Why Evolution Is True (21 page)

Where does this genetic variation come from?
Mutations—
accidental changes in the sequence of DNA that usually occur as errors when the molecule is copied during cell division. Genetic variation generated by mutation is widespread: mutant forms of genes, for example, explain variation in human eye color, blood type, and much of our—and other species’—variation in height, weight, biochemistry, and innumerable other traits.

On the basis of many laboratory experiments, scientists have concluded that mutations occur randomly. The term “random” here has a specific meaning that is often misunderstood, even by biologists. What this means is that
mutations occur regardless of whether they would be useful to the individual.
Mutations are simply errors in DNA replication. Most of them are harmful or neutral, but a few can turn out to be useful. The useful ones are the raw material for evolution. But there is no known biological way to jack up the probability that a mutation will meet the current adaptive needs of the organism. Although it’s better for mice living on sand dunes to have lighter coats, their chance of getting such a useful mutation is no higher than for mice living on dark soil. Rather than calling mutations “random,” then, it seems more accurate to call them “indifferent”: the chance of a mutation arising is indifferent to whether it would be helpful or hurtful to the individual.

The third and last aspect of natural selection is that the genetic variation must affect an individual’s probability of leaving offspring. In the case of mice, Kaufman’s predation experiments showed that the most camouflaged mice would leave more copies of their genes. The white color of beach mice, then, meets all the criteria for having evolved as an adaptive trait.

Evolution by selection, then, is a combination of randomness and lawfulness. There is first a “random” (or “indifferent”) process—the occurrence of mutations that generate an array of genetic variants, both good and bad (in the mouse example, a variety of new coat colors); and then a “lawful” process-natural selection—that orders this variation, keeping the good and winnowing the bad (on the dunes, light-color genes increase at the expense of dark-color ones).

This brings up what is surely the most widespread misunderstanding about Darwinism: the idea that, in evolution, “everything happens by chance” (also stated as “everything happens by accident”). This common claim is flatly wrong. No evolutionist—and certainly not Darwin—ever argued that natural selection is based on chance. Quite the opposite. Could a completely random process alone make the hammering woodpecker, the tricky bee orchid, or the camouflaged katydids and beach mice? Of course not. If suddenly evolution was forced to depend on random mutations alone, species would quickly degenerate and go extinct. Chance alone cannot explain the marvelous fit between individuals and their environment.

And it doesn’t. True, the raw materials for evolution—the variations between individuals—are indeed produced by chance mutations. These mutations occur willy-nilly, regardless of whether they are good or bad for the individual. But it is
the filtering of that variation by natural selection
that produces adaptations, and natural selection is manifestly not random. It is a powerful molding force, accumulating genes that have a greater chance of being passed on than others, and in so doing making individuals ever better able to cope with their environment. It is, then, the unique combination of mutation and selection—chance and lawfulness—that tells us how organisms become adapted. Richard Dawkins provided the most concise definition of natural selection: it is “the non-random survival of random variants.”

The theory of natural selection has a big job—the biggest in biology. Its task is to explain how
every
adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. Selection must explain the evolution of complex physiological traits: the clotting of blood, the metabolic systems that transform food into energy, the marvelous immune system that can recognize and destroy thousands of foreign proteins. And what about the details of genetics itself? Why do pairs of chromosomes separate when eggs and sperm are formed? Why do we have sex at all, instead of budding off clones, as some species do? Selection has to explain behaviors, both cooperative and antagonistic. Why do lions hunt cooperatively in a pack, and yet when intruding males displace resident males from a social group, why do the intruders kill all the unweaned cubs?

And selection has to mold these features in a particular way. First, it has to create them—most often gradually—step by step from precursors. As we have seen, each newly evolved trait begins as a modification of an earlier feature. The legs of tetrapods, for example, are simply modified fins. And each step of the process, each elaboration of an adaptation, must confer a reproductive benefit on individuals possessing it. If this doesn’t happen, selection won’t work. What were the advantages of each step in the transition from a swimming fin to a walking leg? Or from an unfeathered dinosaur to one having both feathers and wings? There is no “going downhill” in the evolution of an adaptation, for selection by its very nature cannot create a step that doesn’t benefit its possessor. In the world of adaptation, we never see the sign that’s the bane of freeway drivers: “a temporary inconvenience—a permanent improvement.”

If an “adaptive” trait evolved by natural selection instead of having been created, we can make some predictions. First, in principle we should be able to imagine a plausible step-by-step scenario for the evolution of that trait, with each step raising the
fitness
(that is, the average number of offspring) of its possessor. For some traits this is easy, like the gradual alteration of the skeleton that turned land animals into whales. For others it is harder, especially for the biochemical pathways that leave no trace in the fossil record. We may never have enough information to reconstruct the evolution of many traits, or even, in extinct species, to understand precisely how those traits functioned. (What were the bony plates on the back of the
Stegosaurus
really for?) It is telling, however, that biologists haven’t found a single adaptation whose evolution absolutely
requires
an intermediate step that reduces the fitness of individuals.

Here’s another requirement. An adaptation must evolve by increasing the
reproductive output of its possessor.
For it is reproduction, not survival, that determines which genes make it to the next generation and cause evolution. Of course, passing on a gene requires that you first survive to the age at which you can have offspring. On the other hand, a gene that knocks you off
after
reproductive age incurs no evolutionary disadvantage. It will remain in the gene pool. It follows that a gene will actually be favored if it helps you reproduce in your youth but kills you in your old age. The accumulation of such genes by natural selection, in fact, is widely thought to explain why we deteriorate in so many ways (“senesce”) as we reach old age. The very genes that help you sow your wild oats when young may give you wrinkles and an enlarged prostate gland later in life.

