D3217: Regulatory effects of insulin and NPY-like signaling on mosquito attraction to humans

Aedes aegypti mosquitoes are deadly disease vectors, infecting millions annually with pathogens that cause diseases including Zika, dengue, and chikungunya. Female Ae. aegypti require vertebrate blood to develop eggs and complete a reproductive cycle. The evolutionary pressure to find and bite a host drives robust attraction to humans. After a complete blood meal, female host-seeking is dramatically suppressed, a temporary behavioral phenomenon that could be exploited for vector control. Several signaling pathways activated by a blood-meal are implicated in regulating biting behavior, but the biological mechanisms underlying suppression remain unclear. Recent work showed that activation of a conserved neuropeptide Y-like (NPY-like) receptor, known to regulate satiety, can suppress mosquito attraction to human hosts. Genetic and pharmacological manipulations of NPY-like signaling disrupt blood digestion, host-seeking, and nutrient-sensing. In mosquitoes insulin-like peptides coordinate blood digestion and physiological preparations for egg development, but a role for insulin in host-seeking behavior has yet to be established. My project will investigate how insulin and NPY-like signaling pathways interact to alter mosquito behavior after a blood-meal. To understand if insulin acts in a parallel or downstream pathway to NPY-like signaling, we are pharmacologically manipulating insulin and NPY-like pathways together and independently to determine behavioral effects on host attraction. Resolving the interaction between insulin and NPY-like pathways will help us understand how these pathways coordinate to produce behavioral suppression.