Babel's Dawn

Tamed Males

Many people interested in the origins of language have noticed the humanity’s peculiar sexual arrangements and wondered if they had anything to do with language’s start. What arrangement are those? Humans engage in a variety of heterosexual arrangements—polygamy, monogamy, polyandry—but we don’t organize our societies around systems in which males and females mate widely and randomly with each other (bonobos do that), nor do the males fight among themselves over who gets to mate with anyone and who does not (gorillas do that). To put it technically, adult human societies are organized in many ways but whatever way they choose they minimize competition between sperm. How could that have anything to do with language?

Well, Terrence Deacon has looked at the relation between sexual organization and the need for symbols to enable that organization. Chris Knight has investigated the impossibility of language under the standard ape society structure in which males contribute very little to survival. They fight among themselves and take what they want from the females. Until that system changed, Knight argues, language as a social tool was impossible. This blog has also insisted many times that the trust and sharing that language requires is only possible if the chief form of evolutionary selection was group selection rather than selection at the individual level.

At the technical level, all three of us have been saying that to have language you have to get rid of competition between sperm. So the breakthrough analysis of the Y chromosome’s genetic structure that has just appeared in Nature (introduction here ) is a real support to these ideas. It turns out that the human and chimpanzee Y chromosomes have diverged so much and so fast that it is as though we shared a last common ancestor from 310 million instead of 6 million years ago. What’s more, while chimpanzee sperm has been streamlining for ever  tighter competition, the human Y chromosome looks to be competition free. This kind of finding is exactly the kind of thing that Deacon, Knight, and this blog have been looking for.

For full stories on the report see The Washington Post and The New York Times.

Genes and Language

Genes work as part of a eco-system, not as lines of code in a computer program. Some of its outputs are predictable, some are not.

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Here’s a bit of unexpected news. An authoritative book almost 500 pages long and listing over 150 genes related to language has recently been published in Spanish. It is not (yet?) available to English language readers. It’s a good reminder that not all the important work on language origins is being conducted in English. Antonio Benitez-Burraco has published Genes y Lenguaje Aspectos Ontogenéticos, Filogenéticos y Cognitivos [Genes and Language: Ontogenetic, Phylogenetic, and Cognitive Issues] in Barcelona. I wouldn’t know about it at all if it were not for a review by Victor. M. Longa  in the latest issue of the online journal, Biolinguistics. Should I master Spanish so that I can read it? Probably, but for the moment I’m going to have to settle for the 8 page review (here)..

The FOXP2 Molecular Network Begins Taking Shape

The FOXP2 gene as illustrated by Simon Fisher (Oriel College, Oxford), the investigator who first isolated the FOXP2 gene.

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A letter to the current issue of Nature has caused a stir among those interested in the evolution of language. It looks at the FOXP2 gene in more detail than any paper has ever done before. It also inspires at least as many questions as it answers, but now at least we have better questions. Also it has dealt yet another blow to the theory that language depends on distinct cognitive modules that permit internal thought and that later interface with motor modules (vocalizing or signing) for “externalizing” what you are thinking. If anything is becoming apparent from FOXP2, it is that language and motor activities are deeply entangled. It also provides more reason to doubt the original recent date ascribed to the gene's mutations.

The letter, titled, “Human-specific transcriptional regulation of C[entral] N[ervous] S[ystem] development genes by FOXP2,” was written by a large team represented by Genevieve Konopka and Daniel Geschwind (abstract here). The journal also had a summary article on the study, “The Importance of Being Human,” by Martin H. Dominguez and Pasko Rakic (abstract here).

