The sense of taste comprises at least five distinct qualities: sweet, bitter, sour, salty, and umami, the taste of glutamate. For bitter, sweet, and umami compounds, taste signaling is initiated by binding of tastants to G-protein-coupled receptors in specialized epithelial cells located in the taste buds, leading to the activation of signal transduction cascades. α-Gustducin, a taste cell-expressed G-protein α subunit closely related to the α-transducins, is a key mediator of sweet and bitter tastes. α-Gustducin knock-out (KO) mice have greatly diminished, but not entirely abolished, responses to many bitter and sweet compounds. We set out to determine whether α-gustducin also mediates umami taste and whether rod α-transducin (αt-rod), which is also expressed in taste receptor cells, plays a role in any of the taste responses that remain in α-gustducin KO mice. Behavioral tests and taste nerve recordings of single and double KO mice lacking α-gustducin and/or αt-rod confirmed the involvement of α-gustducin in bitter (quinine and denatonium) and sweet (sucrose and SC45647) taste and demonstrated the involvement of α-gustducin in umami [monosodium glutamate (MSG), monopotassium glutamate (MPG), and inosine monophosphate (IMP)] taste as well. We found that αt-rod played no role in taste responses to the salty, bitter, and sweet compounds tested or to IMP but was involved in the umami taste of MSG and MPG. Umami detection involving α-gustducin and αt-rod occurs in anteriorly placed taste buds, however taste cells at the back of the tongue respond to umami compounds independently of these two G-protein subunits.
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