Wired for Culture: Origins of the Human Social Mind (38 page)

Thinking of language as a trait for promoting cooperation might give us insight into what the great, but sometimes exasperatingly gnomic, philosopher Ludwig Wittgenstein meant when he said, “If a lion could speak we could not understand him.” Maybe it is this: if a lion could speak it would not be a lion, but something more like us—we wouldn’t understand it as a
lion
. We wouldn’t understand it as a lion because lions behaving as lions don’t really have much to discuss beyond what they already achieve with their forms of communication. If they did have more to discuss, they wouldn’t be lions, but something more like Mole, Badger, and Ratty. In fact, most of the communication in animal social systems is about signaling location, or who is dominant to whom, or disputes about food, territory, or mates. These are issues that can be settled by signals of grunts, chirps, whistles, odors, chest-thumping and head-butting, bites and grimaces, and that is why animals have these systems of communication rather than language. Why talk when a roar will suffice?

An unforgettable passage from Alexander Kinglake’s
Eothen
captures the sense in which language is not merely for communicating. Meaning “from the East,”
Eothen
is a first-person account of this young Englishman’s Grand Tour of the Near East in 1834. Kinglake decided to travel by camel across the Sinai to Cairo, accompanied by a servant. After being out in the desert for several days, he describes seeing

a mere moving speck on the horizon… . Soon it appeared that three laden camels were approaching, and that two of them carried riders; in a little while we saw that one of the riders wore European dress, and at last the riders were pronounced to be an English gentleman and his servant… . As we approached each other, it became with me a question whether we should speak. I thought it likely that the stranger would accost me and in the event of his doing so I was quite ready to be as sociable and chatty as I could be, according to my nature;
but still I could not think of anything particular that I had to say to him
. Of course, among civilized people, the not having anything to say is no excuse at all for not speaking, but I was shy and indolent, and felt no great wish to stop and chat like a morning visitor in the midst of those broad solitudes. The traveler perhaps felt as I did, for, except that we lifted our hands to our caps and waved our arms in courtesy, we passed each other quite as distantly as if we had passed in Bond Street. [italics added]

As it turns out, the two protagonists eventually did speak, but only because their camels slowed up and turned around! Even then, the other man’s greeting was the meager “I dare say you wish to know how the Plague is going on at Cairo?”

It is little short of extraordinary that these two ships could almost pass in the night without speaking to each other, and strains credulity when we appreciate the setting. Kinglake’s only partly ironic use of the word “accost” to describe being spoken to tells us something of the diffident and private character of Englishmen of his day (not entirely extinct even now). But there is something more to this example than reserve. Kinglake is right: there is an element of being accosted when one is spoken to out of the blue, and this is precisely because language can zero in so quickly on matters that we might wish to keep private, matters that were they made public could damage our reputation, give away our plans or simply provide information to someone that could benefit them at our expense. Not knowing the other man on the camel, Kinglake might have concluded that he really didn’t have anything to say to him. Confronted with the same realization, the other man did what we all do when we have nothing to talk about: his remark was the equivalent of talking about the weather.

LANGUAGE, DNA, AND REGULATION

IN THIS
section I want to examine a remarkable similarity between the nature of human language and an unusual feature of our genetic systems. That similarity is that both evolved specifically to promote replicators’ interests within their vehicles—genes in their bodies on the one hand, and people in their societies on the other. Thus, we will see that the nature of our language is precisely what we would expect of a system that evolved to allow us to vary our expression—or the way we are seen—inside our cultural survival vehicles, and in a way that benefits us, just as genes can vary their expression inside our bodies in ways that benefit them. Understanding this similarity will explain why human language had to be different from all other forms of animal communication and why it had to adopt a form that we also find in our genes.

To begin this story, we need to appreciate a puzzling feature of our genetic inheritance. Our genomes represent the sum total of the genetic information on our twenty-three pairs of chromosomes. In our species, these chromosomes contain somewhere around 21,000 genes. What is perhaps surprising is that this is scarcely more than the 19,000 genes in
Caenorhabditis elegans,
a small worm about 1/32 of an inch long that lives in soil; the 15,000 genes of a fruit fly; and only four times more than the number of genes in a yeast, which is just a simple microscopic single-celled organism that causes your fruit to ferment. In spite of having similar numbers of genes to the two animals, our bodies are almost unimaginably more complicated, comprising trillions of cells making an uncountable number of connections, and building hundreds of different kinds of tissues, from eyes and muscles, to hearts (a special kind of muscle), to kidneys. Our brains alone account for many hundreds of billions of these cells, and counting the connections they make to each other is something like trying to count all the stars in the universe. By comparison,
C. elegans’
body is composed of fewer than 1,000 cells. And yeast of course doesn’t even have cells (just the single cell), much less arms or legs, digestive tracts, blood vessels, or brains.

We learn two unexpected lessons from this: one is that we are woefully underspecified. Our genes alone cannot possibly carry enough information to specify all the connections that make up our bodies. The other is that an organism’s complexity seems not to be related in any obvious way to how many genes it has. How, then, do we achieve our vastly greater biological complexity than a simple worm or fruit fly? The answer appears to reside in how we
use
our genes, and not in how many we have. For instance, all mammals have about the same number of genes, and yet they differ remarkably in how they have used them to produce their different sizes, shapes, and capabilities. How we use our genes is why we can share over 98 percent of our genes with chimpanzees but differ so utterly from them. We even have over 80 percent of our genes in common with mice, and 75 percent in common with the much-loved marsupial, the platypus. Moving outside of the mammals, you share 60 percent of your genes with a fruit fly, and even 50 percent with bananas!

