Is a single gene, FOXP2, the secret to human speech?
In the last several decades, we humans have lost a certain amount of footing when it comes to the uniqueness of our species. Making and using tools, having distinct cultures—such things were formerly thought to be exclusively the domain of Homo sapiens. Yet spear-wielding chimps and potato-washing monkeys now testify to the fact that other primates use tools and have culture as well.
Among our few remaining distinctions is our ability to speak a complex language. Successful efforts to teach sign language to gorillas aside, no other species—primate or otherwise—is able to communicate as elaborately, or with equal complexity in articulation, vocabulary, or grammar, as we do. Among evolutionary biologists, the natural question that our verbal virtuosity raises is this: Exactly when—and how—did our ancestors first learn to speak?
The question is slippery because, unlike more tangible behaviors like tool use, speech leaves no physical record for paleontologists to find and date. However, researchers have in fact found some clues to the mystery of human speech, buried not in the ground but in the human genome.
The crack in the case originated in London, England, where dwells a large family uniquely afflicted with an unusual speech and language pathology. Among the three generations of this family—known as the KE family—about half suffer from a severe difficulty in speaking, to the point that others generally cannot understand them at all. The difficulties seem to be both neuromuscular and cognitive, including impaired ability to move the face and mouth and inability to process words according to grammatical rules.
In 2001, researchers announced that they had pinpointed the cause of the KE family’s plight, a single gene called FOXP2, located on chromosome 7. Those afflicted carry a mutation that’s the equivalent of a single-letter “typo” in just one of the 6 billion pairs of proteins that make up the human genome. By obstructing the action of another gene, the protein coded for by FOXP2 actually interferes with the development of neural and/or neuromuscular pathways for speech.
The KE family’s mutation occurs in a region of the FOXP2 gene that is “highly conserved” across many species, meaning that it doesn’t vary much at all; even species as different as yeast and orangutans show little difference in their FOXP2 genes. Wait, you say: Other animals have the FOXP2 gene, too? They do, and in fact, the versions shared by humans, mice, dogs, primates, and most other mammals are almost identical. The human version of the FOXP2 gene differs from the primate version by only two base pairs, and yet scientists speculate that one of these renders a significant developmental difference.
A cornerstone of the argument that the FOXP2 gene may have helped humans develop the gift of gab is the fact that the human variant of FOXP2 seems to have undergone what is called a “selective sweep.” When a particularly beneficial mutation arises in a species, it spreads rapidly and quickly replaces the original version, as those without the advantage fall victim to natural selection. A selective sweep doesn’t just eliminate the alternative base-pair arrangement, it also reduces the variation among other neighboring genes. Based on this and other evidence, researchers conclude that the human version of FOXP2 originated and spread rapidly among our hominid ancestors between 10,000 and 100,000 years ago.
Was it this chance arrival of a lucky mutation in a single gene that triggered the development of human speech? Maybe, maybe not. Other anatomical changes—the position of the larynx and the ability to voluntarily open and close the nasal cavity, to name two—are key to speech as well, and other genes affecting cognitive and motor skills are likely part of the story. Yet it does seem that this single mutation may have allowed Homo sapiens to talk its way into the role of dominant species on earth.