Mice can鈥檛 talk, but a transgenic rodent could shed light on the evolution of language. A team of German researchers has created mice with a human gene implicated in speech problems and thought to play a role in the evolution of language.
Mice have their own form of the gene, called FOXP2, but they and all other animals lack key changes found only in humans and our evolutionary cousins, Neanderthals.
Some researchers speculate that these differences may help explain why humans are the only animal able to communicate with complex languages, and not simple grunts, barks or songs.
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鈥淭he mouse model is the only chance we really have to find out what the human version of FOXP2 does differently from the chimp version,鈥� says , a molecular biologist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, who led the new study.
Human disorders
FOXP2, which makes a protein that switches on numerous other genes, came into prominence when researchers found a mutated copy of the gene in a British family with a history of severe language disorders. Family members with the mutation have trouble speaking and understanding language.
In an attempt to home in on the function of the gene, Enard鈥檚 team bred mice that make the human-specific version.
It was a long shot. The change could have been so small that transgenic mice turned out effectively identical to normal rodents, Enard says. Or, the human version of Foxp2 might not have worked at all, effectively knocking out the gene; and mice without any Foxp2 die weeks after birth. 鈥淲hen I started the project, I thought if I find anything at all I鈥檒l be a really happy man,鈥� Enard admits.
Learning link
His team compared hundreds of traits in the transgenic and normal mice, and found a handful of differences between them 鈥� many in the rodents鈥� brains and behaviour.
For instance, mice with human FOXP2 produce neurons that are more readily calmed by repeated electrical stimulation, compared to neurons from normal mice. While with just one working copy of FOXP2, which mimics humans with genetic language deficits, mice produce neurons that do the opposite. This process, called long-term depression, is involved in learning physical movements.
鈥淗ere鈥檚 a process that goes wrong with speech deficits and maybe was improved in the human version,鈥� Enard says.
Mice with the human version of FOXP2 also belt out deeper ultrasonic calls than normal mice, Enard鈥檚 team found. Yet he is not sure how this could relate directly to human speech: 鈥淢ouse vocalisations are at best similar to baby cries,鈥� he says (See also Romantic rodents give secret serenades).
Moreover, Enard sees his team鈥檚 experiments as a first step toward untangling FOXP2鈥榮 complex role in human speech and evolution. 鈥淲e will never be able to fully recreate human evolution in a mouse,鈥� he says.
Long way to go
calls the new research 鈥渇ascinating鈥�, but he is holding his applause until the findings are replicated. 鈥淭hey raise some interesting issues and I think it鈥檚 worth further study, but I鈥檓 not willing to speculate on human evolution at this point,鈥� he says.
, a neuroscientist at University College London, thinks that FOXP2 is probably involved in controlling the brain circuits involved in the movements underlying vocalisations, including speech.
鈥淭he question is how an idea is translated into an utterance. That鈥檚 very difficult, I don鈥檛 think we are anywhere near understanding that,鈥� she says.
Journal reference: (DOI: 10.1016/j.cell.2009.03.041)
