Genetics of Original Sin (12 page)

Putting together natural diversity and struggle for life, Darwin arrived at the conclusion, evident for us today but visionary at the time, that, in any natural situation where there is competition for limited resources, those varieties most apt to survive and, especially, produce progeny under the prevailing conditions must automatically become preponderant (
fig. 7.1
). Hence the subtitle Darwin gave to his book:
The Preservation of Favoured Races in the Struggle for Life.
In this new view, selection, rather than being purposefully directed toward a predefined end, as in its artificial, human-devised form (such as dog breeding and the like), is taken to occur naturally, automatically, without preconceived intention. Here is where Darwin's ideas encountered the strongest resistance, lasting up to the present day; they implied a lack of purpose in nature.

Darwin conceived his theory during his famous voyage, from 1831 to 1836, on the
Beagle,
which notably led him to visit the Galápagos Islands. It is there that he made one of his most perceptive observations, namely that the finches on each island had, during their long geographical isolation, acquired differently shaped beaks adapted, in each case, to the locally available food, a paradigmatic instance of natural selection (
fig. 7.2
). Nevertheless, Darwin continually put off the publication of his theory, patiently accumulating more evidence that would either support it or disprove it, in the true spirit of objective science. It is only when Darwin was informed that his colleague Alfred Russel Wallace (1823–1913) had conceived the same theory that he decided to rush into print. Much has been written about the poor place accorded to Wallace by posterity. He certainly deserves credit for having independently thought of natural selection as an evolutionary mechanism. But to Darwin goes the immense merit of actually giving body to the idea by laboriously building a monumental set of evidence in its favor.

Fig. 7.1.
Natural selection.
This diagram illustrates the obligatory consequences of replication. As long as replication occurs faultlessly, information is faithfully transmitted from generation to generation. It is the source of genetic continuity. When, as must inevitably happen, replication is not faultless, the imperfect copies produced generate diversity, leading to competition among the variant forms for available resources. As a result of this competition, the variant form or forms best able to survive and, especially, produce progeny under prevailing conditions necessarily emerge. This is natural selection. A fact of capital importance is that copying imperfections (mutations) are chance events or, more precisely, occur in a manner in no way related to any sort of adaptive anticipation of a future environmental challenge (see intelligent design,
chapter 8
).

Fig. 7.2.
Natural selection illustrated.
The Galápagos finches. One of the main findings made by Darwin during his historic voyage on the
Beagle
(1831–1836) was that the finches on each of the Gálapagos Islands had different beak shapes, adapted to the available food. He reasoned that these adaptations had emerged by natural selection during the long period of isolation of the birds. From Charles Darwin's
On the Origin of Species
.

Today, the reality of natural selection leaves no room for doubt. Among countless examples arrayed in its support one can cite, as having taken place under our very eyes, the many cases of antibiotic resistance that developed in only a few decades after
penicillin was first used during the last war, opening the way to the discovery of a string of other, similar drugs. In each case, introduction of a new antibiotic for therapeutic use was rapidly followed by the development of pathogens resistant to the antibiotic, clearly originating from rare, naturally resistant varieties that prevailed when exposed to doses of the antibiotic that killed the more sensitive bacteria. Paradoxically, hospitals have become sites where some of the most dangerous infections may be caught, as they provide an environment particularly enriched in antibiotics and, therefore, particu-larly conducive to the selection of the most antibiotic-resistant pathogen varieties. Similar cases of resistance have been observed with herbicides, insecticides, and other pesticides, even with chemotherapeutic agents, to which resistance may build in a matter of months in the cancer cells of treated patients.

Another often-quoted example of natural selection is industrial melanism, a phenomenon that affected some English peppered moths (
Biston betularia
) that exist in two different varieties, one white, the other black. In the nineteenth century, when smoke and soot produced by the Industrial Revolution covered all surfaces with a black coating, the white moths almost completely disappeared, while the black ones flourished. The situation has reversed since the end of the Second World War, when laws were enacted to clean the air. The explanation is simple. Predators that feed on moths more readily detect the white ones on a dark background and the black ones on a light background.

A key trait of natural selection, already suspected by Darwin and now confirmed by all that has been learned since, is that
the mutations on which natural selection operates are due to
chance
(see
fig. 7.3
). Thus, one cause of mutations, inevitable, as well as unpredictable, is faulty replication. The molecular mechanism that drives this process is of astonishing fidelity, one wrongly inserted base in about one billion, the equivalent of copying the
Concise Oxford Dictionary
fifty times by hand, making a single mistake! Yet, replication mistakes are a significant cause of mutations because of the huge number of bases contained in genomes. Thus, every time a human cell divides, about half a dozen errors are made in the replicated genome. Fortunately, most of these mistakes are of no consequence. But they contribute to genomic diversity through the germ line.

