Beneficial mutations?

To append the last post, concerning the issue of mutation as the engine that drives macroevolution, an excerpt from a terrific article by Jerry Bergman, Ph.D. which you will find here.


Evidence for Beneficial Mutations

It is also widely known that beneficial mutations are extremely rare. Some workers have estimated that far less than .01 percent of all expressed mutations are helpful to the organism. As Francisco Ayala (1978) noted “mutation is the ultimate source of all genetic variation,” but useful genetic variation “is a relatively rare event....” (p.63). Dobzhansky (1957) likewise concluded that “the mutants which arise are, with rare exceptions, deleterious to their carriers, at least in the environments which the species normally encounters” (p. 385). The conclusion that very few beneficial mutations occur in nature is still held by many today. In Strickberger’s words “new mutations that have an immediate beneficial effect on the organism seem generally to be quite rare” (2000, p. 227).

In order to locate all alleged examples of beneficial mutations, I carried out a computer search of the literature. My review covered all published scientific studies that dealt with beneficial mutations. The definition of beneficial mutation used was a mutation that was regarded as beneficial by the authors surveyed. Key words used in the computer search included synonyms of beneficial, such as “favorable, helpful, usable, valuable, adaptive, good, advantageous, supportive, positive,” etc. The search of two data bases totaling 18.8 million records found that, of all articles discussing mutations, only 0.04 percent, or 4 in 10,000 articles on mutations, were located that discussed beneficial or favorable mutations. Some overlap exists in the data bases searched, consequently the actual total number of records searched was less than 18.8 million. The overlap in the search was estimated by extrapolating from the records found. Assuming that the same level of overlap exists in the entire database, a total of approximately 16 million records was searched. These searches may have missed some relevant articles but are useful to indicate trends.

All of the 126 examples located were then reviewed, focusing on evidence for information-gaining beneficial mutations. It was found that none of them contained clear, empirically supported examples of information-gaining, beneficial mutations. Most “examples” of actual, beneficial mutations were loss mutations in which a gene was disabled or damaged, all of which were beneficial only in a limited situation.

A review of both textbooks and journal articles on evolution demonstrated that the most common examples of beneficial mutations were sickle cell anemia, bacterial resistance to antibiotics, Ancon short legged sheep, viral/bacterial immunity, and a “putative beneficial mutation for lipid transport” (Galton, et. al., 1996; Strickburger, 2000).

An example of a mutation that was beneficial in specific situations was damage to the Chemokine receptor 5, (CCR5), the principle co-receptor in T-cells that causes cells with CD4 receptors (primarily T-cells) to be unable to take the human immunodeficiency virus (HIV) into the cell. As a result, a person with this mutation has an abnormally high immunity to HIV infection (Huang, 1996; Wilkinson, 1998).

Discussion of the Beneficial Mutation Literature Review

Most of the literature covered the topic of beneficial mutations in general, and did not document specific mutations. The second largest category was literature dealing with loss mutations that were beneficial to humans only in certain situations. An example of such loss mutations, illustrating that many “beneficial mutations” were not beneficial for the animal, was a muscle mutation in the Belgian Blue breed of cattle. This is very valuable to beef farmers because it results in 20 to 30% more muscle than average. The meat is also very tender and lower in fat (Seitz, et al., 1999; McPherron, et al., 1997). A different mutation in the same gene is also responsible for the very muscular Piedmontese breed of cattle.

Muscle growth is regulated by a number of proteins, including myostatin. The Belgian Blue strain mutation deactivates the myostatin gene. Consequently, there is less regulation of the muscle growth, and the muscle bulk becomes abnormally large. Genetic engineers have bred muscular mice by using the same principle. Like seedless fruit and many similar mutations, this one is beneficial to humans only and not to the cattle. Among the mutation’s several negative side effects is a reduction of the animal’s fertility. Although this Belgian Blue mutation produces “beneficial” effects for farmers and consumers, it is the result of information loss—as are mutations that produce seedless fruit. Therefore, it is the opposite of the production of new beneficial information that would be necessary to achieve macroevolutionary changes.

