@article {1774,
	title = {The receptors and coding logic for bitter taste.},
	journal = {Nature},
	volume = {434},
	year = {2005},
	month = {2005 Mar 10},
	pages = {225-9},
	abstract = {<p>The sense of taste provides animals with valuable information about the nature and quality of food. Bitter taste detection functions as an important sensory input to warn against the ingestion of toxic and noxious substances. T2Rs are a family of approximately 30 highly divergent G-protein-coupled receptors (GPCRs) that are selectively expressed in the tongue and palate epithelium and are implicated in bitter taste sensing. Here we demonstrate, using a combination of genetic, behavioural and physiological studies, that T2R receptors are necessary and sufficient for the detection and perception of bitter compounds, and show that differences in T2Rs between species (human and mouse) can determine the selectivity of bitter taste responses. In addition, we show that mice engineered to express a bitter taste receptor in {\textquoteright}sweet cells{\textquoteright} become strongly attracted to its cognate bitter tastants, whereas expression of the same receptor (or even a novel GPCR) in T2R-expressing cells resulted in mice that are averse to the respective compounds. Together these results illustrate the fundamental principle of bitter taste coding at the periphery: dedicated cells act as broadly tuned bitter sensors that are wired to mediate behavioural aversion.</p>
},
	keywords = {Animals, Food Preferences, G-Protein-Coupled, Humans, Inbred BALB C, Inbred C57BL, Knockout, Mice, Palate, Physical Stimulation, Receptors, Species Specificity, Substrate Specificity, Taste, Tongue},
	issn = {1476-4687},
	doi = {10.1038/nature03352},
	author = {Mueller, Ken L and Hoon, Mark A and Erlenbach, Isolde and Chandrashekar, Jayaram and Zuker, Charles S and Ryba, Nicholas J P}
}
@article {1776,
	title = {The receptors for mammalian sweet and umami taste.},
	journal = {Cell},
	volume = {115},
	year = {2003},
	month = {2003 Oct 31},
	pages = {255-66},
	abstract = {<p>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.</p>
},
	keywords = {Animals, Flavoring Agents, G-Protein-Coupled, Gene Deletion, Humans, In Situ Hybridization, kappa, Knockout, Mice, Opioid, Protein Isoforms, Protein Subunits, Receptors, Sodium Glutamate, Sucrose, Taste, Taste Buds},
	issn = {0092-8674},
	author = {Zhao, Grace Q and Zhang, Yifeng and Hoon, Mark A and Chandrashekar, Jayaram and Erlenbach, Isolde and Ryba, Nicholas J P and Zuker, Charles S}
}
