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, 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 inherited a disrupted version of the gene from one parent. FOXP2 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 out for the human version. Svante Paabo, in whose laboratory the mouse was engineered, promised several years ago 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 the journal Cell by Wolfgang Enard, also of the Leipzig institute, and a large team of German researchers who studied 300 features of the humanized mice. FOXP2, a gene whose protein product switches on other genes, is important during the embryo’s development and plays an active part in constructing many tissues, including the lungs, stomach and brain. The gene is so vital that mice in which both copies of the gene are disrupted die after a few weeks.