The molecular basis of parasitism in the nematode Strongyloides ratti. (360G-Wellcome-094462_Z_10_Z)

This work aims to discover the molecular basis of nematode parasitism. Nematodes are common and important pathogens of humans. Anti-nematode therapy relies on a few drugs to which there is already resistance. Parasitic nematodes have evolved adaptations (e.g. altered metabolism, immune defence) to be successful parasites. While adaptations to animal parasitism is understood in these rather broad categories, the specific molecular bases of these adaptations is not known. A key question is, wh at molecules do parasitic nematodes use to be successful parasites? The genus Strongyloides spp. include important human parasites. There is also a well studied rodent model, S. ratti. Uniquely among parasitic nematodes, the Strongyloides life-cycle includes both a parasitic female stage and a genetically identical free-living female stage. Differences between these two female forms must be epigenetic, presumably controlled by altered transcription and translation. We will compare the proteom e and transcriptome of the parasitic and free-living females of S. ratti. From this we will define the genes and gene products of the parasitic female stage. This approach exploits the currently advanced S. ratti genome sequencing project. This work will give an understanding of the molecular basis of nematode parasitism, and so define new potential drug targets.