Human speech is thought to have emerged 100,000 to 200,000 years ago, some five million years after chimps and humans took divergent paths on the tree of evolution.
Credit: iStockphoto
PARIS: Two minute evolutionary changes in a gene that is otherwise identical in humans and chimps could explain why we have fully fledged power of speech while other primates do not.
The findings may also point to new drug targets for hard-to-treat diseases that disrupt speech, such as schizophrenia and autism, said a study detailed in the British journal Nature today.
A decade ago, researchers discovered that members of an extended family beset with a rare inherited speech disorder all shared the same defect in a gene called FOXP2.
Speech disorder
Investigators then found that a small number of patients with another speech-related disease, developmental dysphasia, also had mutations in the gene.
Separately, biologists studying FOXP2 in our closest evolutionary cousin, the chimpanzee, noticed that only two among the hundreds of amino acids in the protein coded by the gene differed across the two species.
The question emerged: Could this minor genetic variation be the key that enables human speech? Some experts suggested the telltale pair of amino acids – the building blocks of proteins – were evidence of a fast track evolution toward language.
Others, though, argued that the molecules played no part in our ability to talk. To find out which idea might be right, Daniel Geshwind, a professor at the University of California, Los Angeles, designed the first-ever experiments comparing the 'ancestral' FOXP2 in chimps with the evolved variant in humans.
Gene driver
"We thought this would be a direct way to test the relevance of these two amino acids in the protein's function," Geschwind said. The lab tests focussed on genetic expression, the process by which a gene's DNA sequence is converted into proteins.
The researchers also looked at FOXP2's role as a master gene that activates or silences other genes. "What we found is that FOXP2 drives these genes to behave differently in the two species," said Geschwind.
In humans, the gene triggered changes in regions of cerebral cortex known to control high cognitive functions and language. Surprisingly, it also affected another part of the human brain, the striatum, involved in both cognition and motor coordination.
