A new study has shown that a small mutation in the gene FOXP2 is responsible for the human capacity for language. The study, published in the November 12th edition of Nature, is the result of a collaboration between researchers at UCLA and Emory University‘s Yerkes Primate Research Laboratory. According to researchers, FOXP2 regulates the expression of other genes, meaning that different forms of FOXP2 result in different patterns of expression of the genes it regulates. In the case of humans and chimps, different forms of FOXP2 are the reason that we can talk and chimps cant.
It is believed that further research on FOXP2 will allow scientists greater insight into the causes of speech disorders, especially as a result of autism and schizophrenia. According to Genevieve Konopka, the first author on the study and a postdoctoral fellow in neurology at the David Geffen School of Medicine at UCLA, “Genetic changes between the human and chimp species hold the clues for how our brains developed their capacity for language. By pinpointing the genes influences by FOX P2, we have identified a new set of tools for studying how human speech could be regulated at the molecular level” To read the UCLA press release, please click here.