This report supports a growing consensus among evolutionary anthropologists that hominid divergence from the other great apes was fueled 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.
The group found a surprisingly large amount of genetic variation among humans within the prodynorphin gene's promoter. They examined prodynorphin genes from Chinese, Papua New Guineans, (Asian) Indians, Ethiopians, Cameroonians, Austrians and Italians.
The group also sequenced and cloned prodynorphin genes from chimpanzees, gorillas, orangutans, rhesus macaques, pigtail macaques and guinea baboons. The researchers found that high genetic variation in the prodynorphin promoter was unique to humans. Other primates' promoters were far more homogeneous.
Exactly how prodynorphin influences human perception is unknown. Evidence for its various effects comes entirely from clinical studies of people who have mutations in the gene. Past clinical studies have also indicated a positive correlation between lower prodynorphin levels in the brain and susceptibility to cocaine dependence.
Matthew Rockman, David Goldstein and Gregory Wray (Duke University); Nicole Soranzo (University College London); and Fritz Zimprich
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Source:Indiana University