Another example of a so-called “beneficial” mutation that was discovered in 1889 in Atchison, Kansas, is a mutant hornless Hereford cow. Hornless cattle suffer fewer injuries in herds, and for this reason many cattleman had been surgically dehorning their herd. The new breed eliminated this requirement, and it soon became a common domesticated breed (Walker, 1915, p. 68). In the wild, though, the Hereford cow would be at a distinct disadvantage.

The most well known loss mutation was discovered in 1791 by Seth Wright, a Massachusetts farmer. He noted that a male lamb in his flock had short, bent legs resembling a dachshund (Walker, 1915, p. 68). He realized that a flock of bowlegged sheep could not jump high fences, which could save the sheepherder time and money because only short barriers would be needed to contain them. He carefully raised this sheep, and, as the trait was evidently caused by a dominant gene, he was able to produce a new sheep “breed,” which is now called Ancon sheep (Hickman, et al., 2001). It is now realized, however, that this so-called breed is actually a usually lethal deformity that causes achondroplasia, and this “breed” has rapidly gone extinct in spite of efforts to save it.

The Number of Mutations NeoDarwinism Requires to Evolve a Species

A total of 1.7 million species of animals have been identified from comparative studies of preserved specimens (Blackmore, 2002). Researchers estimate that somewhere between 3 million and 30 million species now exist. The most common estimate is around 13 million (Margulis and Schwartz, 1998, p. 3; Blackmore, 2002).

According to an Amersham bioscience report (2001, p. 1), it is estimated that there are thousands of different proteins used in the human body (see also “Preteome” AAAS Science Netlinks). Nuclear pore complexes alone comprise 50 to 100 different proteins (Allen, 2000, p. 1651). All of them are produced by the estimated 35 to 45 thousand human genes that, according to neoDarwinists, evolved from other, less-complex, and often shorter genes. Shermer (2002, p. 229) estimates that “trillions of distinct modifications” were required to evolve humans alone. Presumably, each modification would require many mutations.

A significant fraction of open reading frames has been judged not to match any another sequence in the database, indicating that a significant number of all proteins may be unique to each genus of animal (Bailey, 2001; Siew and Fischer, 2003, p. 7). Thus, as many as 200 million different proteins may exist. From 150,000 to 250,000 extinct animal species have also been identified and reported in the paleontological literature. NeoDarwinists estimate that as many as 99 percent of all species that have ever lived are extinct (Margulis and Sagan, 2002, p. 52; Raup, 1977, p. 50). Although some claim the number is far lower, assuming this estimate to be valid would put the number of species that have ever lived at over 200 trillion!

Given the estimate that roughly an average of 1,000 transitional forms are required to evolve a species (a number that is a rough estimate and is dependant on various assumptions)—this would mean that 2x1017 transitional forms have existed. If 1,000 mutations are required for each transitional form, this would translate into 2x1020 beneficial mutations that are required. And not one clear beneficial mutation or transitional form has yet been convincingly demonstrated, although likely some do exist. The paucity of clearly helpful mutations must be considered in context with the estimate that 2x1020 mutations that are required to produce the natural living world existing today and the number of animals that are speculated to have once existed.

Given a low estimate of 1,000 steps required to evolve the average protein (if this were possible) over 2x1014 beneficial mutations would have been needed to evolve just the proteins that are estimated to exist today. So far only 60 species, including the nematode worm, humans, yeast, rice, mustard plant, and bacteria have had their DNA fully sequenced. As more life forms are sequenced, the above estimates may go either up or down. The same evolutionary problem exists in attempting to use mutations to explain the origin of the genes required to make fat, nucleic acid, carbohydrate families, and other compounds that are produced by living organisms and are necessary for life.