Drosophila TRPA1 channel mediates chemical avoidance in gustatory receptor neurons

TitleDrosophila TRPA1 channel mediates chemical avoidance in gustatory receptor neurons
Publication TypeJournal Article
Year of Publication2010
AuthorsKim SHoon, Lee Y, Akitake B, Woodward OM, Guggino WB, Montell C
JournalProc Natl Acad Sci U S A
Volume107
Pagination8440-5
Date Published05/2010
ISSN1091-6490
KeywordsAnimals, Animals, Genetically Modified, Drosophila melanogaster, Drosophila Proteins, Female, Neurons, Oocytes, Receptors, Cell Surface, Taste, Temperature, TRPC Cation Channels, Type C Phospholipases, Xenopus laevis
Abstract

Mammalian sweet, bitter, and umami taste is mediated by a single transduction pathway that includes a phospholipase C (PLC)beta and one cation channel, TRPM5. However, in insects such as the fruit fly, Drosophila melanogaster, it is unclear whether different tastants, such as bitter compounds, are sensed in gustatory receptor neurons (GRNs) through one or multiple ion channels, as the cation channels required in insect GRNs are unknown. Here, we set out to explore additional sensory roles for the Drosophila TRPA1 channel, which was known to function in thermosensation. We found that TRPA1 was expressed in GRNs that respond to aversive compounds. Elimination of TRPA1 had no impact on the responses to nearly all bitter compounds tested, including caffeine, quinine, and strychnine. Rather, we found that TRPA1 was required in a subset of avoidance GRNs for the behavioral and electrophysiological responses to aristolochic acid. TRPA1 did not appear to be activated or inhibited directly by aristolochic acid. We found that elimination of the same PLC that leads to activation of TRPA1 in thermosensory neurons was also required in the TRPA1-expressing GRNs for avoiding aristolochic acid. Given that mammalian TRPA1 is required for responding to noxious chemicals, many of which cause pain and injury, our analysis underscores the evolutionarily conserved role for TRPA1 channels in chemical avoidance.

DOI10.1073/pnas.1001425107
Alternate JournalProc. Natl. Acad. Sci. U.S.A.
PubMed ID20404155
PubMed Central IDPMC2889570
Grant ListDC007864 / DC / NIDCD NIH HHS / United States