PTC tasting

[2] In 1932, Albert Blakeslee conducted a large-scale study involving the inheritance of PTC tasting within families that concluded that PTC tasting sensitivity is very likely a complex Mendelian trait whose variance is overwhelmingly dependent on a single gene locus; however, it is likely that a few other genes have a smaller effect as well.

This similarity suggests that whatever gene controls for PTC tasting must have some sort of a selective advantage in order to have either evolved and been maintained for millions of years since before humans and chimps diverged into separate species, or to have evolved in two separate events after species divergence.

Substances that resemble PTC today are in some vegetables from the cabbage family (Brassicaceae), such as broccoli and Brussels sprouts.

In 2003, Dennis Drayna and his colleagues at the National Institutes of Health (NIH),[10] as well as a team of researchers led by Un-kyung Kim,[11] discovered that a variation at the TAS2R38 gene locus is responsible for an overwhelming majority of the variance in PTC tasting sensitivity (50-80%).

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.

The test isolates DNA from cheek cells by a simple salt mouthwash and amplification of 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.