Other sources of mutations are chemical alterations of DNA molecules caused by physical agents, such as ultraviolet light, X-rays, or radioactivity, by chemical agents, called mutagenic for this reason, by biological agents, such as viruses, or by faulty rearrangements in the course of recombination. Most of these agents are also carcinogenic; they cause cancer, which is often due to a mutation in the cell that initiates formation of the tumor. All these modifications are due to specific causes; but they are accidental, in the sense that they are not intentional. They are not directed toward a goal, which would be, for instance, adaptation to certain outside circumstances or accomplishment of a given evolutionary step. We shall see in the next chapter that this is a crucial point with respect to the theory of intelligent design. Note, however, that natural selection has allowed emergence of pseudo-intentional mechanisms whereby, for example, a stress situation increases the frequency of mutations, thereby enhancing the possibility that a mutation will occur that produces progeny able to survive the stress.

Fig. 7.3.
The evolutionary lottery.
A schematic representation of natural selection (see
fig. 7.1
), illustrating the two possible extreme outcomes, depending on whether chance offers only a small subset or an essentially complete array of all possible mutations to screening by natural selection. The phenomenon is ruled by contingency in the first instance, by optimization in the second.

Given that chance offers natural selection the array of mutations on which it will operate, important implications follow (
fig. 7.3
). One self-evident implication is that only a mutation included in the array offered by chance can be selected. There could be better solutions to the environmental challenge to which the organism is exposed, but if chance does not provide the
appropriate mutations, none of those solutions can materialize.

An important corollary of this implication is that the probability of a response being the best possible one depends on how many mutations are offered by chance. If all possible mutations are offered, then the response will be optimal and, therefore, reproducible if the same challenge were to arise again. This, at first sight, would seem to be an extremely unlikely situation. Somehow, when it comes to mutations affecting genomes of up to billions of bases, we intuitively think of an immense number of possibilities, of which only a small subset actually takes place at any given time. This has long been the received truth among leading evolutionists, who have all insisted on the utter contingency of the evolutionary process. The late American paleontologist and best-selling author Stephen Jay Gould vividly illustrated this view in his famous tape analogy: rewind the tape and allow it to be played again, and a completely different story will unfold.

This view ignores the enormous numbers of individuals and generations that may participate in evolution and the very long times involved. Just to give an example, a simple calculation shows that it takes twenty billion cell divisions for a given base in a given site of a genome to be replaced with a 99.9 percent probability by another given base (point mutation) as a result of a replication mistake. This may seem like a huge number. Actually, it corresponds to the number of divisions that take place in two hours in our bone marrow in the course of red blood cell renewal. In science, as in other human endeavors, intuition may be misleading.

Also, the structure of genomes is often such as to limit the number of mutations. Remember the example given above of mutability increasing in a stress situation. This could not be so if genomes were liable to suffer all possible mutations all
the time. Another factor that warrants consideration is that many different mutations often produce the same effect.

Because of these reasons, favorable mutations happen more frequently than one might be inclined to expect. In the evolutionary game, tempting chance may actually pay. Experimenters have long been empirically aware of this, when trying indiscriminate exposure to a mutagen to achieve a given result—and often succeeding. Thus, in the days when penicillin was first produced, a major breakthrough was achieved by massively exposing samples of the penicillin-producing mold to X-rays, “carpet-bombing” fashion. Mutants producing twenty times more penicillin than the parent variety were obtained by this simple device, thus suddenly making the miracle-drug available at affordable cost. Many other such examples are known.

When we look at the facts, we do indeed find that there must have been many cases in which chance has offered natural selection a large enough sample of the possible mutations to allow a near-optimal outcome. Look at biodiversity, this extraordinary collection of millions of different living species found in almost every possible habitat, from rain forests and swamps to the driest of deserts, from boiling volcanic springs to polar ice fields, from pristine mountain streams to drying brine, stinging acids, caustic alkalis, or heavy metal–laden industrial wastes. This diversity is often cited as evidence for the contingency of the evolutionary process. What it illustrates much more eloquently is the incredible adaptability of living forms, which, in the face of innumerable different challenges have so often succeeded in coming up with a survivable response.