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Evolution of taste receptor may have shaped human sensitivity to toxic compounds

Researchers have found new evidence suggesting that the ability to taste bitter compounds has been strongly advantageous in human evolution.

Animals rely on chemical perception, including the senses of taste and smell, for protection against the harmful compounds found in nature. It is widely believed that behavioral and dietary choices may have reduced the importance of such chemical perception in higher primates, and particularly in humans.

In new work, researchers including Nicole Soranzo of University College London and Bernd Bufe of the German Institute of Human Nutrition have shed light on the potential role natural selection has played in forming our present sensitivities and protecting us from harmful natural chemicals. The research team analyzed the nucleotide sequence of a human gene encoding a bitter-taste receptor that mediates recognition of a class of naturally ubiquitous, but toxic, cyanide-releasing compounds. By analyzing sequences from a large sample of individuals representing 60 human populations, the researchers found evidence that specific variants of the receptor gene have been strongly favored in the early stages of human evolution. Employing additional gene sequence analyses, the authors estimated that the favorably selected versions of the receptor gene arose prior to the expansion of humans out of Africa.

The researchers went on to show experimentally that such variants of the receptor, when expressed in individual cells, conferred an increased sensitivity toward several harmful compounds found in nature.

The work strongly supports a pivotal role for bitter-taste perception in toxin avoidance in humans, an attribute that could have come into particular play during periods of expansion into new environments. More broadly, the work contributes to the debate on the mechanisms governing the evolution of chemical sensory perception and on the role of diet as a selective force in human evolution.


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Source:Cell Press


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