The report from researchers at Indiana University Bloomington and three other academic institutions appears in the December issue of Public Library of Science Biology.

The gene encodes prodynorphin, an opium-like protein implicated in the anticipation and experience of pain, social attachment and bonding, as well as learning and memory.

“Humans have the ability to turn on this gene more easily and more intensely than other primates,” said IU Bloomington computational biologist Matthew Hahn, who did the brunt of the population genetics work for the paper. “Given its function, we believe regulation of this gene was likely important in the evolution of modern humans’ mental capacity."

Prodynorphin is a precursor molecule of the neurotransmitters alpha-endorphin, dynorphin A, and dynorphin B, collectively called opioids because their action is similar to stimulatory effects caused by the drug opium.

The notion that humans are more perceptive than other primates would hardly be news. But the list of genes known to have tracked or guided humanity’s separation from the other apes is a short one.

Genes controlling the development of the brain almost always turn out to be identical or nearly so in chimpanzees and human beings. And as it turns out, the protein prodynorphin is identical in humans and chimps.

It’s the prodynorphin gene's promoter sequence – upstream DNA that controls how much of the protein is expressed – where the big differences are. “Only about 1 to 1.5 per cent of our DNA differs from chimpanzees,” Hahn said. “We found that in a stretch of DNA about 68 base pairs in length upstream of prodynorphin, 10percent of the sequence was different between us and chimps.”

Hahn said this ‘evolutionary burst’ is responsible for differences in gene expression rates.

This report supports a growing consensus among evolutionary anthropologists that hominid divergence from the other great apes was fuelled not by the origin of new genes, but by the quickening (or slowing) of the expression of existing genes.

Hahn and his colleagues at Duke University, University College London and Medical University of Vienna first became interested in primate prodynorphin after noticing an unusual amount of variation in the human version’s promoter.

The scientists decided to examine the prodynorphin gene in human beings around the world and in non-human primates to see whether such variation was commonplace and whether that variation affected gene expression.

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