Abstract
Trematode infections can induce profound physiological and molecular changes in their hosts, with potential consequences for the host’s offspring. Bucephalus minimus, a trematode infecting the bivalve Cerastoderma edule, causes severe tissue damage, energy depletion, and castration in late stages of infection. These disruptions are expected to impact epigenetic regulation, including DNA methylation, however, little is known about the extent of such modifications or their potential intergenerational effects.This study aimed to investigate the impact of B. minimus infection on DNA methylation and gene expression in C. edule, comparing infected and non-infected adults and their offspring using NEBNext Enzymatic Methyl-seq (EM-seq) and RNA-seq approaches. In infected adults, widespread hypomethylation was observed, with differentially methylated genes involved in metabolism, membrane transport, and autophagy, suggesting parasite-driven modulations of host physiological pathways. In contrast, offspring of infected individuals displayed increased levels of gene hypermethylation, particularly in genes associated with immune signalling, stress response, and kinase activity. These differences may reflect intergenerational epigenetic priming, potentially enhancing immune capacity in offspring. Although only one gene was found to be differentially methylated in both generations, the overall pattern indicated that parasite-induced stress may alter the epigenetic landscape across generations. These finding provide preliminary evidence that parasitic infection can influence host DNA methylation and gene expression both directly and indirectly via inheritance. While further research is needed to determine the functional significance and stability of these changes, these results underscore the potential role of epigenetic regulation in host–parasite coevolution and developmental plasticity in marine invertebrates.
Oral presentation.