Masters of the Planet (18 page)

All physical innovations originate in mutations—spontaneous changes—that constantly occur in our DNA, the hereditary molecule that makes up the chromosomes that reside in the nuclei of our cells (including the sex cells that combine at fertilization to produce each new individual). Particular stretches of the long DNA molecule equate to individual “genes,” the units of heredity that were already envisaged long before the organization of DNA was understood. It used to be thought that the genes lay along the chromosomes pretty much like beads on a string, and that each gene was coded for the production of one of the protein molecules that serve as building blocks for the multifarious kinds of tissues that make up the developing body. This tidy image fit nicely with the gradualist predictions of the Synthesis. According to this interpretation, natural selection was simply a matter of eliminating most mutations while promoting others; and evolutionary change summed out to the gradual accumulation of favorable mutations within lineages, as one bead was incrementally replaced by another. However, since the basic structure of DNA was decoded in the early 1950s, we have learned that things are not that simple at all.

This brings us back to a subject I've already briefly introduced. It has long been known that most protein-coding genes act to determine more than one physical characteristic, and that most physical features are determined by several genes. But it was widely assumed that there must have been a general relationship between the number of genes and the complexity of the organism, and the recent discovery that humans, with their billions of cells, have only around 23,000 protein-coding genes— about the same number as a tiny nematode worm with only 1,000 cells—
came
as quite a shock. What's more, the protein-coding genes turned out to make up only about two percent of the whole genome, as the totality of the DNA in our cells is called. How could so few genes govern the development of an organism as intricate and complicated as a human being? And what was the rest of the “junk” DNA doing?

The answers to the two questions are closely related. Some ingenious recent investigations have shown both that the effects of a coding gene depend largely on when and how long it is active in development, and that part of the “junk” DNA is significantly involved in switching protein-coding genes on and off during that process. It also turns out that a coding gene's effects depend on how active it is during the time it's enabled by those “switch” genes, and that yet other stretches of “regulatory” DNA govern the vigor with which the coding genes are expressed in the development of the tissues. What is more, differences in the expression of the same basic gene may have huge consequences for the phenotype (the observed features of the individual). It has turned out, for example, that the genes governing the development of chimpanzee and human brains differ much more in expression than they do in structure. Compared to their counterparts in chimpanzees, some 200 genes involved in human brain development were found in one study to be upregulated,” and thus much more active; interestingly, this difference was lower in the brain than in other tissues of the body such as testes, heart, and liver, suggesting that the brain is under peculiar constraints as far as change itself is concerned.

The system of DNA-governing-DNA is the key to how so few coding genes can do so much work. This division of labor also explains why the genomes of
all
organisms have turned out to be strikingly similar. As recently as two or three decades ago, geneticists assumed that the genes determining what a fly and a human looked like would be completely different; but we have learned since that both animals are playing to a remarkable extent with the same genetic deck. When you consider that flies and humans share a common ancestor (albeit one that lived more than half a billion years ago) this is less surprising in retrospect than it seemed at the time it was discovered. But it is nonetheless amazing that such hugely dissimilar organisms can have about a third of the same
basic
genes in common. Of course, those genes vary structurally among species—which is why they are useful to systematists trying to figure out the relationships among the organisms they study. But, especially among close relatives, the difference in the phenotypic results produced by the coding genes may be due as much to the combinations in which they act, and to variations in their timing and expression, as to their basic structures.

This fact provides the key to understanding how Nature occasionally makes those leaps that so concerned Thomas Huxley. In the 1940s, the geneticist Richard Goldschmidt found himself roundly excoriated for suggesting that subtle genetic modifications might produce large phenotypic differences; after all, this was the heyday of the Synthesis, and Goldschmidt's choice of the term “hopeful monster” to characterize the transformed organism was perhaps unfortunate. Now, however, it is well established that structurally small genetic changes can produce new adaptive types, and that such innovations can at least occasionally be evolutionarily advantageous. The classic example is furnished by the stickleback, a small fish that boasts sharp spines, derived from the pelvic skeleton, that make it hard for predators to swallow. Some bottom-living sticklebacks, however, find those spines a distinct disadvantage—they can, for example, be grabbed by dragonfly larvae anxious to feed on their possessors. As a result the bottom-livers have lost the spines, apparently quite rapidly and recently. The modification is hardly trivial, involving as it does the elimination of an important part of a complex structure. But this major physical alteration has recently been shown to have occurred in the absence of
any
change in the coding genome. Instead, a small stretch of regulatory DNA has been deleted. This has left the basic gene intact to do its essential task, but it has eradicated the development of spines by reducing its activity in a specific area of the body. A tiny change in the genome has produced major phenotypic results. Most changes on this scale will actually be disadvantageous, and mechanisms of this kind certainly do not exclude the importance in stickleback evolution of mutations with smaller, more localized, effects. However, in the bottom-feeding sticklebacks' case this particular change just happened to have been an advantageous one, and clearly it spread very rapidly.

Perhaps
the Turkana Boy's radically new bodily conformation can be attributed to a genetic event of similar kind. A minor mutation had occurred in the Boy's lineage that, through altering gene timing and expression, had radically changed its possessor's morphology—and had, entirely accidentally, opened new adaptive avenues to them. So maybe we don't need to ask ourselves why there are no harbingers of the Boy's radically new body morphology in the known fossil record. Perhaps there simply
weren't
any such intermediates—or at least none that we could reasonably expect to find on the coarse time scale that the fossil record represents. Something routine and unremarkable on the genomic level had occurred among the Boy's precursors; and it just happened to change the course of hominid history.

