The Language Instinct: How the Mind Creates Language (55 page)

Let’s zoom in even closer. What primal solderer laid down the pools of neurons and the innate potential connections among them? This is one of the hottest topics in contemporary neuroscience, and we are beginning to get the glimmerings of how embryonic brains get wired. Not the language areas of humans, of course, but the eyeballs of fruit flies and the thalamuses of ferrets and the visual cortexes of cats and monkeys. Neurons destined for particular cortical areas are born in specific areas along the walls of the ventricles, the fluid-filled cavities at the center of the cerebral hemispheres. They then creep outward toward the skull into their final resting place in the cortex along guy wires formed by the glial cells (the support cells that, together with neurons, constitute the bulk of the brain). The connections between neurons in different regions of the cortex are often laid down when the intended target area releases some chemical, and the axons growing every which way from the source area “sniff out” that chemical and follow the direction in which its concentration increases, like plant roots growing toward sources of moisture and fertilizer. The axons also sense the presence of specific molecules on the glial surfaces on which they creep, and can steer themselves like Hansel and Gretel following the trail of bread crumbs. Once the axons reach the general vicinity of their target, more precise synaptic connections can be formed because the growing axons and the target neurons bear certain molecules on their surfaces that match each other like a lock and key and adhere in place. These initial connections are often quite sloppy, though, with neurons exuberantly sending out axons that grow toward, and connect to, all kinds of inappropriate targets. The inappropriate ones die off, either because their targets fail to provide some chemical necessary for their survival, or because the connections they form are not used enough once the brain turns on in fetal development.

Try to stay with me in this neuro-mythological quest: we are beginning to approach the “grammar genes.” The molecules that guide, connect, and preserve neurons are proteins. A protein is specified by a gene, and a gene is a sequence of bases in the DNA string found in a chromosome. A gene is turned on by “transcription factors” and other regulatory molecules—gadgets that latch on to a sequence of bases somewhere on a DNA molecule and unzip a neighboring stretch, allowing that gene to be transcribed into RNA, which is then translated into protein. Generally these regulatory factors are themselves proteins, so the process of building an organism is an intricate cascade of DNA making proteins, some of which interact with other DNA to make more proteins, and so on. Small differences in the timing or amount of some protein can have large effects on the organism being built.

Thus a single gene rarely specifies some identifiable part of an organism. Instead, it specifies the release of some protein at specific times in development, an ingredient of an unfathomably complex recipe, usually having some effect in molding a suite of parts that are also affected by many other genes. Brain wiring in particular has a complex relationship to the genes that lay it down. A surface molecule may not be used in a single circuit but in many circuits, each guided by a specific combination. For example, if there are three proteins, X, Y, and Z, that can sit on a membrane, one axon might glue itself to a surface that has X and Y and not Z, and another might glue itself to a surface that has Y and Z but not X. Neuroscientists estimate that about thirty thousand genes, the majority of the human genome, are used to build the brain and nervous sytem.

And it all begins with a single cell, the fertilized egg. It contains two copies of each chromosome, one from the mother, one from the father. Each parental chromosome was originally assembled in the parents’ gonads by randomly splicing together parts of the chromosomes of the two grandparents.

We have arrived at a point at which we can define what grammar genes would be. The grammar genes would be stretches of DNA that code for proteins, or trigger the transcription of proteins, in certain times and places in the brain, that guide, attract, or glue neurons into networks that, in combination with the synaptic tuning that takes place during learning, are necessary to compute the solution to some grammatical problem (like choosing an affix or a word).

So do grammar genes really exist, or is the whole idea just loopy? Can we expect the scenario in the 1990 editorial cartoon by Brian Duffy? A pig, standing upright, asks a farmer, “What’s for dinner? Not me, I hope.” The farmer says to his companion, “That’s the one that received the human gene implant.”

For any grammar gene that exists in every human being, there is currently no way to verify its existence directly. As in many cases in biology, genes are easiest to identify when they correlate with some difference between individuals, often a difference implicated in some pathology.

We certainly know that there is something in the sperm and egg that affects the language abilities of the child that grows out of their union. Stuttering, dyslexia (a difficulty in reading that is often related to a difficulty in mentally snipping syllables into their phonemes), and Specific Language Impairment (SLI) all run in families. This does not prove that they are genetic (recipes and wealth also run in families), but these three syndromes probably are. In each case there is no plausible environmental agent that could act on afflicted family members while sparing the normal ones. And the syndromes are far more likely to affect both members of a pair of identical twins, who share an environment and all their DNA, than both members of a pair of fraternal twins, who share an environment and only half of their DNA. For example, identical four-year-old twins tend to mispronounce the same words more often than fraternal twins, and if a child has Specific Language Impairment, there is an eighty percent chance that an identical twin will have it too, but only a thirty-five percent chance that a fraternal twin will have it. It would be interesting to see whether adopted children resemble their biological family members, who share their DNA but not their environments. I am unaware of any adoption study that tests for SLI or dyslexia, but one study has found that a measure of early language ability in the first year of life (a measure that combines vocabulary, vocal imitation, word combinations, jabbering, and word comprehension) was correlated with the general cognitive ability and memory of the birth mother, but not of the adoptive mother or father.

