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Gene Knockout Leaves Mice Speechless
21 June 2005 (All day)
Speech and language are considered distinctively human traits. But a gene involved in human speech now appears to play a key role in mouse communication as well, according to a new study. If correct, the finding would add to growing evidence that this so-called "speech gene" is involved in communication in a wide variety of animal species.
The study team, led by neuroscientist Joseph Buxbaum of the Mount Sinai School of Medicine in New York and including coworkers at the University of Pennsylvania Medical Center in Philadelphia and Manhattanville College in Purchase, New York, genetically engineered mice to carry defective versions of the FOXP2 gene. In humans, mutations in this gene cause a language disorder that seems to impair motor control of speech and verbal understanding. The researchers bred two types of FOXP2 "knockout" mice: One group was homozygous, meaning the mice carried two copies of the disrupted gene; the second group was heterozygous, with one functional and one defective gene.
As the team reports online this week in Proceedings of the National Academy of Sciences, the homozygous mice didn't make the ultrasonic sounds that young mice emit when separated from their mothers. Moreover, these mice suffered from severe motor defects and did not live to adulthood. Even the heterozygotes had communication problems: They emitted significantly fewer sounds over a given time period compared to normal mice. And when the team examined the brain tissue of the homozygous knockout mice, it found striking developmental abnormalities in the cerebellum, especially in the Purkinje cells, which are involved in fine motor control.
Buxbaum and his coworkers point out that FOXP2 is also expressed in the brains of songbirds such as finches and canaries, and further studies of the gene in mice might provide a better understanding of its role in human communication.
Geneticist Simon Fisher of the Wellcome Trust Center for Human Genetics at Oxford University in the United Kingdom agrees that there is much to learn about the function of FOXP2 from animals like the mouse. But Fisher, a member of the team that originally isolated FOXP2 in humans, says that he "would be cautious about concluding" that the new findings represent "a direct parallel with the kinds of speech problems observed in humans with FOXP2 disruption."
More information on FOXP2