Independent Evolution of Bitter-taste sensitivity in Humans and Chimpanzees
Background:One of the first described and widely accepted balanced polymorphism genes are those encoding for bitter-taste sensitivity. During its initial description it was observed by Fisher et al In 1939 that both humans and chimpanzees share this mutation, and share also its origin before the human-chimpanzee divergence. They accurately described that this trait, phenotypically expressed by bitter taste to phenylthiocarbamide (PTC), is controlled by 2 alleles present at the same loci in both species. The authors of this article however disputed the fact that Fisher et al At similar loci, are not shared with humans. It is worth noting that the balanced polymorphism here is maintained by the usefulness of this trait in averting poisonous food for animals and food selection and diet choices for humans. Introduction:
Two alleles at the TAS2R38 locus control the PTC sensitivity in humans. The same locus in responsible for controlling the taster and non-taster phenotype in chimpanzees. These genes encode for G-protein-coupled receptors in the taste buds. Evidence points to variation in this gene even at a humanoid levels and early humans during their evolution leading to variation in PTC taste sensitivity among humans and primates as well. When this was described by Fisher et al, they postulated an equally prevalent dominant and recessive allele of the taster gene in both humans and chimpanzees. They also pointed to the fact that this can only happen if the mutation is shared by both before they diverged. Methods, Discussion and analysis:
The human locus, or hTAS2R38 gene, is a 1kb located on chromosome 7. The genotypic variation in PTC sensitivity is related to variations at 3 positions: 49, 262 and 296 leading to either a hTAS2R38(PAV) meaning proline, alanine and valine; or hTAS2R38(AVI) meaning alanine, valine, and isoleucine. In vitro and in vivo studies showed that the...
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