Horizontal gene transfer of a functional cki homolog in the human pathogen Schistosoma mansoni

Abstract

Schistosomes, parasitic flatworms responsible for the neglected tropical disease schistosomiasis, are protected by a skin-like tegument, and tegument maintenance is controlled by a schistosome ortholog (p53-1) of the tumor suppressor TP53. To understand p53-1 function, we characterized a schistosome cyclin dependent kinase inhibitor homolog (cki). Knockdown of cki resulted in hyperproliferation, that, combined with p53-1 knockdown yielded tumor-like growths, indicating that cki and p53-1 are tumor suppressors in Schistosoma mansoni. Interestingly, cki homologs are ubiquitous in parasitic flatworms but are absent from their free-living ancestors, suggesting cki may have come from horizontal gene transfer. This suggests that the evolution of parasitism in flatworms was aided by an unusual means of metazoan genetic inheritance. TeaserHorizontal gene transfer may have played an important role in the evolution of parasitic flatworms