| Literature DB >> 14636554 |
Grace Q Zhao1, Yifeng Zhang, Mark A Hoon, Jayaram Chandrashekar, Isolde Erlenbach, Nicholas J P Ryba, Charles S Zuker.
Abstract
Sweet and umami (the taste of monosodium glutamate) are the main attractive taste modalities in humans. T1Rs are candidate mammalian taste receptors that combine to assemble two heteromeric G-protein-coupled receptor complexes: T1R1+3, an umami sensor, and T1R2+3, a sweet receptor. We now report the behavioral and physiological characterization of T1R1, T1R2, and T1R3 knockout mice. We demonstrate that sweet and umami taste are strictly dependent on T1R-receptors, and show that selective elimination of T1R-subunits differentially abolishes detection and perception of these two taste modalities. To examine the basis of sweet tastant recognition and coding, we engineered animals expressing either the human T1R2-receptor (hT1R2), or a modified opioid-receptor (RASSL) in sweet cells. Expression of hT1R2 in mice generates animals with humanized sweet taste preferences, while expression of RASSL drives strong attraction to a synthetic opiate, demonstrating that sweet cells trigger dedicated behavioral outputs, but their tastant selectivity is determined by the nature of the receptors.Entities:
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Year: 2003 PMID: 14636554 DOI: 10.1016/s0092-8674(03)00844-4
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582