Insect vectors of disease find their human hosts primarily through chemosensory cues. Further, most rely heavily on chemosensation in both larval and adult stages. Therefore, it is of utmost importance to understand how these cues contribute to insect behavior. The long-range objective of this project is to illuminate some of these workings. Because the mechanisms of chemosensation in insects are highly conserved, we are conducting these studies in the most genetically tractable insect model, Drosophila. First, I will test the hypothesis that the previously uncharacterized subfamily of chemoreceptors, the IR20a subfamily, is expressed in larval chemosensory neurons, primarily taste neurons. I will also test the hypothesis that the taste neurons that express IR20a genes express other receptors as well. Secondly, I will extend preliminary observations that suggest that some IR20a genes are developmentally regulated. Using tools developed for this, I will also test the hypothesis that IR proteins are localized to dendrites of neurons that express them. Lastly, I will test the hypothesis that the cells are undergoing caspase-dependent apoptosis to account for the declining expression of IR20a genes in late larval development.
Hundreds of millions of people each year suffer from diseases transmitted by insects, many of which locate their human hosts through chemosensory cues. A better understanding of the principles of insect chemosensation could lead to better means of controlling these insects and the diseases they transmit. )
