Why can humans talk but apes can't?

Of all the possibilities that make up human uniqueness, the most striking is that we can speak. This makes humans really different from other species, even our closest relatives in the evolutionary timeline - the apes, don't have this ability.

Detailed studies of genetic material and fossils have dated human evolution from chimpanzees (Homo and Pan respectively) to about 7-8 million years ago (as shown in the image below). family tree below). Due to their close ancestry to humans, scientists have repeatedly been excited and curious when testing chimpanzees' language abilities.

The tree of the family Hominidae shows that humans (Genus: Homo) diverged from chimpanzees (Genus: Pan) about 7-8 million years ago

Specifically, in a recent project, researchers tried to teach sign language to a chimpanzee named Nim Chimpsky (named after Noam Chomsky!), raised as a child in human social environment. It's surprising that despite persistent and rigorous training, Nim is incapable of combining words using grammatical rules, that is to say. In contrast to Nim, deaf children with little exposure to speech were able to easily express grammar in their sign language. This leads us to ask: if chimpanzees are indeed so closely related to us humans, why are we the only ones capable of speaking? What secret does the human genetic material contain that makes us so magically able to converse?

With the question "why speaking is a unique human ability", the first hint came when scientists studying language disorders stumbled upon a unique case. They found a family (called the KE family) where, over three generations, about half of the members had severe speech and language disorders. These people show a disorder in the coordination of the muscles of the face when speaking, known as "motor coordination disorder" or "dyslexia". This makes it impossible for the listener to understand what they are saying. In addition, affected members show difficulty in following grammar rules. The ability to move facial muscles to speak and follow grammatical rules sets humans apart from other primates. This is remarkable research.

Curious about the genetic basis of the decline in the KE family, the researchers conducted their genome analysis. They found that both males and females in the KE family were equally affected, so they focused on autosomal (non-sex) chromosomes. The three-generation KE family tree shown below shows affected members (black). Scientists suspect that the disorder is caused by a region on chromosome 7, found in all 27 affected members. They call it the "SPCH1" region. However, this region contains about 70 genes and it is not possible to find out which genes here actually cause dyskinesia.

KE family tree of three generations. The circle shows the female and the square shows the male. Black shape indicates members affected by speech function

A later report from one unrelated individual about speaking difficulties similar to the KE family helped the researchers continue this investigation. Genetic analysis of this affected individual revealed a break in chromosome 7, between a gene known as "FOXP2" (Forkhead b OX P2). Scientists now know that the FOXP2 gene in the SPCH1 region is responsible for this.

What follows is also the main part of the FOXP2 association puzzle, and the keynote comes from analyzing the genetic code contained in the gene and determining how it has changed over the course of evolution. The researchers traced the evolutionary origins of the FOXP2 gene by comparing it across species - mice, rhesus monkeys, orangutans, gorillas, chimpanzees and humans. Intriguingly, this is an extremely "conservative" gene, all of the chimpanzee, gorilla and rhesus FOXP2 proteins differing from only 2 (out of 715) amino acids from the human FOXP2 protein. Furthermore, humans, in all different regions, were compared and all showed the same FOXP2 gene encoding two unique amino acids.

The FOXP2 gene is present in all animals, but none can speak except humans. This leads experts to believe that a single change in amino acids at those two positions could play an important role in human speech.

Surprisingly, despite the differences in the coding genes, FOXP2 has been shown to function similarly in several animal species. A detailed study of the FOXP2 gene in mice showed that it plays an important role in the proper development of brain cells in the fetus, which are later responsible for the motor abilities of mice. The researchers also created "animal models" with mutated FOXP2 genes in mice and songbirds that mimic the KE family.

The mice showed severe deficits in learning motor tasks and decreased vocal abilities. The mutant songbirds couldn't learn to pronounce or sing their own "songs", nor could they even imitate them properly when taught by a "tutor bird".

All of this important evidence has prompted experts to believe that FOXP2 plays an important role in controlling the vocal motor of species.

Given that humans possess a single amino acid sequence encoded by the FOXP2 gene, it is important to explore its function in humans. It would be imprecise and fair to extrapolate findings from other animals with a different sequence in their FOXP2 to explain its function in humans. To explore the influence of the FOXP2 gene on human brain function, the scientists scanned the brains of affected members of the KE family as they performed a number of language tasks and compared them with Family members are not affected. The results showed that in the member with impaired speech function, their Broca area was reduced - this is an important brain area for our ability to speak. This area, when injured in humans, will lead to the inability to speak, called aphasia.

FOXP2 mutations affect the activity of Broca's region, a motor region implicated in aphasia.

Other studies have also shown that FOXP2 also regulates the function of a number of other genes, so when disrupted, it also leads to language difficulties, such as autism (ASD) and language difficulties. specific language impairment (SLI). These findings suggest that FOXP2 gene expression is important for the normal functioning of the human brain regions that underlie our ability to speak.

Although language ability in humans is considered a complex skill that cannot be controlled by genes, the truth is that much of this ability has been bestowed upon us by the presence of a unique sequence of genes. most of the FOXP2 gene on chromosome 7. The FOX family of genes acts as regulators of several other genes, "turning them on and off" at times of need. This rule also leads to the proper development and functioning of our speech neurons, including those in Broca's area.

It's also important to note that FOXP2 is not a "single gene" responsible for voice. Several other genes controlled by FOXP2 also contribute to our language abilities. However, FOXP2 is 'highest' in the hierarchy of genes that control the development of brain structures important for fine facial and mouth movements required for speech. It is the only gene expressed only in humans, different from chimpanzees only in two amino acids, helping us to better control our mouth movements.

It is also what sets us apart from other species, both apes and chimpanzees - our closest living "relatives".