The story so far: The FOXP2 gene is a highly stable gene, changing very little over millions of years, but it has changed twice since the last common ancestor with chimpanzees and bonobos, and it turns out to be important to the proper development of language. It cannot be directly responsible for speech, however, because it works by regulating the activity of other genes. (See: The Human FOXP2 Gene) The gene’s role in vocalization has been strengthened by evidence that FOXP2 is crucial in songbirds for enabling young birds to learn how to imitate the songs of their elders, (see: Birds Also Use FOXP2) and making echolocation sounds in bats (see: The Latest on the FOXP2 Gene). A year ago British researchers identified a “downstream” gene (CNTNAP2) regulated by FOXP2. Their report ended by saying that their work was a first step in understanding molecular networks affecting language. (See: A Second Gene Supports Language). Now it is time for another step.

Another Speech-Related Gene Identified

I've been trying to track down information on a presentation this week in Honolulu at the American Society of Human Genetics Convention. Raymond Clarke of New South Wales, Australia reports that a gene, called the "tospeak" gene has been identified as being important in proper shaping of the vocal tract and voice box. The gene itself is exclusive to primates, and the human version differs from that of other primates. In a response to an e-mail query from me, Dr. Clarke says,“The birth and evolution of the tospeak gene may represent the key evolutionary change to the human genome and our anatomical capacity to speak." It sounds suspiciously enthusiastic to my ears, but until I learn more I can't say. 

I'm looking. 

Humanized Mice

In my next post I planned to discuss a paper in the latest issue of Cell titled, "A Humanized Version of FOXP2 affects Cortico-Basal Ganglia Cells in Mice" (abstract here). A large team lead by Wolfgang Enard of the Max Planck Institute has substituted a human FOXP2 gene for a mouse FOXP2. I was amused to see that one result has been to display decreased exploratory behavior, but of course we cannot yet make any statements based on this technique yet. It is the start of a long inquiry. But I see that Carl Zimmer has posted a pretty good report on the paper on his blog, "The Loom" (here) and since I have something else I also want to discuss anyway, I'm going to refer the curious to that post.

FOXP2 Gene Over 1.5 Million Years Old?

The Neanderthal genome includes the human version of the FOXP2 gene. In my most recent post on that finding (see: Narrowing Down the Suspects) I said:

The original dating of the appearance of the FOXP2 gene in its human form put it between 200 and 100 thousand years ago. Many arguments about the recency of language have claimed authority based on that date, and now find their cards are very weak. ... In November 2006 this blog reported on a paper presented at a conference in Stellenbosch, South Africa claiming that the original dating effort on FOXP2 had been grossly in error and the true date of the human version of the gene was 1.8 to 1.9 million years ago. ... I have emailed the paper’s main author, Karl Diller, to ask for an update on his work, but have not yet had a response.

Now I have gotten a response. In a nutshell, he is sticking by his earlier findings:

It is true that the [original] date for FOXP2 was widely cited before the
Neanderthal results, but I would say that hardly anyone believes anymore
that the FOXP2 mutations were recent. The accepted date for the common
ancestor with Neanderthals is ~660,000 years ago. We stand by the genomic
evidence and our date of 1.8 or 1.9 million years ago for the FOXP2
mutations.

More

Carl Zimmer reminds me of a letter Molecular Biology and Evolution (here) arguing that the Neanderthal gene is a contaminant from inbreeding with Homo sapiens. These things will be argued for some time, and as I said in my Narrowing Down the Suspects post:

... all dates on this gene are likely to be taken with several grains of salt without multiple, independent confirmations.

Narrowing Down the Suspects

A Neanderthal man, as depicted at the American Museum of Natural History. If we put this fellow in some clothes and sent him on his way, how would he do?

As reported previously on Babel’s Dawn, the draft version of the Neanderthal genome was presented in Chicago last week (press release here) and it confirms the earlier finding that Neanderthal’s share the same FOXP2 gene found in humans. FOXP2 is the most important gene known to support language. Without it in its human form, rapid speech and the ability to learn speech sounds is limited. The gene’s presence in Neanderthals is very strong evidence that the human lineage was speaking fluently before the Neanderthals split from the line that became Homo sapiens.  The original dating of the appearance of the FOXP2 gene in its human form put it between 200 and 100 thousand years ago. Many arguments about the recency of language have claimed authority based on that date, and now find their cards are very weak.

