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Apologetics Press :: Sensible Science

15 Answers to John Rennie and Scientific American’s Nonsense—Argument #10
by Bert Thompson, Ph.D. and Brad Harrub, Ph.D.

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Introduction
Argument #1
Argument #2
Argument #3
Argument #4
Argument #5
Argument #6
Argument #7
Argument #8
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Argument #9
Argument #10
Argument #11
Argument #12
Argument #13
Argument #14
Argument #15
Conclusion & References


10. [Creationists suggest that] mutations are essential to evolution theory, but mutations can only eliminate traits. They cannot produce new features.

Rennie commented:

On the contrary, biology has catalogued many traits produced by point mutations (changes at precise positions in an organism’s DNA)—bacterial resistance to antibiotics, for example. Mutations that arise in the homeobox (Hox) family of development-regulating genes in animals can also have complex effects. Hox genes direct where legs, wings, antennae and body segments should grow. In fruit flies, for instance, the mutation called Antennapedia causes legs to sprout where antennae should grow. These abnormal limbs are not functional, but their existence demonstrates that genetic mistakes can produce complex structures, which natural selection can then test for possible uses (2002, 287[1]:282, parenthetical items in orig.).

In trying to go from single-celled “primitive” organisms to Homo sapiens, evolutionists commonly point to mutations as the catalyst for transforming one species into another. Simpson and Beck stated: “Mutations are the ultimate raw materials for evolution” (1965, p. 430). Evolutionist Luigi Cavalli-Sforza, head of the international human genome diversity project, remarked in his book, Genes, Peoples, and Languages:

Evolution also results from the accumulation of new information. In the case of a biological mutation, new information is provided by an error of genetic transmission (i.e., a change in the DNA during its transmission from parent to child). Genetic mutations are spontaneous, chance changes, which are rarely beneficial, and more often have no effect, or a deleterious one. Natural selection makes it possible to accept the good ones and eliminate the bad ones (2000, p. 176, emp. added).

Dr. Cavalli-Sforza is correct on one of his points, and incorrect on another. It is true that genetic mutations “most often have no effect.” Neutral mutations, as they are known, are of little use to evolutionists (see Hitching, 1982, pp. 62-63), as they themselves are dependent on still further mutations in order to be fully expressed and “useful” (in an evolutionary sense). But Dr. Cavalli-Sforza was incorrect when he stated that “new information is provided by an error of genetic transmission.” It most certainly is not! As Sarfati commented:

The issue is not new traits, but new genetic information. In no known case is antibiotic resistance the result of new information. There are several ways where an information loss can confer resistance. We have pointed out in various ways how new traits, even helpful, adaptive traits, can arise through loss of genetic information (which is to be expected from mutations) [2002a, parenthetical comment and emp. in orig.].

Mutations do not result in new information! And this is what evolution is all about. Mutations in bacteria, for example, may result in antibiotic resistance. But in the end, the resistant microorganisms are still the same species of microorganisms they were before the mutations occurred. Alan Hayward correctly noted:

...mutations do not appear to bring progressive changes. Genes seem to be built so as to allow changes to occur within certain narrow limits, and to prevent those limits from being crossed. To oversimplify a little: mutations very easily produce new varieties within a species, and might occasionally produce a new (though similar) species, but—despite enormous efforts by experimenters and breeders—mutations seem unable to produce entirely new forms of life (1985, p. 55, emp. added, parenthetical item in orig.).

In the end, after mutations have occurred, no macroevolution has taken place. None! [For a discussion of the concept of mutations and microbial antibiotic resistance, see Harrub and Thompson, 2002.]

Elsewhere, we have dealt with the concept of Hox genes, which Mr. Rennie also mentioned (see Harrub and Thompson, 2002), and so we will not deal with that subject again here in any great length. Simply put, Hox genes are pieces of DNA that either promote or inhibit other genes, which, in turn, play a role in the development of a particular organism. For instance, in the fruit fly there is a Hox gene that promotes wing development. And so, during the early stages of the fruit fly’s development, this gene signals the manufacture of wing structures. Scientists have been able to use this information to produce flies without wing, or even flies with two sets of wings. And, Hox genes even can result in already-existing information being switched on in the wrong place. But let’s not lose sight of the forest for the trees. Producing a two-winged fly, or adding a pair of legs to the head of an animal, is a far cry from explaining how plants, animals, and bacteria all descended from a nonliving source.

Hox genes themselves do not produce the information that results in such complex structures as legs, wings, antennae, or body segments (to use Mr. Rennie’s examples). Hox genes do not act in a “biological vacuum.” They rely on many other genes and proteins as valuable pieces of the overall outcome. For instance, a light switch is great for turning on a light—but only if you have the necessary wires and bulb in place “downstream” from that switch. Without those, the switch is nothing more than, well, a switch. Hox genes, like light switches, are reliant on certain postcursors (other genes that already are present). Hox genes cannot do everything “by themselves.” Keep in mind there is a well-balanced feedback mechanism in place inside every living cell. If more proteins are needed, genes are “turned on” so that those proteins can be produced. When genes mutate, this delicate balance of proteins is affected adversely, causing the production of either too much or too little of these much-needed proteins.

Just because a Hox gene can alter the development of some structure, that does not mean necessarily that all of the items necessary for that structure will be present in the newly mutated animal. For instance wings, legs, or eyes may be transplanted to various regions of the body. But experiments have shown that the muscles and nerves necessary for those structures to function normally are not routinely manufactured. So while a non-flying animal might possess a mutated Hox gene, and thus develop wings, the muscles needed for those wings to function would not necessarily be present—thereby making this new structure worthless. Hox genes are not the “magic bullet” that Mr. Rennie and his evolutionist colleagues make them out to be.


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