Independent evolution of bitter-taste sensitivity in humans and chimpanzees

Stephen Wooding, Bernd Bufe, Christina Grassi, Michael T. Howard, Anne C. Stone, Maribel Vazquez, Diane M. Dunn, Wolfgang Meyerhof, Robert B. Weiss, Michael J. Bamshad

Research output: Contribution to journalArticlepeer-review

108 Scopus citations

Abstract

It was reported over 65 years ago that chimpanzees, like humans, vary in taste sensitivity to the bitter compound phenylthiocarbamide (PTC)1. This was suggested to be the result of a shared balanced polymorphism, defining the first, and now classic, example of the effects of balancing selection in great apes. In humans, variable PTC sensitivity is largely controlled by the segregation of two common alleles at the TAS2R38 locus, which encode receptor variants with different ligand affinities2-4. Here we show that PTC taste sensitivity in chimpanzees is also controlled by two common alleles of TAS2R38; however, neither of these alleles is shared with humans. Instead, a mutation of the initiation codon results in the use of an alternative downstream start codon and production of a truncated receptor variant that fails to respond to PTC in vitro. Association testing of PTC sensitivity in a cohort of captive chimpanzees confirmed that chimpanzee TAS2R38 genotype accurately predicts taster status in vivo. Therefore, although Fisher et al.'s observations1 were accurate, their explanation was wrong. Humans and chimpanzees share variable taste sensitivity to bitter compounds mediated by PTC receptor variants, but the molecular basis of this variation has arisen twice, independently, in the two species.

Original languageEnglish (US)
Pages (from-to)930-934
Number of pages5
JournalNature
Volume440
Issue number7086
DOIs
StatePublished - Apr 13 2006

ASJC Scopus subject areas

  • General

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