Talking through the genes

TWO SMALL chemical changes – that may be all that was needed to give early humans the power to talk. The complexity of human language is something that sets us apart from our nearest relative, the chimpanzee. And yet the trigger that allowed this evolutionary gift may have come down to just two amino-acid changes in a single protein, writes DICK AHLSTROM

New research that explains how this might have happened is published this morning in the journal Nature. These subtle chemical changes altered the way that a particular protein works inside the body, with the capacity for speech the ultimate result.

Dr Dan Geschwind, from the University of California, Los Angeles, and colleagues were studying the protein FOXP2. It is known to have an effect on speech, given that malfunctions in FOXP2 are linked to disorders of speech and language.

Yet chimps also produce the FOXP2 protein. The research team compared the structure of human and chimp FOXP2 and discovered two small amino-acid changes in the human form. These two small changes alone seem sufficient to cause a completely different set of downstream effects when comparing humans and chimps.

"Because FOXP2 has an important role in speech and language in humans, the identified targets may have a critical function in the development and evolution of language circuitry in humans," the authors write in Nature.

It had been known for some time that FOXP2 changed rapidly at about the same time that language emerged in modern humans.

“Ours is the first study to examine the effect of these amino-acid substitutions in FOXP2 in human cells,” Geschwind says. “We showed that the human and chimp versions of FOXP2 not only look different but function differently too.”

The researchers found that chimp FOXP2 set off one set of downstream reactions, while human FOXP2 set off another that was entirely different. The proteins trigger cascades of changes as genes are switched on or off in response to them or to other proteins that arise because of them.

“This suggests that FOXP2 drives these genes to behave differently in the two species,” Geschwind says.

OUR ABILITY TOform language depends on many physiological changes, however, and it seems that the modification in human FOXP2 allowed these changes to come through.

Geschwind and his team tracked down the genes that changed in the presence of human FOXP2 using microarrays, and these genes influenced a variety of areas, including the development of the human central nervous system.

“Moreover, this study reveals enrichment of differential FOXP2 targets with known involvement in cerebellar motor function, craniofacial formation and cartilage and connective tissue formation, suggesting an important role for human FOXP2 in establishing both the neural circuitry and physical structures needed for spoken language,” the authors report.

These biochemical processes are extremely complex and depend on many hundreds, if not more, genes to switch on or off in unison.

It is also difficult to understand what might have caused those two amino acids to change and so alter the human form of FOXP2.

Presumably, it was a chance mutation that opened the way towards the development of speech. Once initiated, it would have taken some time for the alterations to take hold but, when established, language would have conferred a tremendous survival advantage for any species able to use it.

The authors acknowledge that it “remains controversial” to make definitive assumptions about the two amino-acid changes being enough to produce language, but the new information they provide makes it more plausible that this little change was enough to give us the gift of the gab.