The Loom

Mice, Monkeys, and Muttering

This week a few more tantalizing clues about the origin of language popped up.

I blogged here and here about a fierce debate over the evolution of language. No other species communicates quite the way humans do, with a system of sounds, words, and grammar that allows us to convey an infinite number of ideas. While particular languages are the products of different cultures, the basic capacity for language appears to be built into our species. Some scientists argue that language is primarily the product of natural selection working within the hominid lineage over the past few million years. Others suggest (argue might be too strong a word) that a lot of the components of language may have already been in place before our ancestors parted evolutionary ways with other apes. That would leave natural selection with a relatively small role in giving rise to human language.

Debates in evolutionary biology can be fierce and sometimes even ugly, and as a result they can give the misleading impression that the two sides are as different as black and white. Usually, however, the debate is over how much natural selection was responsible for shaping a feature in its current form and function. Take the evolution of bird feathers. Birds use them for flight, and they are exquisitely adapted for flight in their subtlest details. But fossils suggest that dinosaurs had feathers long before birds flew. So natural selection for flight did not produce feathers. As the ancestors of today’s birds started flying, however, natural selection probably then sculpted their feathers for better performance in the air.

In the case of the language debate, both sides agree that hominids inherited a set of capacities that may now play a role in language. Both sides agree that at least some natural selection helped shaped those capacities. The question is how far to either side the balance actually was. The best way to set that balance is to find more clues about the origin of language.

The first clue comes from squeaky mice.

In 2001 scientists identified a gene involved in spoken language. They found it by studying a Pakistani family in which half the members suffered from a disorder that interfered with their ability to understand grammar and to speak. The scientists tracked the disorder back to a single mutation to a single gene, which is now known as FOXP2.

FOXP2 belongs to a family of genes found in animals and fungi. They all produce proteins that regulate other genes, giving them a powerful role in the development of the body. FOXP2 in particular exists in other mammals, in slightly different forms. In mice, for example, the part of the gene that actually encodes a protein is 93.5% identical to human FOXP2.

The following year another group of scientists compared the human version of FOXP2 to the sequence in our close primate relatives. They found that chimpanzees have a version of the gene that’s hardly different from the gene in mice. But in our own lineage, FOXP2 underwent some fierce natural selection. By comparing the minor differences in FOXP2 carried by different people, the scientists were able to estimate when that natural selection took place–roughly 100,000 years ago. That’s about the time when archaeological evidence suggests that humans began using language. (For a good review of all this work, go here.)

What exactly was FOXP2′s role in the evolution of language? A group of scientists decided to see what sort of role it played in other animals. They genetically engineered mice lacking FOXP2 (some had one copy, others had none). Then they watched the mice develop. As the scientists reported this week, the mice experienced many changes, but the most tantalizing one reported in a paper this week was in their squeaks. Mice communicate with one another a great deal with ultrasonic sounds, and their squeaks can convey a lot of information. They are particularly important for pups, so that they can get help from their mothers. Pups missing FOXP2 had serious trouble squeaking for Mom when the scientists removed them from their nests. The trouble did not lie anywhere in their vocal tract, which developed normally. The scientists found instead that the neurons in a region of the brain at the back of the head known as the cerebellum hadn’t developed properly. The cerebellum is known to play a vital role in motor control, so perhaps that mice couldn’t manipulate their throats properly.

Before this study, scientists already knew that FOXP2 was important to the development of other animals, but now the evidence suggests that the gene was already playing a role in communication in the common ancestor of mice and humans, perhaps 80 million years ago. Given that the FOXP2 gene in chimpanzees and mice is barely different, it seems to have evolved little in our ancestry from 80 million years ago to 6 million years ago. That’s interesting when you consider that primates have some pretty elaborate communication systems, and that a clever chimpanzee can be taught a simple language by humans. Perhaps FOXP2 was continuing to play a role in the brain’s control of the voice anatomy, while other genes were evolving to handle other aspects of communication. And if FOXP2 in fact only underwent significant evolution in our lineage after we split from other apes, the new research may give a clue as to what happened during the evolution. People with mutations to FOXP2 have trouble controlling their mouths, and they had trouble with grammar. Perhaps it took on this second role in the past 100,000 years.

As I blogged here, scientists have looked for more clues to the function of FOXP2 with brain scans. They compared activity in the brains of people with mutations to FOXP2 to people with normal versions of the gene as both sets of people did different language tasks, such as thinking of verbs that go with nouns. The scientists found that a change to FOXP2 changes the way the brain handles language. Specifically, in people with mutant copies of the gene, a language processing area of the brain called Broca’s area is far less active than in people with normal FOXP2.

Broca’s area has a long history in neuroscience. In 1861 the French physician Pierre Broca treated a man who had suffered a stroke that robbed him of his ability to say anything except the word “Tan.” (He said it so much that he was nicknamed Tan.) Despite this devastating blow to his faculty of language, he could still understand the speech of other people. After Tan’s death, Broca autopsied his brain to find exactly what part of the brain had been damaged. It turned out that the stroke had destroyed part of Tan’s left frontal lobe. Broca looked at other patients with the same condition (known as aphasia), and found that they too suffered damage in the same area–what came to be known as Broca’s area.

Scientists are still trying to figure out what Broca’s area actually does in language. It’s possible that it does several things at once, or that it’s actually a collection of smaller regions that have different jobs. While Broca’s area may help us control our mouths, that’s not its only role. In the recent scanning experiment I mentioned, it became active even when people just thought about words.

The second clue this week comes from Broca’s area—or at least the corresponding part of a monkey’s brain.

Monkey brains and human brains are similar enough that scientists can find some of the regions in one species in the other, albeit in a different size and shape. There’s been a lot of debate, however, about whether a counterpart to Broca’s area exists in monkeys. If it didn’t, that would suggest that it must have emerged in our own lineage after the split with the ancestors of living monkeys.