The K family, three generations of SLI sufferers, whose members say things like
Carol is cry in the church
and can not deduce the plural of
wug
, is currently one of the most dramatic demonstrations that defects in grammatical abilities might be inherited. The attention-grabbing hypothesis about a single dominant autosomal gene is based on the following Mendelian reasoning. The syndrome is suspected of being genetic because there is no plausible environmental cause that would single out some family members and spare their agemates (in one case, one fraternal twin was affected, the other not), and because the syndrome has struck fifty-three percent of the family members but strikes no more than about three percent of the population at large. (In principle, the family could just have been unlucky; after all, they were not randomly selected from the population but came to the geneticists’ attention only
because
of the high concentration of the syndrome. But it is unlikely.) A single gene is thought to be responsible because if several genes were responsible, each eroding language ability by a bit, there would be several degrees of disability among the family members, depending on how many of the damaging genes they inherited. But the syndrome seems to be all-or-none: the school system and family members all agree on who does and who does not have the impairment, and in most of Gopnik’s tests the impaired members cluster together at the low end of the scale while the normal members cluster at the high end, with no overlap. The gene is thought to be autosomal (not on the X chromosome) and dominant because the syndrome struck males and females with equal frequency, and in all cases the spouse of an impaired parent, whether husband or wife, was normal. If the gene were recessive and autosomal, it would be necessary to have two impaired parents to inherit the syndrome. If it were recessive and on the X chromosome, only males would have it; females would be carriers. And if it were dominant and on the X chromosome, an impaired father would pass it on to all of his daughters and none of his sons, because sons get their X chromosome from their mother, and daughters get one from each parent. But one of the daughters of an impaired man was normal.

This single gene is not, repeat not, responsible for all the circuitry underlying grammar, contrary to the Associated Press, James Kilpatrick, et al. Remember that a single defective component can bring a complex machine to a halt even when the machine needs many properly functioning parts to work. In fact, it is possible that the normal version of the gene does not build grammar circuitry at all. Maybe the defective version manufactures a protein that gets in the way of some chemical process necessary for laying down the language circuits. Maybe it causes some adjacent area in the brain to overgrow its own territory and spill into the territory ordinarily allotted to language.

But the discovery is still quite interesting. Most of the language-impaired family members were average in intelligence, and there are sufferers in other families who are way above average; one boy studied by Gopnik was tops in his math class. So the syndrome shows that there must be some pattern of genetically guided events in the development in the brain (namely, the events disrupted in this syndrome) that is specialized for the wiring in of linguistic computation. And these construction sites seem to involve circuitry necessary for the processing of grammar in the mind, not just the articulation of speech sounds by the mouth or the perception of speech sounds by the ear. Though the afflicted family members as children suffered from difficulties in articulating speech and developed language late, most of them outgrew the articulation problems, and their lasting deficits involve grammar. For example, although the impaired family members often leave off the -
ed
and -
s
suffixes, it is not because they cannot hear or say those sounds; they easily discriminate between
car
and
card
, and never pronounce
nose
as
no
. In other words, they treat a sound differently when it is a permanent part of a word and when it is added to a word by a rule of grammar.

Equally interestingly, the impairment does not wipe out any part of grammar completely, nor does it compromise all parts equally. Though the impaired family members had trouble changing the tense of test sentences and applying suffixes in their spontaneous speech, they were not hopeless; they just performed far less accurately than their unimpaired relatives. These probabilistic deficits seemed to be concentrated in morphology and the features it manipulates, like tense, person, and number; other aspects of grammar were less affected. The impaired members could, for example, detect verb phrase violations in sentences like
The nice girl gives
and
The girl eats a, cookie to the boy
, and could act out many complex commands. The lack of an exact correspondence between a gene and a single function is exactly what we would expect, knowing how genes work.

So for now there is suggestive evidence for grammar genes, in the sense of genes whose effects seem most specific to the development of the circuits underlying parts of grammar. The chromosomal locus of the putative gene is completely unknown, as is its effect on the structure of the brain. But blood samples are being drawn from the family for genetic analysis, and MRI scans of brains from other individuals with Specific Language Impairment have already been found to lack the asymmetry in the perisylvian areas that we find in linguistically normal brains. Other researchers on language disorders, some excited by Gopnik’s claims, others skeptical of them, have begun to screen their patients with careful tests of their grammatical abilities and their family histories. They are seeking to determine how commonly Specific Language Impairment is inherited and how many distinct syndromes of the impairment there might be. You can expect to read about some interesting discoveries about the neurology and genetics of language in the next few years.

In modern biology, it is hard to discuss genes without discussing genetic variation. Aside from identical twins, no two people—in fact, no two sexually reproducing organisms—are genetically identical. If this were not true, evolution as we know it could not have happened. If there are language genes, then, shouldn’t normal people be innately different from one another in their linguistic abilities? Are they? Must I qualify everything I have said about language and its development, because no two people have the same language instinct?

It is easy to get carried away with the geneticists’ discovery that many of our genes are as distinctive as our fingerprints. After all, you can open up any page of
Grey’s Anatomy
and expect to find a depiction of organs and their parts and arrangements that will be true of any normal person. (Everyone has a heart with four chambers, a liver, and so on.) The biological anthropologist John Tooby and the cognitive psychologist Leda Cosmides have resolved the apparent paradox.

Tooby and Cosmides argue that differences between people must be minor quantitative variations, not qualitatively different designs. The reason is sex. Imagine that two people were really built from fundamentally different designs: either physical designs, like the structure of the lungs, or neurological designs, like the circuitry underlying some cognitive process. Complex machines require many finely meshing parts, which in turn require many genes to build them. But the chromosomes are randomly snipped, spliced, and shuffled during the formation of sex cells, and then are paired with other chimeras at fertilization. If two people really had different designs, their offspring would inherit a mishmash of fragments from the genetic blueprints of each—as if the plans for two cars were cut up with scissors and the pieces taped back together without our caring about which scrap originally came from which car. If the cars are of different designs, like a Ferrari and a jeep, the resulting contraption, if it could be built at all, would certainly not get anywhere. Only if the two designs were extremely similar to begin with could the new pastiche work.