Jun 8, 2009, 14:10 GMT
Hamburg - German scientists have used a human speech gene to alter the brains of mice in order to study how our own linguistic is different from mammalian vocalization.
The baby mice who received the human speech gene squeak differently from other mice, though they are obviously incapable of speech, according to a report in the journal Cell.
The goal of the study done by the German researchers at the Max-Planck Institute for Evolutionary Anthropology is not to create a race of talking rodents, but in fact to learn more about human medical disorders which cause speech defects. Mice may never be able to speak, but they may help scientists discover ways to remedy genetically caused speech defects in humans.
'With this study, we get the first glimpse that mice can be used to study not only disease, but also our own history,' writes Wolfgang Enard of the Max-Planck Institute in Leipzig, Germany.
'In the last decade or so, we've come to realize that the mouse is really similar to humans,' he says. 'The genes are essentially the same and they also work similarly.'
There are hundreds of genes involved with human speech. But one human speech gene, FOXP2, was identified a decade ago as the cause of a speech defect in a large London family. Those family members with the genetic aberration have trouble with speech articulation and grammar.
Scientists quickly discovered that some other mammals share this particular gene. But they found that the human gene differs significantly from its shared gene in chimpanzees and mice.
The German researchers in Leipzig introduced this single gene to 300 mouse embryos. The result was that mice with the human FOXP2 show changes in brain circuits that have previously been linked to human speech.
Intriguingly enough, the genetically altered mice also have 'qualitative differences in ultrasonic vocalizations' they use when placed outside the comfort of their mothers' nests. In other words, they squeak differently from other baby mice.
But, Enard says, not enough is known about mouse communication to read too much yet into what exactly those changes might mean.
'Currently, one can only speculate about the role these effects may have played during human evolution,' the German scientists wrote.
'However, since patients that carry one nonfunctional FOXP2 allele show impairments in the timing and sequencing of orofacial movements, one possibility is that the amino acid substitutions in FOXP2 contributed to an increased fine-tuning of motor control necessary for articulation, i.e., the unique human capacity to learn and coordinate the muscle movements in lungs, larynx, tongue and lips that are necessary for speech.
'We are confident that concerted studies of mice, humans and other primates will eventually clarify if this is the case.'
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