Gene Knockout Leaves Mice Squeakless

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Science  01 Jul 2005:
Vol. 309, Issue 5731, pp. 47
DOI: 10.1126/science.309.5731.47d

A new study suggests that the mouse version of a human “speech gene” also plays a key role in murine communication. It adds to evidence that the gene may be widely involved in animal communication.


In humans, mutations in the FOXP2 gene cause impairments in both understanding and motor control of speech. The gene differs only slightly in mice, so researchers led by neuroscientist Joseph Buxbaum of the Mount Sinai School of Medicine in New York City bred two types of FOXP2 “knockout” mice: One group was homozygous—that is, it had two disrupted copies of the gene; the other group had one functional and one defective gene.

The homozygotes did not make the ultrasonic sounds that young mice emit when separated from their mothers, Buxbaum's team found. Moreover, they had severe motor defects and died young. Even those with one normal copy of the gene had problems, making significantly fewer sounds than did normal mice when separated from their mothers, the scientists reported last week in the Proceedings of the National Academy of Sciences. Examination of brain tissue revealed abnormalities in the cerebella of the double knockouts, especially in the Purkinje cells, which are involved in fine motor control.

Simon Fisher of the Wellcome Trust Center for Human Genetics at Oxford University in the U.K., who helped isolate the gene in humans, cautions that the knockouts may not offer a “direct parallel” with human speech problems from FOXP2 disruption. But he says such studies “will be critical for gaining insights into the neuromuscular pathways regulated by this gene.”

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