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The human TAS2R16 receptor mediates bitter taste in response to beta-glucopyranosides.

Bitter taste generally causes aversion, which protects humans from ingesting toxic substances. But bitter flavors also contribute to the palatability of food and beverages, thereby influencing nutritional habits in humans. Although many studies have examined bitter taste, the underlying receptor mechanisms remain poorly understood. Anatomical, functional and genetic data from rodents suggest the existence of a family of receptors that are responsive to bitter compounds. Here we report that a human member of this family, TAS2R16, is present in taste receptor cells on the tongue and is activated by bitter beta-glucopyranosides. Responses to these phytonutrients show a similar concentration dependence and desensitization in transfected cells and in experiments assessing taste perception in humans. Bitter compounds consisting of a hydrophobic residue attached to glucose by a beta-glycosidic bond activate TAS2R16. Thus, TAS2R16 links the recognition of a specific chemical structure to the perception of bitter taste. If the ability of TAS2R16 to detect substances with common molecular properties is typical of the bitter receptor family, it may explain how a few receptors permit the perception of numerous bitter substances.

Pubmed ID: 12379855


  • Bufe B
  • Hofmann T
  • Krautwurst D
  • Raguse JD
  • Meyerhof W


Nature genetics

Publication Data

November 31, 2002

Associated Grants


Mesh Terms

  • Benzyl Alcohols
  • Cell Membrane
  • Chromosomes, Human, Pair 12
  • Chromosomes, Human, Pair 7
  • Cloning, Molecular
  • DNA, Complementary
  • Dose-Response Relationship, Drug
  • Glucosides
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization
  • Microscopy, Confocal
  • Models, Chemical
  • Molecular Sequence Data
  • Phylogeny
  • Receptors, Cell Surface
  • Receptors, G-Protein-Coupled
  • Reverse Transcriptase Polymerase Chain Reaction
  • Spectrometry, Fluorescence
  • Taste
  • Time Factors
  • Tissue Distribution
  • Transfection