Most mutations are harmful

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Claim

Most mutations are neutral or harmful. We could say all, as no laboratory evidence shows beneficial mutation. Humans with mutations resulting in a (theoretically) beneficial third eye are generally not viable, because the mutation(s) which caused the third eye, also caused other deformities, and the fetus is miscarried, stillborn, or dies shortly after birth. A multitude of other (theoretically) beneficial mutations can also be cited.

Source

Responses

  1. The claim is beside the point. Evolution is a two part process—variation and selection—the claim ignores selection processes. The theory of evolution does not need more than a few adaptive or "beneficial" mutations. The number of maladaptive mutations is simply irrelevant - these mutations are selected out and the few adaptive mutations go on.
  2. Whether a mutation is harmful or beneficial or neutral in terms of increasing the functionality or survival of an organism is highly contextual: a mutation that can be harmful in one environment (such as a decreased subcutaneous fat layer on a polar animal) could turn out to be helpful if the environment changes (such as if the temperature increases). Aside from mutations which simply destroy embryonic development or cause premature death, there is no real "objective" measure of whether a mutation is harmful or not.
  3. Similarly, whether or not a mutation is ultimately harmful or beneficial can also be quite complex. Sickle Cell Anemia, although life-threatening when homozygous, can result in a benefit. People who are heterozygous for sickle cell anemia are 25% less likely to get malaria from mosquitoes, as the sickle cells die almost immediately after the malarial parasites enter them.
  4. Most mutations are actually classified as "neutral," given that their effects are not salient enough to effect an organism one way or the other at the present time. However, the accumulation of such small changes can have an effect over time, or could prove beneficial in a different context or because of a subsequent mutation.
  5. Many beneficial gene variants have been studied:
    • The CKR5 gene produces a protein which determines what is able to enter a cell. An allele produced by a single nucleotide deletion in the CKR5 gene confers resistance to HIV (Dean et al. 1996).
    • A point mutation in the LPR5 gene causes high bone density, which could be adaptive in environments where one is likely to be injured. (Boyden et al. 2002)
    • The HbS gene that causes the harmful trait of sickle cell anemia also has the benefit of providing some resistance to the disease malaria (a selective advantage in some environments).
  6. In bacteria, plasmids often mutate to grant antibiotic resistance, which is a beneficial mutation for the bacterium. As a result, penicillin and other antibiotics are now becoming much less useful than it once was.
  7. Mutations in a region of DNA following a gene duplication generally have no ill effect on the organism.
  8. There has been no human (or any vertebrate, for that matter) that has ever lived who had three functional eyes. That the claim even mentions the possibility betrays a gross ignorance of the genetic basis for bilateral symmetry. The claim is clearly a creationist Just So Story that has achieved folk tale status.

Fallacies contained in this claim

External Links

  • Mark Isaak's page for this claim [1]
  • Williams, Robert, n.d. Examples of Beneficial Mutations in Humans. [2]
  • Williams, Robert, n.d. Examples of Beneficial Mutations and Natural Selection. [3]
  • Boyden, Lynn M. et al. High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5.[4]
  • PBS evolution library, "A Mutation Story" [5]

Additional examples of beneficial mutations

References

  1. Boyden, Lynn M., Ph.D, Junhao Mao, Ph.D., Joseph Belsky, M.D., Lyle Mitzner, M.D., Anita Farhi, R.N., Mary A. Mitnick, Ph.D., Dianqing Wu, Ph.D., Karl Insogna, M.D., and Richard P. Lifton, M.D., Ph.D., 2002. High Bone Density Due to a Mutation in LDL-Receptor-Related Protein 5. New England Journal of Medicine 346: 1513-1521, May 16, 2002. [6]
  2. Dean, M. Carrington, M, et al., 1996. Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Science 273: 1856-1862. See also: Cohen, J., 1996. Receptor mutations help slow disease progression. Science 273: 1797-1798.
  3. Elena, S.F., Cooper, V.S. & Lenski, R.E., 1996. Punctuated evolution caused by selection of rare beneficial mutations. Science 272: 1802-1804.
  4. FAO/IAEA, 1977. Manual on Mutation Breeding, 2nd edition. IAEA, Vienna.
  5. Long, P., 1994 (Jan/Feb.). A town with a golden gene. Health 8: 60ff.
  6. Moffat, Anne S., 2000. Transposons help sculpt a dynamic genome. Science 289: 1455-1457.
  7. Morris, H, op cit., pg. 13.
  8. Nachman MW, Crowell SL, 2000. Estimate of the mutation rate per nucleotide in humans. Genetics 156(1): 297-304.
  9. Oliver, A. et al., 2000. High frequency of hypermutable Pseudomonas aeruginosa isolates from 30 chronically infected CF patients. Science 288: 1251. See also: Rainey & Moxon, 2000. When being hyper keeps you fit. Science 288: 1186. See also: LeClerc, J.E. & Cebula, T.A., 2000. Pseudomonas survival strategies in cystic fibrosis (letter), 2000. Science 289: 391-392.
  10. Prijambada ID et al., 1995. Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution. Applied and Environmental Microbiology 61(5): 2020-2022.
  11. Rayl, A.J.S., 2000 (2 Mar.). Mutant gene may curb vascular disease. USA Today, [www.usatoday.com/life/health/doctor/lhdoc103.htm] (link broken)
  12. Weisgraber KH, Rall Jr SC, Bersot TP, Mahley RW, Franceschini G, Sirtori CR, 1983. Apolipoprotein A-I Milano. Detection of normal A-I in affected subjects and evidence for a cysteine for arginine substitution in the variant A-I. J Biol Chem 258: 2508-2513.
  13. Wichman, H. A. et al., 1999. Different trajectories of parallel evolution during viral adaptation. Science 285: 422-424.
  14. Gene duplication. Wikipedia. Retrieved on 2008-04-14

Further Reading

  • Harter, Richard, 1999. Are mutations harmful? [7]
  • Peck, JR & Eyer-Walker, A, 1997. The muddle about mutations. Nature 387: 135-136.

Related claims

See Also

Why is Creationism not a Scientific Theory?

Acknowledgments

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