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.

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.

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.

The switch from ubiquinone to rhodoquinone synthesis that is required for parasitic helminths to survive in anaerobic host tissues is due to alternative splicing of polyprenyltransferase COQ-2.

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

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 quantification of sexual selection reveals that it is important to consider the chosen time frame of measurement as well as the sexual system.

The transition to the aggregative stage of Capsaspora owczarzaki, a close unicellular relative to Metazoa, is associated with significant upregulation of orthologs of genes that are important for multicellularity in metazoans.

The expression of DECTIN-2 family C-type lectin receptors on macrophages and monocytes is inhibited by the Th2 cytokine IL-4, which suggests a mechanism for inhibition of Th17 responses to MINCLE-dependent vaccination responses by underlying helminth infection.

Genome editing in a close unicellular relative of animals suggests a premetazoan function of the Hippo pathway effector YAP/TAZ/Yorkie in the regulation of cytoskeletal dynamics and multicellular morphogenesis but not proliferation.