Further studies have shown that the Turkana Boy's rapid developmental timetable was not unusual. This somewhat apelike rapid growth seems to have been typical for hominids like
Homo ergaster
and
Homo erectus,
and results very similar to those on the Boy's teeth have been obtained from dental analyses of
Homo erectus
specimens from Java. Put together, these observations have substantial implications for what hominids of what paleoanthropologists like to call this “grade” (general kind) and time period may have been like in life. This is particularly true for the indications we have about brain growth, starting very early in the developmental process. Apes grow up much more quickly than humans do, and they go straight from juvenile to adult, omitting a prolonged adolescent developmental phase. Perhaps surprisingly, though, their gestation length is about the same as ours—though the process itself is subtly different. The main difference in the prenatal period is that, in the last trimester of pregnancy, human beings dedicate much more energy to the development of the brain than apes do. The result is that a human neonate already has a larger brain than its ape equivalent. And while this may be perfectly fine on its own, there is a pretty severe limit to the size of any head that can pass without difficulty through the fairly rigid pelvic birth canal.

Today,
Homo sapiens
is pushing uncomfortably hard against that limit, as witness to the distressingly high number of deaths in childbirth in the absence of modern medical supervision. (Somewhere in the world, a woman dies in this appalling way about every 90 seconds.) It has been
suggested
that, with their newly narrow pelvis, even a modest increase in the head size of the neonates they gave birth to might have required
Homo ergaster
mothers to have assistance during the process: a situation that would dictate some sort of midwifery. This is idea has its own implications for social and cognitive complexity, and remains speculative. What is not in doubt, though, is that obstetrical requirements inevitably restrict the amount of brain enlargement that can take place before birth, meaning that to attain their large adult brains, modern humans subsequently need to divert large amounts of energy to brain development over sustained periods of time. The upshot is that an ape is born with as much as 40 percent of the brain volume it will have as an adult, while, despite that accelerated prenatal expansion, the equivalent percentage for humans is only about 25. Hence, in contrast to the slowdown in brain growth after birth that occurs in apes and other mammals, the human brain, exceptionally, keeps on expanding at fetal rates for at least the first year of life. So, while by the end of that first year an ape's brain has already attained 80 percent of its adult size, this compares to only 50 percent in human infants—whose brains will necessarily continue growing much longer, reaching adult size around the age of seven.

The Turkana Boy died at a stage of maturity when his 880 cc brain would already have been very close to adult size, so his fossil remains can't tell us much about his early brain development. But other evidence confirms that individuals of the
Homo ergaster/Homo erectus
grade conformed much more closely to the ape pattern than to the human one in brain development, as well as in other aspects of growth. Thus a recent study of a juvenile
Homo erectus
from Java, who died perhaps as much as 1.8 million years ago at about one year of age, showed that even at this tender age its fast-developing brain was already around 72 to 84 percent of the average adult size for the species.

This accelerated schedule of brain development has implications both for the mental complexity of those ancient members of our genus, and for the kinds of lives they lived. Modern humans are “secondarily altricial,” meaning that infants of our species are produced in relatively small numbers but are helpless or extremely dependent on their parents for an extended period—a period that, in our case, is associated with a great deal of complex learning and transmission of social skills,
including
the acquisition of language. It may also be associated with an increase in the complexity of the social apparatus for bringing up infants, with more generations becoming involved in the process. Great apes become sexually mature, and conclude their key learning period, at about seven years of age. In contrast, modern human beings take almost twice as long to become sexually mature, and considerably longer still to complete their physical and emotional development. The fact that their brains are still immature and incapable of fully assessing risk is, for example, a major reason why teenage drivers have such an appalling accident rate. To be sure, the faster-developing apes are remarkably sophisticated beings, with highly nuanced societies and complex inter-individual relationships; but although they show certain rudiments of what we might in the broadest sense recognize as “culture”—the local, rather than species-wide, transmission of learned traditions—they are clearly not cultural in the highly complex human manner. Certainly, what any living human being needs to know to be an integrated member of society is hugely greater than anything an ape is required to master.

So where did the Turkana Boy and other members of the
Homo erectus
grade fit into the spectrum of developmental timetables? And how would this have affected or fed back into their cognition? Well, if we can take it at face value, the relatively fast maturation of these hominids strongly suggests that, for all their innovative physical similarities to us, on the cognitive side they were very different from today's
Homo sapiens.
They were, indeed, unique: they were neither bipedal apes nor modern humans; and though they had clearly progressed well beyond the ape stage, they led lives that were not mediated by mental equipment that was anything like our own. And while as adults they had brains that in absolute terms were considerably larger than those of the bipedal apes, those brains were not a whole lot bigger when compared to their greater body size. This is a key consideration, because the larger your body is, the more brain you need to control its basic motor and sensory functions.

Of course, the vast range of brain sizes found among cognitively normal modern humans suggests that
within
any species there is no close relationship between brain size and smarts. But
among
species the story is different. If you plot out the relationship between brain and body sizes
among
mammals in general, you find that there is indeed a strong relationship between the two variables. As body sizes increase, so do brain volumes (though typically in mammals brain volumes don't increase as fast as body size). One of the many notable features of
Homo sapiens
is that our large brains place us way above the curve that describes this basic relationship. We have much bigger brains than you would predict for a mammal of our body size. But the Turkana Boy and his kin were less remarkable in this respect. They departed much less strikingly than we do from the typical primate brain–to–body size relationship, although they also diverged from the specifically great ape pattern of relatively smaller brains with increased body size. These early members of our genus may well have been the smartest mammals of their day; but they almost certainly perceived the world, and processed information about it, differently than we do. They were a long way from being simply junior-league versions of ourselves, and we should resist the temptation to view them that way.