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I work on cell competition, a process where relatively less fit cells (losers) are eliminated by relatively fitter neighbouring cells (winners). There are many types of cell competition and in my PhD I will focus on Minute cell competition. In Minute cell competition cells that have lost one copy of a ribosome gene (called Minute) are induced to die by wild-type cells. Minute cell competition acts as a quality control to maintain tissues healthy and is likely to contribute to the elimination of cells with tumorigenic potential. We are interested in understanding how proximity with winner cells modifies the cellular state of Minute cells so that they behave as losers and die. Our approach involves introducing groups of wild-type-cells in a Minute background in developing fly epithelia. In my work I will characterise how cell competition changes specific cellular processes such as translation, autophagy and oxidative stress. I will also look at gene expression changes induced during cell competition in loser Minute cells, to identify novel additional factors affected by winners and involved in cell competition. This work is likely to identify new components that, by modulating cell competition, could be important in maintaining tissue health and in cancer prevention.

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.