I learned this today. FOXP2 is known as the language gene.
FOXP2 stands for Forkhead box protein P2. Forkhead box proteins bind to a specific DNA sequence to control the rate of information. They are important for cell growth, proliferation, differentiation, and longevity. They, and all of the forkhead box proteins, have a region of about 100 amino acids, which is called the forkhead domain. They are transcription factor proteins, which means they activate some genes while suppressing others. FOXP2 is very active in the brain and other tissues before and after birth, and it is vital for the growth of nerve cells. It is also very involved with the plasticity of the brain, making it vital for learning and memory. It is also necessary for the development of the lungs. Mice without the gene don’t have fully developed lungs and die very quickly.
So, why is it called the language gene? This is a tricky question because it isn’t necessarily the only gene that is responsible for our ability to acquire language, but a mutation in it can severely hamper our ability to speak.
The gene was discovered in 2001. A British family known as KE, had a severe speech disorder that appeared to be inherited. It had been in their family for 3 generations, implying that it was a genetic disease. The disease was called developmental verbal dyspraxia and people with it have trouble saying sounds, syllables, and words. The problem is that the brain has difficulty planning to move the lips, jaw, and tongue into the correct place in time for the correct sound. Blood samples were taken from the family and analyzed. In the beginning, scientists thought that there might be a gene responsible for grammar, but this was disproved in 1995. The problem turned out to be more connected to linguistic ability, along with intellectual and anatomical features. In 1998, the location of the gene was narrowed down and in 2001 it was identified as FOXP2. Mutations in this gene were responsible for the speech impairment in the KE family. The gene was obviously important in the acquisition of language.
When this discovery was made, people theorized that the presence of this gene could be what sets humans aside from animals. However, the gene is present in many animals so there must be some other explanation. It turns out that the FOXP2 protein that we have differs from other animals by a few amino acids. We have three more than mice and two more than chimpanzees. That means that whatever advantage these amino acids have given us occurred after we split from primates, which is relatively recently. The gene with the same two extra amino acids that we have was also present in Neanderthals, studies have shown. Does that mean they were able to talk in the same way that we could? I don’t know, but it does show that we evolved this adaption before we split from them. The gene has virtually no variation across all human populations, so it must be doing something. So, what advantage has it given us?
This gene is present in birds, bats, and whales, and a whole host of other animals. In birds, if the gene is made inactive, the birds are no longer able to produce coherent songs. They become garbled and mix up the parts of the songs. In very much the same way as the KE family.
Bats also have the gene, but they don’t communicate with each other. Yet, they do make sounds. On top of that, the FOXP2 gene seems to have a lot of diversity among bat species. It appears that the gene varies and corresponds with different types of echolocation among bat species. Dolphins and whales also use echolocation, they don’t have a special version of FOXP2. This is probably because they produce the sounds for echolocation from inside their foreheads. They don’t have to make complex movements in the same way that the bats do. Bats use echolocation to navigate and hunt fast insects while they are flying. They need to make instant flight adjustments. Could this have something to do with the FOXP2 gene?
The most likely explanation seems to be that the FOXP2 gene is linked to sensory-motor coordination. It is almost always found in the basal ganglia and the cerebellums of animals, the area that is responsible for precise sequences of muscle movements. These areas integrate information coming in from senses with motor commands going out from other parts of the brain.
If this is true and the FOXP2 plays a big part in the development of motor coordination, it would explain why a mutation in it stopped the KE family from being able to speak properly. It is not so much a “language gene” as it allows us to move our mouths, lips, tongues, and jaws to make speech. Having it might not necessarily make us able to talk, but not having it stops us being able to move our faces enough to talk. The extra two amino acids might allow us to make the extra mouth movements that we need to be able to make complex speech.
SO, FOXP2 appears to be a gene that gives us the motor coordination required to talk. There may be other genes that give us the specific ability to talk. It is a fascinating topic. And this is what I learned today.
Photo by EKATERINA BOLOVTSOVA: https://www.pexels.com/photo/photo-of-women-talking-to-each-other-4051134/
Sources:
https://www.nationalgeographic.com/science/article/revisiting-foxp2-and-the-origins-of-language
https://www.sciencedirect.com/science/article/pii/S096098221831546X
https://en.wikipedia.org/wiki/FOXP2
https://en.wikipedia.org/wiki/KE_family
https://en.wikipedia.org/wiki/Developmental_verbal_dyspraxia
https://en.wikipedia.org/wiki/FOX_proteins
https://en.wikipedia.org/wiki/Fork_head_domain
https://www.frontiersin.org/articles/10.3389/fnbeh.2016.00197/full
https://www.nature.com/articles/news.2009.1079