Defender's Guide to Science and Creationism

Mark Vuletic

Assertion

Mutations are never beneficial.

Analysis

I. Disavowal by a creationist organization

There are enough examples of beneficial mutations that creationists now generally seem to acknowledge their existence, and turn to other lines of argument. The young-earth creationist organization Answers in Genesis, for instance, has declared this an argument that "should definitely not be used." They advise in its place a retreat to the vague argument that mutations cannot increase genetic information. However, there are still some holdouts, and this claim still seems to enjoy wide currency among the creationist masses, so it is worth discussing.

II. A few examples of beneficial mutations

 Here are some examples of beneficial mutations, most of which I found through a very cursory search of the scientific literature:

  1. The acquisition by Flavobacterium of the ability to hydrolyze certain industrial waste products:

    Microorganisms have acquired new enzymes that allow them to metabolize toxic industrial wastes never occurring in nature (e.g. chlorinated and fluorinated hydrocarbons), and are an increasingly important method of pollution control (Ghosal et al., Science 228: 135-142, 1985). Susumi Ohno (Proc. Natl. Acad. Sci. 81:2421-2425, 1984) found that one such new enzyme, nylon linear oligomer hydrolase, resulted from a frame-shift mutation. Frame-shift mutations scramble the entire structure of a protein, and so the enzyme is a random construct! As would be expected, this new enzyme is imperfect and has only 1% the efficiency of typical enzymes, but the important thing is that it works (Bakken)

    Since the mutation documented by Ohno allows the microorganisms in question to consume short nylon oligomers as a primary food source, it certainly qualifies as a beneficial mutation. It is interesting to note that the acquisition of this new metabolic activity has been duplicated in the laboratory (although it is not clear whether it involved the same kinds of microorganisms, the same frame-shift mutation, or the same enzyme). Richard Harter reports:

    In the experiments, non-nylon-metabolizing strains of Pseudomonas were grown with nylon oligomers available as the primary food source. Within a relatively small number of generations, they developed these enzyme activities. (Harter 1999)

    The creationist organization Answers in Genesis disputes the validity of the kind of mutation cited by Bakken, but as near as I can tell, their objections have been answered adequately by Ian Musgrave. I am in the process of reviewing the primary literature to make sure, but in the meantime, readers who would like to judge for themselves (and that should be all of you) can access the AiG article and Musgrave's response at the above links. Of course, interesting though this example is, it is probably wrong to put too much stress on it, since beneficial frame-shift mutations are generally thought by evolutionists to be particularly rare, even by the standards of beneficial mutations.

  2. Researchers working with the nematode Caenorhabditis elegans have identified "four genes, that, when mutated, can make these worms use energy more efficiently, feed and swim at a slower pace -- and live many times their normal life-span. Some of the experimental nematodes lived for almost 2 months, far longer than their expected 9 days" (Pennisi 1996:949; see also Lakowski 1996:1010-1013).

  3. A mutation increasing AIDS resistance in humans:

    Population geneticist Stephen O'Brien of the National Cancer Institute, his NCI colleagues Michael Dean and Mary Carrington, and their collaborators provide strong confirmatory evidence that people who have two mutant copies of the gene for CCRS (also known as CKRS), the chemokine receptor that HIV uses when it initially infects white cells, are highly resistant to HIV infection. Another, entirely new, finding is that people who get infected with HIV, but have one mutant copy of the CCRS gene, progress to AIDS more slowly than do people without the mutation. (Cohen 1996:1797)

III. Context-dependence of what counts as a deleterious mutation

Even some of the most seemingly deleterious mutations can have great adaptive value in certain environments. For instance, mutations that cause stunted wing growth in Drosophila increase the fly's ability to survive on islands where high winds are present (Ruse 1982:92). This helps to explain why decades of irradiating Drosophila in the laboratory produced only less fit mutants: in a population's normal environment, virtually all mutations must be neutral or deleterious, because the population is already extremely well adapted to its environment (Moore 1983:11-13). But the same mutations that are deleterious in the normal environment may become beneficial on the geographical fringes of a population, or in the event of environmental change throughout the entire geographical range of the population (a hurricane might wipe out all of the winged Drosophila on an island). It also offers a partial explanation for why evolution should be expected to proceed in a punctuated manner on the geological time scale.

IV. Neutral or beneficial macromutations

Even certain classes of macromutations can be neutral or beneficial. Richard Dawkins presents an example with snake vertebrae:

The number of vertebrae in different species of snakes varies from 200 to 350. Since all snakes are cousins of each other, and since vertebrae cannot come in halves or quarters, this must mean that, from time to time, a snake is born with at least one more, or one fewer, vertebra than its parents. These mutations deserve to be called macro-mutations, and they have evidently been incorporated in evolution because all these snakes exist. (Dawkins 1996:103)

V. The sickle-cell mutation

This is a good place to talk about the sickle-cell mutation. This mutation seems to be a stock in textbooks, probably because it is an example not only of beneficial mutation, but of heterozygote fitness. Creationists have routinely panned this example, arguing that a mutation that impairs the function of hemoglobin can hardly be called a beneficial mutation. For instance, creationist David A. Demick writes

The mutation responsible for sickle cell anemia has been put forward as an example of evolution. The problems with this is obvious, as the sickle cell mutation, like the many other described hemoglobin mutations, clearly impairs the function of the otherwise marvelously well-designed hemoglobin molecule. It can in no way be regarded as an improvement in our species, even though its incidence is enhanced in malaria endemic parts of central Africa by natural selection. (Demick 1999:3)

The problem with Demick's not wanting to count the sickle cell mutation as a beneficial mutation is actually highlighted in the last sentence of the quoted text: "its incidence is enhanced in malaria endemic parts of central Africa by natural selection." Let me repeat with added emphasis: "its incidence is enhanced in malaria endemic parts of central Africa by natural selection." How can Demick say this and yet seem to contend that it is not a beneficial mutation? Here is something that many people do not understand about mutations: the same mutation can be beneficial in one environment and harmful in another. There may well be no such thing as a mutation that is beneficial in every environment. The diversity of life is generally driven by differences in environment within a species, leading to selection for different mutations, and ultimately driving the varieties that occupy the different environments into different species.

References

Bakken GS. Creation or Evolution? Berkeley: National Center for Science Education. [Pamphlet]

Cohen J. 1996. Receptor mutations help slow disease progression. Science 273(5283):1797-1798.

Dawkins R. 1996. Climbing Mount Improbable. New York: W. W. Norton & Co.

Demick DA. 1999. The blind gunman. Impact 308. February 1999.

Harter R. 1999. Are mutations harmful? www.talkorigins.org/faqs/mutations.html.

Lakowski B and Hekimi S. 1996. Determination of life-span in Caenorhabditis elegans by four clock genes. Science 272(5264):1010-1013.

Max EE. 1999. The evolution of improved fitness by random mutation plus selection. www.talkorigins.org/faqs/fitness.html.

McGowan C. 1984. In the Beginning...: A Scientist Shows Why the Creationists are Wrong. Buffalo: Prometheus.

Moore JA. 1983. Evolution, education, and the nature of science and scientific inquiry. In Zetterberg 1983:3-17.

Pennisi E. 1996. Worm genes imply a master clock. Science 272(5264);949-950.

Ruse M. 1982. Darwinism Defended: A Guide to the Evolution Controversies. London: Addison-Wesley.

Last updated: 21 Mar 2008

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