Trpm5: The sweet taste of successful signaling

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Perez et al. have found that Trpm5, the fifth member of the melastatin-related TRP channel subfamily, is coexpressed with taste signaling molecules such as α-gus, Gγ₁₃, phospholipase C-β₂ and IP3R3, and that it is also selectively expressed in taste tissue. This indicates that Trpm5 may be a capacitative calcium entry channel.

Salty and sour tastes result from an influx of sodium or hydrogen ions through channels in taste-receptor cells (TRCs) found in taste bud epithelia. However, sweet, bitter and umami (the taste of glutamate) flavours are thought to be detected by specific G-protein coupled receptors. There are several known downstream signaling components that are responsive to sweet and bitter compounds, including the G protein alpha -gustducin ( alpha -gus), G alpha ₁₃, G beta ₁₃, PLC- beta ₂, PDE1A, IP₃R3 and cyclic nucleotide-regulated channels. The consequent release of calcium ions from internal stores has previously been implicated in TCR responses to both bitter and sweet compounds, but additional unknown signaling molecules may also be involved in Ca²⁺ related TRC signal transduction.

To identify candidate taste transduction elements in mice, Perez et al. employed differential screening of cDNAs from individual taste receptor cells through differential hybridization with probes from alpha -gus⁺ and alpha -gus^- TRCs, which have previously been used to identify G beta ₃ and G alpha ₁₃ as taste signaling molecules. Among the differentially expressed genes isolated was the TRP channel Trpm5, a channel family implicated in capacitative calcium entry (CCE).

The group found that Trpm5, the fifth member of the melastatin-related TRP channel subfamily (formerly known as Mtr1), is coexpressed with taste signaling molecules such as alpha -gus, G gamma ₁₃, phospholipase C- beta ₂ and IP₃R3. Trpm5 is selectively expressed in taste tissue in a subset of TRCs. Consistent with the function of other TRP channels, Perez et al. establish that Trpm5 functions as a calcium channel activated by the depletion of internal Ca²⁺ stores, although the mechanism of this activation remains unknown.

In conclusion, Perez et al. propose that Trpm5 may well be a capacitative calcium entry (CCE) channel with a likely role in taste signalling elicited by bitter and possibly other taste stimuli, although additional studies will be necessary to confirm this.

The Signaling Gateway Team

References

Pérez, Cristian A. et al. A transient receptor potential channel expressed in taste receptor cells. Nature Neuroscience, 5, 1169–1176 (November 2002); 10.1038/nn952 | PubMed |