PGC1α Controls Sucrose Taste Sensitization in Drosophila

Perceived palatability of food controls caloric intake. Sweet taste is the primary means of detecting the carbohydrate content of food. Surprisingly, sweet taste sensitivity is responsive to extrinsic factors like diet, and this occurs by unknown mechanisms. Here, we describe an unbiased proteomic investigation into sweet taste sensitivity in the fruit fly. We identify a dopamine/cyclic AMP (cAMP)/CREB axis acting within sweet taste neurons that controls taste perception but is largely dispensable for acute taste transduction. This pathway modulates sweet taste perception in response to both sensory- and nutrient-restricted diets and converges on PGC1α, a critical regulator of metabolic health and lifespan. By electrophysiology, we found that enhanced sucrose taste sensitivity was the result of heightened sweet taste intensity and that PGC1α was both necessary and sufficient for this effect. Together, we provide the first molecular insight into how diet-induced taste perception is regulated within the sweet taste neuron. [Display omitted] •Diet manipulation can alter sucrose sensitivity•Sucrose sensitization requires dopamine signaling•Gαs, PKA, CREB, and PGC1α mediate sensitization within sweet taste neurons•PGC1α is necessary and sufficient to drive taste sensitization Wang et al. show that manipulation of diet composition can alter subsequent sweet taste sensitivity. This effect involves dopamine signaling pathways and PGC1α. These findings explain how diet composition can impact future sweet taste perception.