Transgenic mice containing a human speech gene could give clues about the evolution of language. A team from the Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany, replaced the mouse gene FOXP2 with the human equivalent - a gene implicated in speech problems, and thought to be linked to the evolution of human language. The replacement changed aspects of mouse brain function as well as the sounds that mice used to communicate with each other. The team published its work in the journal Cell.
In 1998 FOXP2 was identified as the cause of a speech defect in a large British family with a history of severe language disorders. Family members who had trouble speaking and understanding language had inherited a mutated copy of the gene from one parent. FOXP2 is also known to have an effect on communication in other animals. When the gene was disabled in mice embryos the newborn mice had trouble making the ultrasonic squeaks needed to get help from their mother, and when scientists blocked FOXP2 expression in the brains of songbirds they did a worse job of singing.
Since the FOXP2 gene sequence seems to be involved in communication, and is very similar in all mammals, except humans and Neanderthals where it is markedly different, evolutionary biologists have speculated that it may help explain why humans are the only animal capable of speaking with complex language rather than simple songs, barks and grunts.
Wolfgang Enard and his team were motivated to breed mice that make the human-specific version of FOXP2 in an attempt to nail down the gene's function. 'The mouse model is the only chance we really have to find out what the human version of FOXP2 does differently from the chimp version,' says Enard, referring to the lack of a good way to genetically engineer chimps, even if it were not ethically questionable.
Enard's team compared 300 traits between the transgenic and normal mice and found that the human version of FOXP2 was a perfect substitute in all the mouse's tissues except for the brain, leading to some differences in brain function and behaviour. The engineered mice had squeaks of a lower frequency and were also found to explore less, perhaps explained by the lower levels of dopamine in their brains - dopamine is a neurotransmitter we need to control our bodies and pursue 'rewarding' things such as food.
Dopamine is produced in the basal ganglia, a clump of neurons at the base of the brain, and scientists studying people with FOXP2 defects noticed that a part of the basal ganglia, known as the striatum, is altered. In the striatum of the 'humanised' mice certain kinds of neurons had longer branches and sprouted more new connections with other neurons, when compared to normal mice. This might point to one step that helped give rise to language since people who produce less dopamine in the basal ganglia are better at breaking down complex speech into smaller chunks that the brain can interpret as words being said.