Mutations are not adaptive:
In the twentieth century, the theory of evolution predicted that mutations are not adaptive or directed. In other words, mutations were believed to be random with respect to the needs of the individual. As Julian Huxley put it, “Mutation merely provides the raw material of evolution; it is a random affair, and takes place in all directions. … in all cases they are random in relation to evolution. Their effects are not related to the needs of the organisms.” (Huxley, 36) Or as Jacques Monod explained:
chance alone is at the source of every innovation, of all creation in the biosphere. Pure chance, absolutely free but blind, at the very root of the stupendous edifice of evolution: this central concept of modern biology is no longer one among other possible or even conceivable hypotheses. It is today the sole conceivable hypothesis, the only one that squares with observed and tested fact. And nothing warrants the supposition—or the hope—that on this score our position is likely ever to be revised. (Monod, 112)
Ronald Fisher wrote that mutations are “random with respect to the organism’s need” (Orr). This fundamental prediction persisted for decades as a recent paper explained: “mutation is assumed to create heritable variation that is random and undirected.” (Chen, Lowenfeld and Cullis)
But that assumption is now known to be false. The first problem is that the mutation rate is adaptive. For instance, when a population of bacteria is subjected to harsh conditions it tends to increase its mutation rate. It is as though a signal has been sent saying, “It is time to adapt.” Also, a small fraction of the population increases its mutation rates even higher yet. These hypermutators ensure that an even greater variety of adaptive change is explored. (Foster) Experiments have also discovered that duplicated DNA segments may be subject to higher mutation rates. Since the segment is a duplicate it is less important to preserve and, like a test bed, appears to be used to experiment with new designs. (Wright)
The second problem is that organisms use strategies to direct the mutations according to the threat. Adaptive mutations have been extensively studied in bacteria. Experiments typically alter the bacteria food supply or apply some other environmental stress causing mutations that target the specific environmental stress. (Burkala, et. al.; Moxon, et. al; Wright) Adaptive mutations have also been observed in yeast (Fidalgo, et. al.; David, et. al.) and flax plants. (Johnson, Moss and Cullis) One experiment found repeatable mutations in flax in response to fertilizer levels. (Chen, Schneeberger and Cullis) Another exposed the flax to four different growth conditions and found that environmental stress can induce mutations that result in “sizeable, rapid, adaptive evolutionary responses.” (Chen, Lowenfeld and Cullis) In response to this failed prediction some evolutionists now are saying that evolution somehow created the mechanisms that cause mutations to be adaptive.
References
Burkala, E., et. al. 2007. “Secondary structures as predictors of mutation potential in the lacZ gene of Escherichia coli.” Microbiology 153:2180-2189.
Chen, Y., R. Lowenfeld, C. Cullis. 2009. “An environmentally induced adaptive (?) insertion event in flax.” International Journal of Genetics and Molecular Biology 1:38-47.
Chen, Y., R. Schneeberger, C. Cullis. 2005. “A site-specific insertion sequence in flax genotrophs induced by environment.” New Phytologist 167:171-180.
David, L., et. al. 2010. “Inherited adaptation of genome-rewired cells in response to a challenging environment.” HFSP Journal 4:131–141.
Fidalgo, M., et. al. 2006. “Adaptive evolution by mutations in the FLO11 gene.” Proceedings of the National Academy of Sciences 103:11228-11233.
Foster, P. 2005. “Stress responses and genetic variation in bacteria.” Mutation Research / Fundamental and Molecular Mechanisms of Mutagenesis 569:3-11.
Huxley, Julian. 1953. Evolution in Action. New York: Signet Science Library Book.
Johnson, C., T. Moss, C. Cullis. 2011. “Environmentally induced heritable changes in flax.” J Visualized Experiments 47:2332.
Monod, Jacques. 1971. Chance & Necessity. New York: Vintage Books.
Moxon, E., et. al. 1994. “Adaptive evolution of highly mutable loci in pathogenic bacteria.” Current Biology 4:24-33.
Orr, H. 2005. “The genetic theory of adaptation: a brief history.” Nature Review Genetics 6:119-127.
Wright, B. 2000. “A biochemical mechanism for nonrandom mutations and evolution.” J Bacteriology 182:2993-3001.