A mysterious feature of our genomes that we might think of as their “dark matter”—that as-yet-unidentified substance that is thought to account for a majority of the matter in the universe—is emerging as a principal reason why we can share so many genes with these other species and yet be so different. The common view of our genomes as being packed with genes that provide the instructions to make our bodies turns out to be only a small part of the story. Our genomes contain vast stretches of DNA that are not organized into genes, and are not used for making the protein building blocks of our bodies. This is the dark matter, better known as “junk DNA,” and it comprises a startling 99 percent of our genome, and the genomes of most other “higher” organisms. It is extraordinary but true that only about 1 percent of our genomes is made up of the things we normally think of when we talk about genes. Junk DNA’s existence had been appreciated since the early part of the twentieth century, but the discovery in the late 1970s that it was present in such vast quantities was seen as “mildly shocking” even by the editor of the prestigious scientific journal
Nature
.

Much of the junk DNA exists in the form of small genetic parasites called transposons that can infect our genomes in much the same sense that a virus infects our bodies. They go by names such as
LINE-1
(
long interspersed nuclear element),
SINE
(
short interspersed nuclear element
),
P
-
elements
, and
Mariner
. They derive the name
transposon
from their capability to make a copy of themselves that gets inserted at a different place in the genome. They have been present in plants and animals for millions of years, being inherited from generation to generation and even from species to species as new species arise from old. What these genetic parasites all have in common is, like any good replicator, they are good at getting themselves copied. This is the way they reproduce, and they will do this simply because it is what they have evolved to do in competition with other transposons. They are doing this inside your body as you read this, and it is an inevitable fact of natural selection that, once transposons exist, your genome will fill up with the ones best at reproducing themselves.

It has long been a puzzle why we put up with junk DNA rather than evolve ways to remove it. One answer is that most of the time the parasites don’t affect us, they merely accumulate inside our genomes. Even then, we still have to carry this extra DNA around and replicate it along with our genes whenever one of our cells divides. Worse, on rare occasions, when one of our transposons makes a copy of itself, that new copy can get inserted inside one of our genes. This can disrupt the gene’s normal function and sometimes cause harmful effects. Some unusual cases of hemophilia and even of bowel cancer have been blamed on
LINE-1
transposons moving around inside our genomes. In fact, we now know that we have evolved “genomic immune systems” to help control transposons, much as we have bloodborne immune systems that help us fight off diseases and infections. Still, the junk DNA accumulates in our genomes because our genomic immune systems don’t catch them all and because they typically don’t remove the junk DNA, just render it inert.

But modern genomic studies have begun to supply yet another answer to why we might allow at least some of the junk to build up in our genomes. It appears our genes use it to help them make our bodies. Our meager supply of genes is not capable on its own of specifying all the necessary parts to build a body, much less the precise times they are needed and all of the connections these parts make with each other. Genes make proteins, and proteins are the building blocks of our bodies. Our hair, muscles, nerves, fingernails, blood cells, and skin are all made of different kinds of proteins. Nearly every cell in your body carries a complete copy of your genome, but only some of your genes are used in any given place in your body and at any given time. This means there must be something that tells the genes that make your eyes not to switch on in the back of your head, or genes for teeth to stay silent in your toes. Something has to provide the instructions to get genes to team up to produce complex structures such as hearts and kidneys, or the chemical networks that create our metabolism. There is no little homunculus perched on a stool inside us calling out instructions from a manual. Instead, the vast quantities of junk DNA in our genomes fortuitously seem to contain a nearly unlimited variety of different messages whose language our genes have learned.

The complexity of our bodies might be built, then, on the enormous expansion of junk DNA that began hundreds of millions of years ago in our distant ancestors. Careful research shows that by complicated chemical means a gene can use stretches of the junk DNA to regulate or control when, where, and how much it is
expressed
. A gene is expressed when it makes a protein, and just as a person uses language to express a thought, genes seem to use the vast vocabulary of sequences of junk DNA to express themselves in exactly the right amounts and at exactly the right times and places in our bodies. Our genes are using the junk DNA to promote
their
interests within our bodies because genes that make better bodies are more likely to survive and be passed on to the next generation. Incredible as it might sound, junk DNA has been a source of great evolutionary innovation, and we all might just owe our existence, at least in part, to it. Differences in gene regulation are why two animals like chimpanzees and humans can be about 98.5 percent identical in the sequences of their genes and yet be so different on the outside. Junk DNA might even have enabled the ancient biological transition from single-celled organisms like yeast to complex multicellular organisms such as ourselves, elephants, lizards, and monkeys. Yeast and other single-celled organisms don’t have arms and legs, brains and eyes, and it turns out they have very little junk DNA. This is not to say junk DNA exists for
our
good, or even for the gene’s good. It exists because it is good at making copies of itself, and genes have merely been able to exploit its presence.

Before we can grasp the significance of gene regulation to the story of human language, we need to understand one more feature of our genetic system. That feature is that our DNA is a
digital
system of inheritance. A digital signal is one, like Morse code, in which information is transmitted in distinct packets. Morse code relies on just two of these packets, a dot and a dash, and for that reason is a
binary
digital signal. Our DNA’s digital signal, rather than having just two packets, uses four distinct molecules called
bases
or
nucleotides
, and these are normally abbreviated
A
,
C
,
G
, and
T
. Digital signals are needed whenever a system requires great fidelity and great variety. The first of these, fidelity, refers to the ability to be transmitted over and over without losing the signal. Digital signals have fidelity because they have a measure of being self-correcting. If when transmitting a dot in Morse code a little bit of error creeps in, the receiver can usually recognize from the context of the broader message that the signal is still a dot. This means that when that dot is transmitted again, the error will have been removed.