Researchers identify taste receptor responsible for caffeine detection

By studying how taste-receptor mutations impact fruit fly behavior, researchers have identified a taste receptor responsible for the detection of caffeine, a bitter compound known to activate certain taste-receptor neurons, as well as impact various aspects of physiology. The findings are reported by Craig Montell and colleagues at Johns Hopkins University, and appear in the September 19th issue of Current Biology, published by Cell Press.

Many proteins have been identified in mammals and in the genetic model organism Drosophila that belong to a large family of taste receptors, but relatively few of these receptors have been shown to be responsible for the detection of a specific taste compound, or "tastant." One class of tastants for which receptors have not yet been identified is methylxanthines, which include caffeine and related compounds in tea (theophylline) and cocoa (theobromine).

In the new work reported by Montell and colleagues, researchers showed that a specific taste receptor, known as Gr66a, is responsible for the perception of caffeine's bitter taste by fruit flies. The researchers showed that when the gene encoding the Gr66a receptor was disrupted, the mutant flies failed to react normally to the presentation of caffeine, which is a bitter compound that is aversive to flies. Flies with an intact Gr66a receptor gene strongly prefer to consume sucrose (sugar) when given a choice between sucrose and a mixture of sucrose and bitter compounds, but the researchers showed that flies bearing a mutation that disrupted Gr66a failed to show this strong propensity when the bitter mixture contained caffeine. The researchers also showed that activation of the gustatory-receptor neurons that express the Gr66a receptor was impaired in the mutants: Although these gustatory neurons were activated normally by a range of different tastants, they failed to be activated by caffeine, or by the related methylxanthine, theophylline. Another methylxanthin

Contact: Heidi Hardman
Cell Press

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