This week in Nature, scientists report that monkeys do have Broca’s area. They show that the neurons in a patch on the left side of a monkey’s brain are organized in the same ways as Broca’s area. The patch also borders areas that have already been identified as being the same areas that border Broca’s area. The scientists then put microelectrodes in the brain region and ran small currents through it to see what would happen. The monkeys moved their jaws and tongues. So Broca’s area was already controlling the mouth 30 million years ago. At some point later, apparently, it became more adapted for speech in our lineage. Exactly how FOXP2 got involved in Broca’s area remains a mystery.

These two clues don’t show exactly where to set the balance between “pre-adaptation” and natural selection when it comes to language. But they do help reveal the building blocks that were put to use at some point.

Comments

  1. #1 Steve Russell
    June 30, 2005

    Carl, this is a fabulous round-up of this fast-breaking area. Wow!

  2. #2 George
    June 30, 2005

    I am confused about the distinction between the usage “pre-adaption” and natural selection for development of language. Is it not natural selection in either case, but rather a matter of timing? i.e. how much change occured during the human lineage versus in ancestors?

  3. #3 Bill
    June 30, 2005

    Very interesting. I wonder if a mutation of FOXP2 could account for people who have speech impediments like stuttering or lisping? Could repairing the mutation correct the impediment?

  4. #4 Dubya
    July 1, 2005

    D’eh. . .dit. . . uh. Ba. . .NA. . .na.

  5. #5 Zeteo Eurisko
    July 1, 2005

    Absolutely fascinating. My science fiction mind immediately goes to the idea of genetically modifying the FOXP2 gene to make talking monkeys.

    OK. I have to get back to work now…

  6. #6 Morten
    July 1, 2005

    Or how about just sticking a copy of the human FOXP2 into a chimpanzee? Is this doable with current gene technology? Is there any moral reasons we shouldn’t try this?

    On a late-night TV discussion show a few months ago, I believe I heard an invited biologist mentioning that the experiment of using human FOXP2 with mice was in development. Anyone here know anything about that?

  7. #7 Mike Maxwell
    July 1, 2005

    Don’t forget that speech =\= language. There are many signed languages, used by deaf people (and by some hearing people). Signed languages arise ex nihilo when deaf communities are brought together, and bear essentially zero resemblance to spoken languages that exist in the same areas. There was an interesting example of the rise of such a signed language a couple decades ago in Nicaragua, and the changes it underwent during a couple “generations” of learners have been documented.

    So there is no reason to think that speech was necessary for the rise of language, and in fact some researchers have proposed just the opposite–that signed languages were first, or that gestural proto-languages had s.t. to do with the rise of spoken languages.

  8. #8 Jaime Headden
    July 1, 2005

    For some reason, I cannot fathom how this relates to implicit origin of language formation. I understand that the issue of mutated FOXp2 and defects or degeneration of Broca’s Area affect the ability to formulate speech and remember language itself, but these are apparently secondary attributes. All animals appear to communicate, and the neccessity of finding Broca’s Area may represent a degree of modulation communication, rather than the ability to generate it. Indeed, mice lacking a “good” FOXp2 gene still try to communicate, but cannot form the vocal patterns consistent with this, suggesting this gene doesn’t relate at all to the neural processes of communication, only neuromuscular and motor control in the portions of the throat and pharynx [perhaps or perhaps not; looking at birds with more complex vocal "instruments" would help]. The issues of Broca’s Area and aphasia are, indeed, more prominent in the study of the formulation of how the brain works to create structure, but it doesn’t affect reception of language, and in this, it seems, there is lacking information on the issue of language origins.

    This also appeared on Hawks’ blog, and it seems both Carl and Hawks steer away from discussing this feature in relation to non-vocal communication. It can be said that purely guesture-related communication exists, and indeed sign langauges have been around a lot longer than the development of modern signing, and body posture and facial expression have always played a large component of how we perceive communication and thus set the “tone” for receipt and formulation of language. These most likely represent several different regions of the brain, and probably from all over the motor cortex and frontal lobe, as well as the cerebellum itself, implying not only an ancient, but implicit, nature of language that the human lineage has only adapted into a nearly pure vocal system of complexity nascent even in Antrhropoidea.

  9. …” 80 million years ago. Given… ” “The monkeys moved their jaws and tongues. So .. the mouth 30 million years ago”… In the last 80 millions years we learnt very well to talk, I hope that in the next 50-80 million years we’ll learn very well to listen. Which is the gene for listening?

    Domenico Schietti – 2010 Eliminazione Povertà

  10. #10 Jessika
    July 6, 2005

    Intriguing story!

  11. #11 Joseph Hilferty
    July 8, 2005

    Very nicely done. I might quibble on a few points concerning the KE family and FOXP2, but I think it’s more important to think about Broca’s area in this case.

    First, it is well-known that not everyone who suffers a lesion to Broca’s area will manifest Broca’s aphasia. Conversely, some people manifest the symptoms of Broca’s aphasia yet they do not have a lession to Broca’s area. This is not to say that Broca’s area is not important on average for speech and grammar. It is, but only on average.

    Second, Broca’s area is known to “light up” in tasks involving musical chord progressions. And it also has been confirmed that it is involved in other sequencing tasks. Nobody knows the answer but the forté (on average) of Broca’s area just might be to sequence things.

    In case anybody’s interested in references, check out my thesis:

    http://budling.nytud.hu/~kalman/course/konstr/thesis_Hilferty.pdf

  12. #12 flag
    July 13, 2005

    I believe I heard an invited biologist mentioning that the experiment of using human FOXP2 with mice was in development.