DUBBED 鈥渢he language gene鈥�, Foxp2 has been seen as key to the evolution of speech and language since its discovery in 2001. Now transgenic mice have been produced that make the human version of the gene, with dramatic results: their calls sound different from those of normal mice, and certain learning pathways in the brain appear to be enhanced.
The work offers tantalising clues to the gene鈥檚 importance 鈥� but it also highlights the difficulty of using animal models to probe a uniquely human trait.
Foxp2 rose to fame when it was found to be mutated in a British family (known as KE) with a history of severe language disorders. Wolfgang Enard of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and colleagues homed in on its genetic sequence and discovered that the human version has two key changes found in no other species (Nature, vol 418, p 869).
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To probe whether the human version of Foxp2 does anything special, Enard bred mice that make it. It was a long shot 鈥� the mice could have been indistinguishable from normal ones, or the gene might not have worked at all 鈥� but he struck lucky.
鈥淭he mice could have been indistinguishable from normal ones, but the researchers struck lucky鈥�
When his team compared hundreds of traits in the transgenic and normal mice, they found key differences in the rodents鈥� (Cell, ). For example, the mice with human Foxp2 produce neurons that are more readily and lastingly calmed by repeated electrical stimulation. This process, known as long-term depression, is involved in learning physical movements.
In mice which have just one working copy of Foxp2, as members of the KE family do, long-term depression was impaired. 鈥淗ere鈥檚 a process that might cause speech deficits when it goes wrong,鈥� says Enard. 鈥淢aybe it was improved by the human version of the gene.鈥�
These effects occurred in the basal ganglia, a brain area implicated in Foxp2鈥榮 effects in other species. Humans with one broken copy of Foxp2 have abnormal activity and anatomy here. And zebra finches that don鈥檛 make enough Foxp2 in their basal ganglia struggle to imitate the songs of other birds.
of University College London, who was part of the team that studied the KE family, thinks the gene may help to establish brain circuits that coordinate the complex movements of the lungs, larynx, tongue and lips needed for speech. Language is far more than exquisite muscular choreography, however. 鈥淭he question is how an idea is translated into an utterance,鈥� she points out. 鈥淚 don鈥檛 think we鈥檙e anywhere near understanding that.鈥�
Neuroscientists have made great strides in linking memory to particular neural processes 鈥� but they are able to study animals capable of forming memories. Speech, on the other hand, is a uniquely human ability, so results from animal studies must be interpreted with great caution.
Intriguingly, Enard found that mice with human Foxp2 issue deeper ultrasonic calls than normal mice. The significance of this is not clear, but he discounts the idea that it could be a step towards human speech. 鈥淢ouse vocalisations are at best similar to baby cries,鈥� he says. 鈥淲e will never be able to fully recreate human evolution in a mouse.鈥