All of our projects emerge from a single general question: how do host genotype and phenotype 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 physiological changes in response to infection, we can explore their in vivo consequences for survival and immune function, and we can connect them with effects on host enodcrine signalling.
Our current work mostly falls into two broad areas. Some projects focus on the biology of effective immune responses, with a particular emphasis on the mechanistic origin of the connection between immune responses and systemic physiological regulation and how immune-induced physiological change is important to support immune function. Other projects focus on how specific bacterial pathogens disrupt cellular and organismal physiology 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.
et al., 2017, Regulation of phagocyte triglyceride by a STAT-ATG2 pathway controls mycobacterial infection, Nature Communications, Vol:8, ISSN:2041-1723, Pages:1-11
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:1097-4180, 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