Two minute changes in a gene that is otherwise identical in humans and chimps could explain why we have full-fledged power of speech while other primates can only grunt or screech, say scientists.
The findings may also point to new drug targets for hard-to-treat diseases that disrupt speech, such as schizophrenia and autism, they said.
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.
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 yammer and yak.
To find out who might be right, Daniel Geshwind, a professor at the University of California in Los Angeles, designed the first-ever experiments comparing the "ancestral" FOXP2 in chimps with the evolved variant in humans.
"We thought this would be a direct way to test the relevance of these two amino acids in the protein's function," Geschwind told AFP by phone.
The lab tests focused 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.
"We speculate that FOXP2 [in humans] might be involved in regulating both the neural motor mechanism of speech as well as some of the physical structure," said Geschwind.
In other words, even if one could transplant a human brain into a chimpanzee, the ape would probably be unable to speak because it lacks the right "articulatory apparatus," he said.
The findings hold real promise for the treatment of disorders that disrupt the ability to use language, the researchers said.
Future research, for example, could scan the circuit of genes affected by FOXP2 for telltale mutations among patients afflicted with autism, schizophrenia or other speech disorders.
"We have been looking most for rare mutations, but I would look first at pure language disorders such as dyslexia," said Geschwind.
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.
The study is published in the British science journal Nature.