"If we could talk to the animals, learn their languages, think of all the things we could discuss..." People have a deep desire to communicate with animals, as is evident from the way they converse with their dogs, enjoy myths about talking animals or devote lifetimes to teaching chimpanzees how to speak. A delicate, if tiny, step has now been taken toward the real thing -- the creation of a mouse with a human gene for language. The gene, known as FOXP2, was identified in 1998 as the cause of a subtle speech defect in a large London family, half of whose members have difficulties with articulation and grammar. All those affected have inherited a disrupted version of the gene from one parent. The gene quickly attracted the attention of evolutionary biologists because other animals also possess the gene, and the human version differs significantly in its DNA sequence from those of mice and chimpanzees, just as might be expected for a gene sculpted by natural selection to play an important role in language.
Researchers at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, have now genetically engineered a strain of mice whose FOXP2 gene has been swapped for the human version. Svante Paabo, in whose laboratory the mouse was engineered, promised that when the project was completed, "We will speak to the mouse."
He did not promise that the mouse would say anything in reply, doubtless because a great many genes must have undergone evolutionary change to endow people with the faculty of language, and the new mouse was gaining only one of them. So it is perhaps surprising that possession of the human version of FOXP2 does in fact change the sounds that mice use to communicate with other mice, as well as other aspects of brain function.
That is the result reported in the current issue of Cell by Wolfgang Enard, also of the Leipzig institute, and a team of researchers who studied 300 features of the humanized mice.
FOXP2, a gene whose protein product switches on other genes, is important during the development of the embryo and plays an active part in constructing many tissues, including the lungs, stomach and brain. It's so vital that mice in which both copies of the gene are disrupted die after a few weeks.
Despite the mammalian body's dependence on having its two FOXP2 genes work just right, Enard's team found that the human version seemed to substitute perfectly for the mouse version in all the mouse's tissues except for the brain.
In the language region of the brain, the basal ganglia, the humanized mice grew nerve cells that had a more complex structure and produced less dopamine, a chemical that transmits signals from one neuron to another. Baby mice utter ultrasonic whistles when removed from their mothers. The humanized baby mice made whistles that had a lower pitch, among other differences, Enard said.
Discovering that humanized mice whistle differently may seem a long way from understanding how language evolved. Enard argues that putting human genes into mice is the only way of exploring the essential differences between people and chimps, our closest relatives. And because there is no good way of genetically engineering chimps the mouse is the testbed of choice, Enard said.
"The most surprising finding, and cause for great optimism, is that the gene does seem to have a great effect on pathways of neural development in mice," said Dr. Joseph Buxbaum of Mount Sinai Medical Center.
Said Gary Marcus, who studies language acquisition at New York University: "People shouldn't think of this as the one language gene but as part of broader cascade of genes. It would have been truly spectacular if they had wound up with a talking mouse."
NEW YORK TIMES
