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Encephalization and the FOXP2 Language Gene
If you happen to be born with abnormal human FOXP2, you will suffer from severe language impairment. That means that the normal human form is a naturally selected mutation, a “target of natural selection.” (A mutation is a randomly occurring change in the gene, resulting in a change in physiology or anatomy or even behaviour.) And that strongly indicates that the innate human capacity for effortless language learning is an adaptation, the product of Darwinian natural selection.
About two million years ago, the hominid brain suddenly (in glacial evolutionary terms) began to get larger and larger, a process called encephalization. This did not occur in any of the other large primates, such as chimpanzees and gorillas. A mutation occurred in hominids around that time, a mutation that may have made encephalization possible.
A gene called MYH16, active in chimpanzees, ensures huge jaw muscle build-up, necessary for powerful chewing. These muscles constrict the skull, something like bungee cords, preventing growth in cranial capacity. In hominids, a mutation appeared in the line that deactivated MYH16. This may have freed the hominid skull to expand. And expand it did, tripling in size over the next 2 million years. To this day, chimpanzees still have the active version of MYH16 and comparatively small skulls. All humans have the deactivated human mutation of MYH16 and comparatively huge skulls.
As well, there’s evidence of a connection between MYH16 and FOXP2. It turns out that if you have abnormal human FOXP2, you not only have grave cognitive language difficulties, but you also have physical problems with your mouth and jaw muscles.
Taken together, the uniquely human variants of MYH16 and FOXP2 look like smoking-gun mutations with respect to encephalization and language development.