For over two decades, scientists have suspected a link between the Foxp2 gene and the development of speech and language in humans. Now, researchers show that introducing the human version of this gene into mice speeds up their learning. The findings, published in Proceedings of the National Academy of Sciences this week, could help explain the evolution of our unique ability to produce and understand speech -- which may be the result of a gene mutation that arose more than half a million years ago.
Nicknamed the language gene, Foxp2 was first identified in a family with severe speech difficulties; they carried only one functional copy of the gene coding for transcription factor forkhead box P2. Since humans split from chimps, there’ve only been two key mutations in this gene, which makes you wonder: What would happen if chimps had our version of the gene?
For starters, a large international team led by MIT’s Ann Graybiel and Svante Pääbo from the Max Planck Institute for Evolutionary Anthropology engineered mice to express “humanized” Foxp2 by introducing two human-specific amino acid changes into the gene. This change affected their striatum, a brain area essential for motor and cognitive behaviors in humans. Different parts of the striatum are responsible for two modes of learning: a conscious form called declarative learning and a non-conscious form called procedural learning.
The team placed the mice through a series of maze experiments. Mice with humanized Foxp2 performed the same as normal mice when just one type of memory was needed. But when both declarative and procedural forms of learning were engaged, mice with humanized Foxp2 learned “stimulus-response associations” much faster than regular mice. For example, knowing whether to turn left or right at a T-shaped junction -- based on the texture of the maze floor and visible lab furniture -- to earn a tasty treat.
Turns out, humanized Foxp2 gene makes it easier to transform new experiences and mindful actions into behavioral routine procedures. The engineered mice learned the route within a week, while regular mice did it in 11.
“This really is an important brick in the wall saying that the form of the gene that allowed us to speak may have something to do with a special kind of learning, which takes us from having to make conscious associations in order to act to a nearly automatic-pilot way of acting based on the cues around us,” Graybiel says in a news release.
By turning other genes on and off, Foxp2 helped tune the brain, adapting it to speech and language acquisition. Speech is often seen as requiring a leap in conscious thought-processing abilities, but it’s also dependent on complex movements of the lips and tongue becoming automatic, Graybiel explains to New Scientist. When we first learn to talk as infants, Foxp2 may have provided us unconscious control over our lips and tongue. Perhaps the gene also helped with the emergence of speech in early humans, the team suggests.
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