- Category: Science & Technology
- Created on Sunday, 31 May 2009 10:00
- Written by Scientific Blogging News Staff
The short story is that one of the unique genes that define human beings, the speech gene known as FoxP2 was grafted into a mouse’s DNA, and the newborne critter started making new and unsual sounds for mice.
This represents an important development by Wolfgang Enard and his colleagues. Nicholas Wade writes in the New York Times:
In a region of the brain called the basal ganglia, known in people to be involved in language, 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, when isolated, made whistles that had a slightly lower pitch, among other differences, Dr. Enard says. Discovering that humanized mice whistle differently may seem a long way from understanding how language evolved. Dr. Enard argues that putting significant human genes into mice is the only feasible way of exploring the essential differences between people and chimps, our closest living relatives.
Of course, implanting this gene did not enable the mouse to talk. Actual speech requires a cascade of genetic changes in humans from even their close chimp cousins (including brain size, physical throat structures, and more).
It confirms the role of FoxP2 in creating sounds, and it will enhance our ability to understand what that gene does in humans, and it will help us understand more deeply how we became human in the evolution from our earlier chimp-like ancestors.
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The following article appeared on Scientific Blogging.
Talking Mice? No, But Their FOXP2 ‘Speech’ Gene Can Tell Us About Our Evolutionary Past
By News Staff | May 28 2009
Following on the heels of ‘missing links’ in the popular media earlier this month, you might expect that research on mice carrying a “humanized version” of a gene believed to influence speech and language will have references to cartoons and mice that talk.
In reality, it’s nothing so outrageous but the research can still teach us about our evolutionary past – even if the mice don’t speak.
Wolfgang Enard of the Max-Planck Institute for Evolutionary Anthropology and colleagues are interested in the genomic differences that set humans apart from their primate relatives. One important difference between humans and chimpanzees they have studied are two amino acid substitutions in FOXP2. Those changes became fixed after the human lineage split from chimpanzees and earlier studies have yielded evidence that the gene underwent positive selection. That evolutionary change is thought to reflect selection for some important aspects of speech and language.
“Changes in FOXP2 occurred over the course of human evolution and are the best candidates for genetic changes that might explain why we can speak,” Enard said. “The challenge is to study it functionally.”
For obvious reasons, the genetic studies needed to sort that out can’t be completed in humans or chimpanzees, he said. In the new study, the researchers introduced those substitutions into the FOXP2 gene of mice. They note that the mouse version of the gene is essentially identical to that of chimps, making it a reasonable model for the ancestral human version.
Mice with the human FOXP2 show changes in brain circuits that have previously been linked to human speech, the new research shows. Intriguingly enough, the genetically altered mouse pups also have qualitative differences in ultrasonic vocalizations they use when placed outside the comfort of their mothers’ nests. But, Enard says, not enough is known about mouse communication to read too much yet into what exactly those changes might mean.
Although FoxP2 is active in many other tissues of the body, the altered version did not appear to have other effects on the mice, which appeared to be generally healthy.
Those differences offer a window into the evolution of speech and language capacity in the human brain. They said it will now be important to further explore the mechanistic basis of the gene’s effects and their possible relationship to characteristics that differ between humans and apes.
“Currently, one can only speculate about the role these effects may have played during human evolution. 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.”