PTC tasting

Genetics

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.

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 nontasters 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 transmembrane 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 a fascinatingly imperfect experimental assay 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), but somehow the taster allele (GGGC) cut. This generates a length polymorphism, and the 2 alleles can be easily separated in an agarose gel.

For best effect, produce the genotypes first and have each student predict their tasting phenotype. Then bring the PTC paper and the students have their points sample ability as strong, weak or nonexistant. Predicting the bitter taste is good, but not perfect.

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.

Harris – Kalmus' threshold solutions and differentiation

In 1949, Harris and Kalmus developed a method for differentiation of bimodal threshold stimuli for tasting PTC. They proposed a series of 13 solutions of these substances with serial water by halves from the initial concentration of 0.13%, so that the solution in the final solution contained only a few molecules of this substance. Pure water was used as the fourteenth test liquid to provide a control. Differentiation between the two phenotypes of "tasters" and "non-tasters" occurred with the fifth solution. Then assuming that the conditional dimorphism controlled by two allele of the corresponding gene locus, the allele which controls the absence of sensitivity to taste PTC is recessive homozygote.

Although the view of the genetics of individual sensitivity to taste PTC changed, practically all the current data on the PTC taste (in)ability established certain of these substances originate from research by Harris and Kalmus, and such investigations are still taken. This is probably because it is not suggested a better method for mass population genetics projects.

Nontaster phenotype distribution (%) in selected populations