Distinct stem cell populations drive larval, somatic, and germline development of the human parasitic flatworm, Schistosoma mansoni.

Gene knock-out of the omega-1 ribonuclease of Schistosoma mansoni eggs resulted in immunologically impaired phenotype, showcasing the novel application of CRISPR/Cas9 genome editing and utility for functional genomics in schistosomes.

An analysis of gene dosage at the DNA, RNA and protein level yields new insights into the early stages of Z-chromosome dosage compensation in schistosome parasites.

Interactions among parasites in snails create cascading effects on their transmission and highlight that biodiversity has complex, context-dependent and important effects on human schistosomiasis transmission dynamics.

A coordinated humoral immune response that includes recognition, effector and cytotoxic factors engages the cell-mediated immune response to defend a snail against infection by schistosome parasites.

Cells that give rise to the infectious form of parasitic flatworms called schistosomes show similar patterns of gene expression to stem cells in free-living flatworms.

The specification of tegumental progenitor cells in Schistosoma mansoni relies on a pair of flatworm-specific transcription factors that are related to genes regulating epidermal specification in free-living flatworms.

Stem cells are found to continually rejuvenate the epidermis of the human parasite Schistosoma mansoni.

An iterative self-assembling algorithm identifies the intrinsic structures in single-cell transcriptomic data and helps to discover new cell populations that are undetectable by existing methods.

A region of the Biomphalaria genome, containing highly divergent haplotypes with different combinations of transmembrane genes, strongly impacts whether these snails can transmit parasitic schistosomes.