Abstracts (first author)
Environmentally induced epigenetic plasticity in the human parasite Schistosoma mansoni
Adaptation to environmental changes is based on the perpetual generation of new phenotypes. We know that phenotypic variability generating mechanisms have not only a genetic but also an epigenetic component, and their relative importance in adaptive evolution is an open question. Variability generating mechanisms are particularly important in host-parasite interaction models in which selective pressures are high and evolution is fast. Epigenetics has been proposed to be the language that is used to communicate between genome and environment. We present here data for a metazoan parasite/host system. The digenetic trematode Schistosoma mansoni is a human parasite that uses the mollusc Biomphalaria glabrata as intermediate host and humans as definitive host. We exposed S. mansoni populations to a stressful but ecological realistic environment: the interaction with an allopatric B. glabrata host in which the parasite develops into the human-infecting cercaria. We then studied phenotypic traits, epigenetic and transcriptional changes that the parasite engages in response to this stressful environment. ChIP-seq studies were performed with antibodies that recognize euchromatic and heterochromatic marks on cercariae released either from the allopatric or sympatric hosts. Differences in chromatin structures were found in roughly 0.1% of the epigenome (excluding repetitive sequences). RNA-seq studies performed on the same stages allowed the identification of about 200 differentially expressed genes between the stressful and normal conditions. Among those we indentified a histone-methyltransferase, providing a potential functional link between stress induced transcriptional and epigenetic modifications. More importantly, our data suggest that chromatin structure changes during the development of the cercariae are inherited by the subsequently formed adult stage.