Abstract
We evaluated the role of IP3 in sugar taste reception in Drosophila melanogaster by inactivating the IP3 signaling using genetic tools. We used the “IP3 sponge,” composed of the modified ligand-binding domain from the mouse IP3 receptor, which was designed to absorb IP3 in competition with native IP3 receptors. Another tool was a transgene that generates double-stranded RNA against IP3 receptor mRNA. Both inhibitors diminished the sensitivity of flies to trehalose and sucrose, as estimated by behavioral assays and electrophysiological recordings from the sugar receptor cells. The result indicates that IP3 signaling is indispensable for sugar reception in Drosophila.