In the twentieth century, the theory of evolution predicted that mutations are not adaptive or directed. In other words, mutations were believed to be random with respect to the needs of the individual. As Julian Huxley put it, “Mutation merely provides the raw material of evolution; it is a random affair, and takes place in all directions. … in all cases they are random in relation to evolution. Their effects are not related to the needs of the organisms.” (Huxley, 36) Or as Jacques Monod explained:
chance alone is at the source of every innovation, of all creation in the biosphere. Pure chance, absolutely free but blind, at the very root of the stupendous edifice of evolution: this central concept of modern biology is no longer one among other possible or even conceivable hypotheses. It is today the sole conceivable hypothesis, the only one that squares with observed and tested fact. And nothing warrants the supposition—or the hope—that on this score our position is likely ever to be revised. (Monod, 112)
Ronald Fisher wrote that mutations are “random with respect to the organism’s need” (Orr). This fundamental prediction persisted for decades as a recent paper explained: “mutation is assumed to create heritable variation that is random and undirected.” (Chen, Lowenfeld and Cullis)
But that assumption is now known to be false. The first problem is that the mutation rate is adaptive. For instance, when a population of bacteria is subjected to harsh conditions it tends to increase its mutation rate. It is as though a signal has been sent saying, “It is time to adapt.” Also, a small fraction of the population increases its mutation rates even higher yet. These hypermutators ensure that an even greater variety of adaptive change is explored. (Foster) Experiments have also discovered that duplicated DNA segments may be subject to higher mutation rates. Since the segment is a duplicate it is less important to preserve and, like a test bed, appears to be used to experiment with new designs. (Wright)
The second problem is that organisms use strategies to direct the mutations according to the threat. Adaptive mutations have been extensively studied in bacteria. Experiments typically alter the bacteria food supply or apply some other environmental stress causing mutations that target the specific environmental stress. (Burkala, et. al.; Moxon, et. al; Wright) Adaptive mutations have also been observed in yeast (Fidalgo, et. al.; David, et. al.) and flax plants. (Johnson, Moss and Cullis) One experiment found repeatable mutations in flax in response to fertilizer levels. (Chen, Schneeberger and Cullis) Another exposed the flax to four different growth conditions and found that environmental stress can induce mutations that result in “sizeable, rapid, adaptive evolutionary responses.” (Chen, Lowenfeld and Cullis) In response to this failed prediction some evolutionists now are saying that evolution somehow created the mechanisms that cause mutations to be adaptive.
References
Burkala, E., et. al. 2007. “Secondary structures as predictors of mutation potential in the lacZ gene of Escherichia coli.” Microbiology 153:2180-2189.
Chen, Y., R. Lowenfeld, C. Cullis. 2009. “An environmentally induced adaptive (?) insertion event in flax.” International Journal of Genetics and Molecular Biology 1:38-47.
Chen, Y., R. Schneeberger, C. Cullis. 2005. “A site-specific insertion sequence in flax genotrophs induced by environment.” New Phytologist 167:171-180.
David, L., et. al. 2010. “Inherited adaptation of genome-rewired cells in response to a challenging environment.” HFSP Journal 4:131–141.
Fidalgo, M., et. al. 2006. “Adaptive evolution by mutations in the FLO11 gene.” Proceedings of the National Academy of Sciences 103:11228-11233.
Foster, P. 2005. “Stress responses and genetic variation in bacteria.” Mutation Research / Fundamental and Molecular Mechanisms of Mutagenesis 569:3-11.
Huxley, Julian. 1953. Evolution in Action. New York: Signet Science Library Book.
Johnson, C., T. Moss, C. Cullis. 2011. “Environmentally induced heritable changes in flax.” J Visualized Experiments 47:2332.
Monod, Jacques. 1971. Chance & Necessity. New York: Vintage Books.
Moxon, E., et. al. 1994. “Adaptive evolution of highly mutable loci in pathogenic bacteria.” Current Biology 4:24-33.
Orr, H. 2005. “The genetic theory of adaptation: a brief history.” Nature Review Genetics 6:119-127.
Wright, B. 2000. “A biochemical mechanism for nonrandom mutations and evolution.” J Bacteriology 182:2993-3001.
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