Given how natural selection works, it shouldn’t produce adaptations that help an individual survive without also promoting reproduction. One example would be a gene that helps human females survive after menopause. Nor do we expect to see adaptations in one species that benefit only members of another species.

We can test this last prediction by looking at traits of one species that are useful to members of a second species. If those features arose by selection, we’d predict that they’ll also be useful for the first species. Take tropical acacia trees, which have swollen, hollow thorns that act as homes for colonies of fierce, stinging ants. The trees also secrete nectar and produce protein-rich bodies on their leaves that provide the ants with food. It looks as if the tree is housing and feeding the ants at its own expense. Does this violate our prediction? Not at all. In fact, harboring ants gives a tree huge benefits. First, herbivorous insects and mammals that stop by for a leafy treat are repelled by a furious ant horde—as I discovered to my chagrin when brushing up against an acacia in Costa Rica. The ants also cut down seedlings around the base of the tree—seedlings which, when larger, could compete with the tree for nutrients and light. It is easy to see how acacias that were able to enlist ants to defend them from both predators and competitors would produce more seeds than acacias lacking this ability. In every case, when one species does something to help another, it always helps itself. This is a direct prediction of evolution, and one that does not follow from the notion of special creation or intelligent design.

And adaptations always increase the fitness of the
individual,
not necessarily of the group or the species. The idea that natural selection acts “for the good of the species,” though common, is misguided. In fact, evolution can produce features that, while helping an individual, harm the species as a whole. When a group of male lions displaces the resident males of a pride, this is often followed by a gruesome slaughter of the unweaned cubs. This behavior is bad for the species since it reduces the total number of lions, increasing their likelihood of extinction. But it’s good for the invading lions, as they can quickly fertilize the females (who come back into estrus when they’re not nursing) and replace the slaughtered cubs with their own offspring. It is easy—though unsettling—to see how a gene causing infanticide would spread at the expense of “nicer” genes, which would have the invading males simply babysit the unrelated cubs. As evolution predicts, we never see adaptations that benefit the species at the expense of the individual—something that we might have expected if organisms were designed by a beneficent creator.

LET’S TAKE A BRIEF DIGRESSION HERE, because it’s important to appreciate that natural selection isn’t the only process of evolutionary change. Most biologists define evolution as a change in the proportion of
alleles
(different forms of a gene) in a population. As the frequency of “light-color” forms of the
Agouti
gene increases in a mouse population, for example, the population and its coat color evolve. But such change can happen in other ways too. Every individual has two copies of each gene, which can be identical or different. Every time sexual reproduction occurs, one member of each pair of genes from a parent makes it into the offspring, along with one from the other parent. It’s a toss-up which one of each parent’s pair gets to the next generation. If you have an AB blood type, for example (one “A” allele and one “B” allele), and produce only one child, there’s only a 50 percent chance it will get your A allele and a 50 percent chance it gets the B allele. In a one-child family, it’s a certainty that one of your alleles will be lost. The upshot is that, every generation, the genes of parents take part in a lottery whose prize is representation in the next generation. Because the number of offspring is finite, the frequencies of the genes present in the offspring won’t be present in exactly the same frequencies as in their parents. This “sampling” of genes is precisely like tossing a coin. Although there is a 50 percent chance of getting heads on any given toss, if you make only a few tosses there is a substantial chance that you’ll deviate from this expectation (in four tosses, for example, you have a 12 percent chance of getting either all heads or all tails). And so, especially in small populations, the proportion of different alleles can change over time entirely by chance. And new mutations may enter the fray and themselves rise or fall in frequency due to this random sampling. Eventually the resulting “random walk” can even cause genes to become
fixed
in the population (that is, rise to 100 percent frequency) or, alternatively, get completely lost.

Such random change in the frequency of genes over time is called
genetic drift.
It is a legitimate type of evolution, since it involves changes in the frequencies of alleles over time, but it doesn’t arise from natural selection. One example of evolution by drift may be the unusual frequencies of blood types (as in the ABO system) in the Old Order Amish and Dunker religious communities in America. These are small, isolated religious groups whose members intermarry—just the right circumstances for rapid evolution by genetic drift.

Accidents of sampling can also happen when a population is founded by just a few immigrants, as occurs when individuals colonize an island or a new area. The almost complete absence of genes producing the B blood type in Native American populations, for example, may reflect the loss of this gene in a small population of humans that colonized North America from Asia around twelve thousand years ago.

Both drift and natural selection produce the genetic change that we recognize as evolution. But there’s an important difference. Drift is a random process, while selection is the antithesis of randomness. Genetic drift can change the frequencies of alleles regardless of how useful they are to their carrier. Selection, on the other hand, always gets rid of harmful alleles and raises the frequencies of beneficial ones.

As a purely random process, genetic drift can’t cause the evolution of adaptations. It could never build a wing or an eye. That takes nonrandom natural selection. What drift
can
do is cause the evolution of features that are neither useful nor harmful to the organism. Ever prescient, Darwin himself broached this idea in
The Origin:

In fact, genetic drift is not only powerless to create adaptations, but can actually
overpower
natural selection. Especially in small populations, the sampling effect can be so large that it raises the frequency of harmful genes even though selection is working in the opposite direction. This is almost certainly why we see a high incidence of genetically based diseases in isolated human communities, including Gaucher’s disease in northern Swedes, Tay-Sachs in the Cajuns of Louisiana, and retinitis pigmentosa in the inhabitants of the island of Tristan da Cunha.