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of outstanding interest. The murine α gustducin gene was cloned, and homologous gene replacement was used to generate a null mutation. Homozygous α gustducin null (knockout) mice were generated and then analyzed behaviorally (two bottle preference) and electrophysiologically (chorda tympani recording) for any taste deficits. The null mice were indistinguishable from wild-type in their responses to salty and sour stimuli. However, the null mice had reduced aversion and diminished chorda tympani responses to the bitter compounds denatonium benzoate and quinine sulfate. The null mice also had reduced preference for, and nerve responses to, the sweet compounds sucrose and SC45647. These experiments demonstrate in vivo that gustducin is a principal mediator of both bitter and sweet taste transduction.
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3, but only in tissue derived from SOA-sensitive `taster' strains. The response to SOA was potentiated by GTPγS and inhibited by GDPβS, suggesting the involvement of a G-protein-mediated transduction pathway.
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3, but only in tissue derived from SOA-sensitive `taster' strains. The response to SOA was potentiated by GTPγS and inhibited by GDPβS, suggesting the involvement of a G-protein-mediated transduction pathway.
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