PTC tasting

This variability of PTC tasting came to the attention of Albert Blakeslee at the Carnegie Institute of Genetics on Long Island, New York. Blakeslee believed that PTC tasting was genetically determined. In 1932 he published a population study that showed that PTC tasting is inherited as a dominant Mendelian trait.[1]

For seven decades, Blakeslee's genetic description of the PTC tasting was widely accepted: tasters having one or two copies of a taster allele, but non-tasters being recessive homozygotes. Then, in 2003, Dennis Drayna and his colleagues at the National Institutes of Health (NIH) cloned the gene, the bitter-tasting ability explains TAS2R38-the 38th member of the family of 2R bitter receptors.

It has been suggested that taste and smell receptors are controlled by TAS2R38, with a small intron gene of about 1000 nucleotides. It is a member of the family of G protein-coupled or 7 trans membrane cross receptors. The binding of a ligand to the extracellular region of the receptor sets an action potential that sends an impulse to the sensory cortex of the brain, where it is interpreted as a bitter taste.

This allows an experimental test for SNP at position 145 that has the highest correlation to the sample 3 polymorphisms. Students obtain isolated DNA from cheek cells by a simple salt mouthwash and amplify a region of the gene TAS2R38. The amplified fragment (amplicon) is incubated with the restriction enzyme HaeIII, comprising the SNP in their recognition sequence GGCC. HaeIII cuts the taster allele (having the sequence GGCC); this generates a length polymorphism, and the 2 alleles can be easily separated in an agarose gel.

Virtually all non-tasters (dd) cannot taste PTC, while homozygous tasters (TT) occasionally report an inability or weak ability to taste the chemical. The heterozygous genotype (Tt) has the "leakiest" phenotype as reduced or absent tasting ability is relatively common. This is formally called a heterozygous effect.