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Nature 440, 930-934 (13 April 2006) | doi:10.1038/nature04655; Received 17 November 2005; Accepted 16 February 2006

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Independent evolution of bitter-taste sensitivity in humans and chimpanzees

Stephen Wooding1, Bernd Bufe2, Christina Grassi3, Michael T. Howard1, Anne C. Stone4, Maribel Vazquez3, Diane M. Dunn1, Wolfgang Meyerhof2, Robert B. Weiss1 & Michael J. Bamshad1,5

  1. Department of Human Genetics, University of Utah, 15 North 2030 East, Salt Lake City, Utah 84112-5330, USA
  2. German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, Nuthetal 14558, Germany
  3. Department of Comparative Medicine, Southwest Foundation for Biomedical Research, San Antonio, Texas 78245-0549, USA
  4. School of Human Evolution and Social Change, Arizona State University, Tempe, Arizona 85287-2402, USA
  5. †Present address: Departments of Pediatrics and Genome Sciences, University of Washington, Seattle, Washington 98195, USA

Correspondence to: Stephen Wooding1Michael J. Bamshad1,5 Correspondence and requests for materials should be addressed to S.W. (Email: swooding@genetics.utah.edu) or M.J.B. (Email: mbamshad@u.washington.edu).

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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, 3, 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.

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