杏吧原创

Bring up a chimpanzee from birth as if it were a human and it will learn many unsimian behaviours, like wearing clothes and even eating with a knife and fork. But one thing it will not do is talk.

In fact, it would be physically impossible for a chimp to talk just like us, thanks to differences in our voice boxes and nasal cavities. There are neurological differences too, some of which are the result of changes to what has been dubbed the 鈥渓anguage gene鈥�.

This story began with a British family that had 16 members over three generations with severe speech difficulties. Usually speech problems are part of a broad spectrum of learning difficulties, but the 鈥淜E鈥� family, as they came to be known, seemed to have deficits that were more specific. Their speech was unintelligible and they had a hard time understanding others鈥� speech, particularly when it involved applying rules of grammar. They also had problems making complex movements of the mouth and tongue.

In 2001, the problem was pinned on a mutation in a gene called FOXP2. We can tell from its structure that the gene helps regulate the activity of other genes. Unfortunately, we do not yet know which ones are controlled by FOXP2. What we do know is that in mice (and so, presumably, in humans) FOXP2 is active in the brain during embryonic development.

Contrary to initial speculation, the KE family had not reverted to a 鈥渃himp-like鈥� version of the gene 鈥� they had a new mutation that set back their language skills. In any case, chimps, mice and most other species have a version of FOXP2 that is remarkably similar to that of humans. But since we split from chimpanzees there have been two other mutations to the human version, each of which alters just one of the many amino acids that make up the FOXP2 protein ().

It would be fascinating to put the human version of FOXP2 into chimps to see if it improves their powers of speech but we cannot do that for both technical and ethical reasons. The human version has been put into mice, though. Intriguingly, the researchers observed that the genetically modified mice pups squeak slightly differently 鈥� there was a small drop in the pitch of their ultrasound squeals.

But this may be less relevant than the changes seen within the mice brains. Last year, changes were found in the structure and behaviour of neurons in an area called the cortico-basal ganglia circuits (). Also called the brain鈥檚 reward circuits, these are known to be involved in learning new mental tasks. 鈥淚f you do something and all of a sudden you get a reward, you learn that you should repeat that,鈥� says , an evolutionary geneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who led the work.

Based on what we already know about these circuits, Enard thinks that in humans FOXP2 plays a role in learning the rules of speech 鈥� that specific vocal movements generate certain sounds, perhaps, or even the rules of grammar. 鈥淵ou could view it as learning the muscle sequences of speech, but also learning the sequence of 鈥楾he cat the dog chased yesterday was black鈥�,鈥� he suggests.

Enard reckons this is the best example yet found of a mutation that fuelled the evolution of the human brain. 鈥淭here鈥檚 no other mutation where we have such a good idea what happened,鈥� he says.