A recent study in neuroscience suggests that a gene mutation which arose over half a million years ago could be the key to the unique ability that humans have to both produce and understand speech. The study, published in Proceedings of the National Academy of Sciences was conducted by Christiane Schreiweis, a former visiting graduate student at MIT and Ulrich Bornschein of the Max Planck Institute for Evolutionary Anthropology in Germany.
What the researchers from MIT and the other European universities which took part in the study suggest is that the human version of a gene named FOXP2 facilitates transforming new experiences into routine procedures. When mice were engineered to express humanized FOXP2, they learned how to run a maze visibly faster than normal mice.
What the findings also show is that FOXP2 is potentially responsible for helping humans by influencing a key component used in learning languages. This component is the transformation of experiences (such as hearing the word ‘glass’ when being shown a glass of water) into a nearly automatic association of the word, with objects looking and functioning like glasses. According to Ann Graybiel, an MIT Institute Professor, member of MIT McGovern Institute for Brain Research and senior author of the study,
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,’ the researcher declared.
It is known that all animal species communicate with each other, but only humans have the singular ability of generating and comprehending a proper language. FOXP2 is one of the numerous genes which scientists think might have contributed to the development of human linguistic skills. The FOXP2 gene was first identified in a group of family members (known as the KE family) who experienced severe difficulties in both speaking and understanding speech – they were found to carry a mutated version of this gene.
It was in 2009 when Svante Pääbo, director of the Max Planck Institute for Evolutionary Anthropology, engineered mice to express the human form of FOXP2, along with his team of researchers. The FOXP2 gene encodes a protein which is different from the mouse version by only two amino acids. The team found that the mice’s slender extensions in the striatum which neurons use to communicate with each other, called dendrites, were actually longer. (The striatum is a part of the brain which is responsible for habit formation). The mice were found to be better than humans at forming new synapses as well.
FOXP2 produces a protein that functions like a transcription factor, which means that it has the possibility to turn other genes on and off. The present study found that this gene appears to turn on genes involved in the regulation of synaptic connections in between neurons. Another finding of the research is that the dopamine activity in a part of the striatum involved in forming procedures is enhanced by the gene. Consequently, the neurons of stiatal regions could be turned off for longer periods in response to prolonged activation, known as long-term depression, which is allocated to learning new tasks and memory formation.
Svante Pääbo is an author of the new PNAS paper as well, while Enard and Graybiel are responsible for the striatum part of the study and the analysis of behavioral effects of replacing FOXP2. As mentioned earlier, the mice with humanized FOXP2 were better at learning to run a T-shaped maze, where mice have to make the decision to turn left or right at a T-shaped junction, based on the texture of the maze floor, in order to earn a food reward.
Collectively, the changes help with tuning the brain distinctly in order to adapt it to speech and language acquisition, according to the researchers. What they are investigating now is whether FOXP2 can interact with other genes to produce its effects on learning and language in other areas. According to Genevieve Konopka, assistand professor of neuroscience at the University of Texas.
‘The study provides new ways to think about the evolution of FOXP2 function in the brain. It suggests that human FOXP2 facilitates learning that has been conducive for the emergence of speech and language in humans. The observed differences in dopamine levels and long-term depression in a region-specific manner are also striking and begin to provide mechanistic details of how the molecular evolution of one gene might lead to alterations in behavior.
Nancy Lurie Marks Family Foundation, The Simons Foundation Autism Research Initiative, The National Institutes of Health, the Wellcome Trust, the Fondation pour la Recherche Medicale and the Max Planck Society are the major organizations to have funded this research.