Speaker: Simon Kershenbaum (Department of Biology, Evolutionary Biology)

Schistosomes infect around 250 million people around the world, with chronic infections leading to debilitating disease. The pathology is largely driven by the eggs laid by fully mature female worms, so understanding the mechanisms of sexual development in schistosomes may reveal novel targets to limit pathology. Beyond the public health implications, investigating the mechanisms of sexual development in schistosomes is of evolutionary interest since most flatworms are hermaphroditic while schistosomes are dioecious (have two separate sexes). However, to date, most research into the development of schistosomes relies either on using mammalian hosts, which is both ethically and financially costly, or in vitro cultures using foetal bovine serum which does not allow the parasites to reach a sexually dimorphic stage. We recently showed that parasites can be cultured from a sexually monomorphic stage to a sexually dimorphic stage using human serum instead of foetal bovine serum. This allows for the assessment of sexual development in vitro. Comparing single-cell RNAseq libraries from parasites cultured in different media shows that key stem cell populations are depleted in parasites cultured in foetal bovine serum, suggesting that despite its widespread use in both drug screening and research, important developmental pathways are perturbed. In light of these findings, we are currently shifting our in vitro experiments to human serum. We are now investigating the earliest developmental differences between male and female schistosomes, finding candidate transcription factors that may regulate sexual development in this human parasite.