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Significance It is currently thought that the transduction of bitter, sweet, and umami stimuli in taste cells depends on G protein-coupled receptor signaling with transient receptor potential melastatin 5 (TRPM5) acting as a common downstream component. However, in the absence of TRPM5, mice have a reduced, but not abolished, ability to detect these stimuli, suggesting that a TRPM5-independent pathway also contributes to taste transduction. Here, we identify a critical role for the TRPM4 channel in the detection of these taste qualities. Deletion of either TRPM4 or TRPM5 impairs sensitivity to bitter, sweet, and umami stimuli, and loss of both TRPM4 and TRPM5 abolishes taste responses to these stimuli. Our results show that both TRPM4 and TRPM5 are required and sufficient for the transduction of bitter, sweet, and umami stimuli.

TRPM4 and TRPM5 are both required for normal signaling in taste receptor cells