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We are interested in (1) the effects of host genetics on the biology of infection; and (2) the physiological control of metabolic balance.
Host genetics and the biology of infection
Different individuals show different levels of resistance to specific infections and exhibit different pathogeneic effects after infection. We are interested in why this is the case. We use the fruitfly Drosophila melanogaster as a model host to study these questions; this allows us to screen for genes that affect the progress of infection in a rapid and unbiased fashion.
All of our experiments originate from a simple genetic screen. Mutant flies are infected with Mycobacterium marinum, a bacterium closely-related to the causative agent of tuberculosis, or with Mycobacterium smegmatis, a related non-pathogen. We select lines of flies that die more quickly or more slowly than wild-type controls and determine the mutation that gives rise to this phenotype. We then try to understand what this phenotype tells us about the function of the mutated gene.
So far, our work on this system has focused on the mechanisms of pathogenesis. We have found that this infection causes progressive loss of metabolic stores, similar to the wasting seen in people with tuberculosis. We have shown that, in the fly, this wasting effect is caused partly by systemic failures in anabolic signals via the insulin effector kinase Akt. We are now working to try to understand how infection causes this defect in anabolic signalling.
Physiological control of metabolic balance
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