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.
The role of chance in evolution is limited by stringent constraints
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 theappropriate 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,
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.
The role of chance in evolution is limited by stringent constraints
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 theappropriate 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,
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