The taste testing shows that the mutations in TAS2R16 had functional significance for the bitter taste perception system," Breslin said. "In this case, the mutation caused a gain of taste function.
When the researchers "mapped" individuals' genetic profiles onto their tasting ability, they found a strong correlation between one of the 15 variants and an increased sensitivity to salicin. The cell-based analysis offered an explanation for this sensitivity: cells with this genetic mutation had nearly twice as many receptors for salicin on their membranes as did cells with other forms of the TAS2R16 gene.
On a population level, the researchers found that the "high-sensitivity" variant for salicin was more prevalent in individuals from East Africa than in those from West Central or Central Africa, and non-Africans possessed only the "high-sensitivity" version of the gene. What's more, in East Africans this high-sensitivity variant, which arose roughly 1.1 million years ago, showed signs of being under a force of natural selection in humans, suggesting it conferred an evolutionary advantage at some point during our past.
"That's another sign that this variant must be tremendously important for human survival because it evolved in our human ancestors so long ago and carried over to us," Campbell said.
The geographic structure of TAS2R16 variants contrasts with the previous work on TAS2R38, variants of which did not appear to fall into any clear geographic pattern. These differences between two genes that both relate to bitter taste perception offer more support to the idea that taste was not the only force driving the evolution of this gene.
"The types of populations we're studying are diverse and they have diverse diets," Tishkoff said, "suggesting that there is likely something else going on here. By getting a handle on how much variation is in these populations, where it is located and what are
|Contact: Katherine Unger Baillie|
University of Pennsylvania