All of our projects emerge from a single general question: how does host genotype affect the biology of bacterial infection? We address this question using the fruit-fly Drosophila melanogaster as a model host. Drosophila offers a number of advantages for this work. Because flies are small, cheap, and have a short generation time, we are able to identify genes that affect infection susceptibility rapidly and without prior bias. These same features allow us to explore the effects of infection on the whole organism—for example, we can identify endocrine changes in response to infection, and we can explore their in vivo consequences for physiological and immune function.
Our current work mostly falls into two broad areas. Some projects focus on the systemic effects of bacterial infection, with a particular emphasis on the mechanistic origin of the connection between immune responses and systemic physiological regulation. Other projects focus on how intracellular bacterial pathogens, especially mycobacteria, subvert phagocyte function to enable their own survival and cause disease. These streams tend to converge on common conserved signalling pathways and cellular mechanisms.
Our research is currently funded by the Wellcome Trust, MRC, and BBSRC. Inquiries from interested potential postdocs or PhD students are welcome.
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et al., 2015, Macrophage-Derived upd3 Cytokine Causes Impaired Glucose Homeostasis and Reduced Lifespan in Drosophila Fed a Lipid-Rich Diet, Immunity, Vol:42, ISSN:1074-7613, Pages:133-144
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et al., 2006, Akt and foxo dysregulation contribute to infection-induced wasting in Drosophila, Current Biology, Vol:16, ISSN:0960-9822, Pages:1977-1985