Babel's Dawn

Duplicate Points of Attention

Some news that I've been waiting for seems to have come along. If so, a number of puzzles may have solutions and some suspicions I've held seem likely to be true. The news appears to be a confirmation of an idea put forth a couple of years ago by Terrence Deacon and which, when I heard it, set me thinking.

Deacon is best known on this blog for his book The Symbolic Species but he is also an expert on evolution and the brain. An interesting idea he has been promoting for a few years is that of "relaxed selection," a means of producing a random change and sheltering that change while it finds a role. Most changes to the genome are point mutations in genes and the results are immediately tested. If a mutation is harmful, it does not spread, while helpful genes do increase in a population. Neutral mutations are neither selected nor filtered out. They may increase over time through chance but probably will never amount to much of importance.

Deacon focuses on a more rare type of change in which a section of a chromosome duplicates. Although relatively rare, doubling has happened many times in evolution's long history. An example Deacon likes is the introduction of color vision into the primate line. It began with an accidental doubling of the genes that govern the retina. Color vision did not result immediately. The original genes provided normal vision. The doubling was basically useless but at least not ruinous. In essence, the doubling worked like a neutral mutation, neither selected nor discarded.

Once the doubling occurs, the doubled genes are of course subject to mutation and can change and sometimes produce something valuable. This process led to the eventual appearance of color vision as a neutral duplication evolved into something well adapted to the forest environment. Deacon calls this process "relaxed selection" because the doubled strand of genes is not immediately rejected and allows time for something new to appear.

Deacon has been arguing that the Homo brain's development is the result of a doubling and relaxed selection. Now comes news that a doubled section of the human genome controlling brain development has been identified. The doubling took place an estimated 2.4 million years ago, early in the history of the Homo line.

As far as I know, James Hurford never linked any of his ideas to Deacon's doubling but I did when I covered one of his presentations on subject and predicate. He talked about it as subject and news (see: The Word-Sentence Continuum). Hurford's approach enabled me to think of sentence and predicate as a kind of doubling.

Standard analysis of sentences defines the subject and predicate as a [noun phrase] + [verb phrase]. That rule allows for simple sentences like [Jesus] [wept] and complex ones like [Alexander and all his army] [defeated the Persians and their allies]. But Hurford got me thinking in a more functional way. News can come in many forms: verbs (e.g., died, as in Our neighbor died), adjectives (red, The leaves turned red), and nouns (book, Jack wrote a book).

Looked at this way, sentences can contain two elements and a link. The elements are the subject and the news. The startling thing is that a sentence can ask the listener to attend to both subject and news at the same time. This double attention is made possible by a link that fits with both ends of the elements: The leaves turned … turned red; Jack wrote … wrote a book. If the link does not work with both elements, the sentence is confusing and the doubled attention breaks: The leaves fell … fell red; Jack splintered … splintered a book.

I'm not proposing that sentences always come from doubled attention. Sometimes the link alone is sufficient for the news—Our neighbor died. Perhaps this kind of sentence is older than a doubled one, but ever since I combined Deacon and Hurford in my thinking I've been keeping an eye out for news that might support the idea that speech reflects a doubling that enables people to hold two points of attention at the same time.

Naturally I sat up straight when I came across a news item headlined, "Doubled Gene Means Extra Smarts," by Tina Hesman Saey. The gene in question is called SRGAP2 and has been previously identified as one of 23 genes that has been duplicated in humans but not in other primates. The gene was partially duplicated 3.4 million years ago and then 2.4 million years ago the partial duplicate was itself duplicated. The first duplicate is not found in all humans, but the second duplicate is fixed (i.e., universal) in the human population. 2.4 million years is considered a short time for a duplicate gene to become fixed, and suggests the change is important. Exactly what the changed gene accomplishes is unclear, but the research team—headed by Megan Dennis—proposes that it thickens the brain's cortex.

From my perspective, the date is good (before speech probably began, but not hopelessly before). It's something to keep an eye on.

The War between the Sexes and Language Origins

Did James Thurber's famous drawing hold  the clue to speech origins?

New theories of language origins are not rare. Here's one that focuses on the "need" to make excuses. What is rare is an interesting one that reflects new information rather than a new bit of whimsy. Human Biology's latest issue is devoted to "Integrating Genetic and Evolutionary Approaches to Language" and among its many notable papers is one that presents an intriguing, new (to me) idea on speech origins. I expect to devote at least one more post to the special issue, but today I want to concentrate on William M. Brown's "The Parental Antagonism Theory of Language Evolution: Preliminary Evidence for the Proposal" (paper here).

The theory is new because it comes at the issue in a new way, not from linguistics or the study of language functions. Its approach reminds me of things that go on in the study of physics, where somebody notices an implication of an equation and the next thing you know people are hunting for black holes. In this case, the focus is on the basic equation of evolution, Hamilton's equation of inclusive fitness. The equation includes an adjustment for relatedness and relatedness is normally treated as one thing. My brother is a closer relation than my first cousin.These relations appear reciprocal. My brother is also related to  my first cousin.

However, I can be related to people in two ways. I have cousins "on my father's side," and a whole different set of cousin's "on my mother's side." Thus, not all my cousins are related to one another. If my father's genes could be distinguished from my mother's, then my father's genes would have different "interests" from my mother's. Normally, these two conflicts would cancel each other out, there being no reason for an offspring to prefer one parent's relatives over the other. Yet conflict is possible if a species has:

• Sex-biased dispersal: e.g., female elephants stay in the group they were born into while males go off into the larger world; and
• Relatedness asymmetries: e.g., adult females are much closer kin to the elephants they encounter than adult male elephants are to any males they encounter.

