A subset of mouse colonic goblet cells expresses the bitter taste receptor Tas2r131

PLoS One. 2013 Dec 18;8(12):e82820. doi: 10.1371/journal.pone.0082820. eCollection 2013.

Abstract

The concept that gut nutrient sensing involves taste receptors has been fueled by recent reports associating the expression of taste receptors and taste-associated signaling molecules in the gut and in gut-derived cell lines with physiological responses induced by known taste stimuli. However, for bitter taste receptors (Tas2rs), direct evidence for their functional role in gut physiology is scarce and their cellular expression pattern remained unknown. We therefore investigated Tas2r expression in mice. RT-PCR experiments assessed the presence of mRNA for Tas2rs and taste signaling molecules in the gut. A gene-targeted mouse strain was established to visualize and identify cell types expressing the bitter receptor Tas2r131. Messenger RNA for various Tas2rs and taste signaling molecules were detected by RT-PCR in the gut. Using our knock-in mouse strain we demonstrate that a subset of colonic goblet cells express Tas2r131. Cells that express this receptor are absent in the upper gut and do not correspond to enteroendocrine and brush cells. Expression in colonic goblet cells is consistent with a role of Tas2rs in defense mechanisms against potentially harmful xenobiotics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Colon / cytology*
  • Goblet Cells / metabolism*
  • Immunohistochemistry
  • In Situ Hybridization
  • Integrases / genetics
  • Integrases / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Receptors, G-Protein-Coupled
  • Tas2r131 protein, mouse
  • Cre recombinase
  • Integrases

Grants and funding

This work was supported by the German Ministry of Education and Research (BMBF, #0315669, to WM and MB). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.