their swimming activity, but remained unresponsive to predator cues when either humic acid or ammonium nitrate were added, even at low concentrations. These interferences due to chemical anthropogenic pollution may pose a threat to the cue recognition systems of prey-predator interactions evolved in amphibian populations.

Contacts

Chairman: Octávio S. Paulo
Tel: 00 351 217500614 direct
Tel: 00 351 217500000 ext22359
Fax: 00 351 217500028
email: mail@eseb2013.com

Address

XIV Congress of the European Society for Evolutionary Biology

Organization Team
Department of Animal Biology (DBA)
Faculty of Sciences of the University of Lisbon
P-1749-016 Lisbon
Portugal

Website

Computational Biology & Population Genomics Group 
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