Therefore, the closely-related sex is likely to be more cooperative than the sex that disperses.

Female elephants, in the example I just gave, are famously cooperative, whereas bull elephants are not. Likewise, among lions, it is the male who enters a pride and is uncooperative, while the lionesses who grew up together cooperate in the hunt.

Does it work the other way too? In chimpanzees it is the male who stays around while the female goes off. And, what do you know, it's the male chimps who hunt together while the females stand aside.

I'm tossing things off the top of my head here, but whenever I find this much under my hat to support an idea, I'm interested and ready to listen.

There is among most mammals, including almost all primates (present company excepted), an obvious relatedness asymmetry: the offspring is related to the female doing the upbringing, while the father is totally absent and doing none of the upbringing. Therefore, the mother has an interest in enjoying some cooperative behavior on the offspring's part, whereas the father, who is unrelated to the mother, has no such interest in cooperation. It is in the father's interest that the offspring be as much of a parasite on the mother as possible without killing her (and leaving the offspring to die soon after), so that the offspring grows up strong. It is this relationship of conflicting interests that the author refers to as "parental antagonism."

Again, however, these interests should cancel each other out as the offspring is equally related to both parents. But there might be a way around this impasse if one parent's version of a gene could silence the other parent's version. In that case, if the mother's gene is silent, the offspring will display parasitic behavior, whereas in the father's gene is silent, the offspring will display cooperative behavior.

The theory is clear and elegant. Genes from the mother (aka matrigenes) promote cooperation; genes from the father (patrigenes), parasitism. In communications, for example, patrigenes would promote signals that make demands and language that backbites, whereas matrigenes would promote signals that end demands by expressing satisfaction and gossip about another's virtues.

Elegant as the idea is, however, I do have some doubts. Functionally speaking, are there really such things as matrigenes and patrigenes? The usual theory is that half a child's genes came from one parent, half from the other. How is the DNA molecule to know which gene came from which parent? In sex chromosomes, yes; in mitochondria too (all from mom). But these don't have anything to do with language.

Brown writes as though a small number of genes have been definitely identified as silenced ("imprinted") because of parental source, but I want to know how this works. Imprinted genes may be as real as black holes, but for the moment they are still only speculative possibilities based on mathematics, not on anything about the mechanisms of inheritance. Any theory of origins based on parental antagonism seems, at best, premature.

Nonetheless, Brown has a theory of "language" origins that depends on parental antagonism and which, remarkably enough, ties into an existing idea, although coming at it from a new angle. A couple of years ago I had a series of posts on Dean Falk's theory (see: Where Shall I Put the Baby; Crying with an Accent; The Oldest Form of Speech.) that pre-linguistic vocalizations began in response to a loss of body hair. Over three million years ago (for reason's unknown) the human lineage appears to have lost most of its body hair, presenting mothers with a new problem. Primate offspring stay with mother by hanging onto her body hair. Once that hair disappeared, the mother had to carry the baby in her hands, and when she had to do something else with her hands—like pick food—she had to set the baby on the ground. This change occurred before the lineage brain began to increase in size and birth became burdensome. Falk's theory is that babies began to vocalize so that the mother could maintain contact while she was on the ground.

The parental antagonism theory enriches this idea a bit. The baby's vocalizations don't just maintain contact; they reassure the mother that the baby is okay, so she does not have to keep coming back and look. I'm not sure that we need parental antagonism to account for such evolution, but the theory does focus directly on point and certainly merits being taken seriously. As Brown says about Falk, "[her] hypothesis is most obviously linked to parental antagonism, in that it involves parental investment and mother-infant bonding."

Brown is not much of a literary stylist, but his paper is well worth wading through.

Where Do We Stand with FOXP2?

A humanized mouse can teach us many things but is  unlikely to actually talk,

I've just read a review article about the Foxp2 gene and its role in the evolution of language and am happy to have been brought up to date. The big assertion in this paper is that Foxp2 is critical for learning vocalizations, maybe not so critical for other aspects of speech and language. (Wolfgang Enard, "Foxp2 and the role of cortical-basal ganglia circuits in speech and language evolution.") The paper is most notable for its presentation of specific facts that support the picture of Foxp2's role:

New Source of News

I see that the Max Planck Institute for Psycholinguistics is opening a new department on Language & Genetics. It will be the only department devoted to understanding the relation beween brain, language, and genetics. Now that's a big bite to chew.

Heading the department will be Simon Fisher, the star of the team that identified the FoxP2 gene and its relation to language. The Max Planck Institute is scattered over northern Europe. This department will be based in  Nijmegen, the Netherlands.

FoxP2 Work Contradicts Idea of a Universal Grammar

At the Utrecht conference there was some discussion about the FoxP2 gene that I have been slow to report because I have been trying to get the story straight. I have had a couple of exchanges with Morten Christiansen about his presentation and with his help I think I understand what he was talking about. The basic argument is that genes shape the brain and the brain shapes the way language is learned, thus genes like FoxP2 contribute the way language is learned. The idea changes the role I’ve seen discussed for FoxP2.

The Biology of Chatter

I was traveling last week and have not been focusing on my blog, but I do want to draw everyone’s attention to a paper published in the current Biolinguistics online journal. Titled, “The Biological Nature of Human Language,” it is signed by 14 authors, many of the distinguished linguists, and begins with an acknowledgment of the contribution of three others. So I suppose this is as close as we are going to get to a consensus from generative grammarians as to where they stand today in thinking about the nature of language. The big news seems to be the shift in emphasis from speech as a symbol processing operation to a biological process.

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.