Early this year NY times reported on how FOXP2 changed the mouse "squeak", exciting the dreamer in me to envision a day Max conversing with me in English:
"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.
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. 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. 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."
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. 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. 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."
Today New Scientist reportson follow up studies:
"Earlier this year, Wolfgang Enard's team at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, spliced this human version of Foxp2 into mice. The mice didn't start speaking, but their sub-sonic vocaliszations changed, as did the shape and activity of neurons in a brain area that goes awry in people with Foxp2-related language disorders.
To discover what Foxp2 does differently in humans, neuroscientists Genevieve Konopka and Daniel Geschwind at the University of California, Los Angeles, grew human brain cells lacking Foxp2 in Petri dishes. To some they added human Foxp2 and to others the chimp version. They then recorded all the genes that were affected. Out of the hundreds of genes controlled by Foxp2, they identified 116 that responded differently to the human version of Foxp2.
This set of genes fits well with Foxp2's suggested role in the evolution of language and speech, says Konopka. Many control brain development or have been linked to cognition. Others are involved in controlling body movement and guiding the development of facial and laryngeal tissues that are essential for articulation.
Evolutionary studies of Foxp2 suggest it acquired its human-specific changes in the last half million years of human evolution – roughly when language is thought to have emerged. Geschwind has done preliminary studies of the evolution of the 116 genes that Foxp2 affects, which suggest they may have a similar history. "It brings up the possibility, which is not at all remote, that these genes may have evolved in concert," he says, adding that this may even be true for other genes involved in language.
While the results hint at a central role for Foxp2 in the evolution of language, Geschwind cautions against calling it "the language gene" as some have in the past. "Either Foxp2 itself is pretty damn important," he says, "or it's part of a regulatory circuit – something else is regulating Foxp2 that no one else has found yet."
Geschwind's team carried out a second experiment, comparing patterns of gene activation in adult human and chimpanzee brain tissue. They found a striking overlap between the genes whose activity was different in the human brain tissue and the set of genes that are controlled differently by human Foxp2.
The finding is preliminary, but if confirmed, it might mean a significant part of the difference between human and chimpanzee brains could be explained by two small changes in one gene, says Wolfgang Enard. "That would be really amazing."
With 116 genes to follow up on, Geschwind and Konopka have their work cut out for them, says Pasko Rakic, a neuroscientist at Yale University. This paper provides a starting point for future molecular studies on the basis of the evolution of language."
To discover what Foxp2 does differently in humans, neuroscientists Genevieve Konopka and Daniel Geschwind at the University of California, Los Angeles, grew human brain cells lacking Foxp2 in Petri dishes. To some they added human Foxp2 and to others the chimp version. They then recorded all the genes that were affected. Out of the hundreds of genes controlled by Foxp2, they identified 116 that responded differently to the human version of Foxp2.
This set of genes fits well with Foxp2's suggested role in the evolution of language and speech, says Konopka. Many control brain development or have been linked to cognition. Others are involved in controlling body movement and guiding the development of facial and laryngeal tissues that are essential for articulation.
Evolutionary studies of Foxp2 suggest it acquired its human-specific changes in the last half million years of human evolution – roughly when language is thought to have emerged. Geschwind has done preliminary studies of the evolution of the 116 genes that Foxp2 affects, which suggest they may have a similar history. "It brings up the possibility, which is not at all remote, that these genes may have evolved in concert," he says, adding that this may even be true for other genes involved in language.
While the results hint at a central role for Foxp2 in the evolution of language, Geschwind cautions against calling it "the language gene" as some have in the past. "Either Foxp2 itself is pretty damn important," he says, "or it's part of a regulatory circuit – something else is regulating Foxp2 that no one else has found yet."
Geschwind's team carried out a second experiment, comparing patterns of gene activation in adult human and chimpanzee brain tissue. They found a striking overlap between the genes whose activity was different in the human brain tissue and the set of genes that are controlled differently by human Foxp2.
The finding is preliminary, but if confirmed, it might mean a significant part of the difference between human and chimpanzee brains could be explained by two small changes in one gene, says Wolfgang Enard. "That would be really amazing."
With 116 genes to follow up on, Geschwind and Konopka have their work cut out for them, says Pasko Rakic, a neuroscientist at Yale University. This paper provides a starting point for future molecular studies on the basis of the evolution of language."
I am not good with languages (more on that later) but my theory is that language scar of mine has paradoxically been a great adhesive for my bond with Max.
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