A Second Gene Supports Language

British scientists have identified a second gene that is crucial to normal language development. The gene, CNTNAP2, joins FOXP2 as critical to understanding the biology of language.

The classic idea about a gene is that it makes a protein. For example, a gene might make the protein that gives some eyes their blue color. FOXP2, however, works differently. Instead of directly making a protein, FOXP2 genes regulate the making of proteins by other genes. A team of researchers at the Wellcome Trust Centre for Human Genetics  has now identified the CNTNAP2 gene as one that FOXP2 regulates. Certain unusual mutations of CNTNAP2 are implicated in both autism and specific language impairment.  The team’s paper, published today (Nov. 5) in the New England Journal of Medicine, concludes that we now have a biological link “between clinically distinct syndromes involving disrupted language.”

Specific language impairment (SLI), affects up to 7% of 5- or 6- year-olds and is much more common than the impaired speech brought on by FOXP2 mutations. SLI is often found among many different members of a family and has long been considered likely to be hereditary. Studies have found no link between SLI and FOXP2. Nevertheless, the authors hypothesized that genetic associations with disorders such as SLI could be found “downstream” from FOXP2 influence. In other words, they suspected that by following FOXP2’s influence on other genes, they might discover the source of further genetically-based language disorders.

Working in the laboratory with human neurons, the team determined that one of the genes regulated by FOXP2 is CNTNAP2. To state it technically: CNTNAP2 is a target of FOXP2. The CNTNAP2 gene does work like a normal gene, making a protein. In its case it makes a kind of protein thought in humans to be “involved in cortical development.” It helps build the brain.

Having identified the gene as possibly important to language the team studied the genetic traits of 184 families known to be affected with SLI. Analysis established that some variants of CNTNAP2 are associated with SLI. Other unrelated work has shown that variant forms of the same gene are implicated in autism.

The test used in the study to identify people with SLI appears to have measured their ability to remember sounds. They scored low in their capacity to hear a nonsense syllable and repeated it. But despite these associations between various language disorders and CNTNAP2, we do not yet know how the genes supports normal speech. Its evolutionary history is also uncertain. In an e-mail to this blog, team leader Simon E. Fisher reports that CNTNAP2 "is one of the largest genes in the human genome, with a lot of intronic sequence [portions not used in coding protein]which might harbour important regulatory elements."

Understandably then, the team ends its report with a very narrow boast:

This work represents a move … toward an understanding of molecular networks that may go awry in neurodevelopmental disorders affecting language.

It is not an answer to the questions asked on this blog, but it is always promising when an explorer cries out, “Hey, over here. I’ve found something.”

 

The Workings of Co-Evolution

Yoruba and Italian peoples can learn each other's languages, but slightly different facial features bias  the evolution of phonemes in slightly different ways.

Here’s a hypothesis that I expect will become known as a law: Language develops in the individual as the interaction between the individual’s genetic bias, the population’s genetic bias, and cultural history. The surprising part of that statement is the reference to population genetics. That idea is the point missed by Chomskyan linguists, cognitive psychologists, and associationists. This statement brings together several themes that have appeared on this blog since the end of last summer, and it explains what happens when language and people co-evolve.

Birds Also Use FoxP2

Finches. Click to hear the two male finches, a zebra finch and a society finch, singing. It seems they need a properly functioning FoxP2 gene to learn their songs, just as humans need the gene to master articulate speech.

The FoxP2 gene is the only genetic basis of speech yet identified, although exactly what it contributes has remained a mystery. Without a normal FoxP2 gene people do not articulate their words well and also have some problems with syntax. It turns out that songbirds also require a properly functioning FoxP2 gene if they are to sing their song accurately and completely, says an article in the December PLoS Biology (available online here) by Constance Scharff and others. Thus, we at last have an experimental method of probing the role of FoxP2 in vocal development. Apparently the gene is important in helping young birds/people learn to imitate the sounds chirped/spoken around them.