Abstract

Intestinal schistosomiasis is a chronic parasitic disease caused by the trematode Schistosoma mansoni. At least 67 million people are infected worldwide. The parasite has a complex life cycle which involve two consecutive obligatory hosts and two transitions between these hosts as free-swimming larvae, being in each step, a new environment to the parasite. Male and female adult worms mature sexually only if in mutual physical contact within the vertebrate host. The interaction with each environment demands strict regulation of gene expression and depends on specific environmental cues, i.e. a multitude of signals from the environment, such as temperature, pH, osmolarity and chemical compounds, and also signals that come from the host, in particular those that serve to recognise and destroy them, i.e. the immune system. This interaction shapes not only the parasite’s morphology, metabolism and behaviour in short-term, but also its development into different phenotypes over the whole life cycle, i.e. subsequent stages that were not directly exposed to the environment. This is because the developmental and evolutionary trajectories of schistosomes are based on an inheritance system being composed of the genome and the epigenome, which will conjointly interpret signals from the environment.

We show here how the epigenome, represented by chromatin structure, changes over the life cycle and through generations, and discuss how epigenetically mediated changes in the phenotype can be generated through modifications in the environment. Immediate consequences of this approach are (i) the development of epidrugs to arrest parasite development and (ii) the awareness that anthropogenic changes in the environment (e.g. control measures) can have rapid and direct and maybe undesired effect on parasite evolution.