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Mutation: Difference between revisions
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Mutations are classified as harmful, beneficial, or neutral. | Mutations are classified as harmful, beneficial, or neutral. | ||
* Harmful - spontaneous changes to [[genes]] will render [[proteins]] dysfunctional, and can lead to physical deformation, cancer, or death. | * Harmful - spontaneous changes to [[genes]] will render [[proteins]] dysfunctional, and can lead to physical deformation, cancer, or death. | ||
* Beneficial - mutations that produce some benefit can theoretically happen even | * Beneficial - mutations that produce some benefit can theoretically happen, even though the protein loses all or some of its function. | ||
* Neutral - mutation where there is no effect (also known as a silent mutation). A neutral mutation either results | * Neutral - mutation where there is no effect (also known as a silent mutation). A neutral mutation either results from a codon that is translated into the same amino acid during [[gene expression]], or a changed amino acid that has no effect on [[protein]] function. The following table shows several codons that are each translated into the same amino acid. In each case, the 3rd [[nucleotide]] in the codon would be a neutral mutation if changed. | ||
<center> | <center> | ||
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|- | |- | ||
| '''Codon''' | | '''Codon''' | ||
| TCT | | TCT | ||
| CTT | | CTT | ||
| CCT | | CCT | ||
| CGT | | CGT | ||
| ACT | | ACT | ||
| Line 31: | Line 31: | ||
| '''Codon''' | | '''Codon''' | ||
| TCC | | TCC | ||
| CTC | | CTC | ||
| CCC | | CCC | ||
| CGT | | CGT | ||
| ACC | | ACC | ||
|- | |- | ||
| '''Codon''' | | '''Codon''' | ||
| TCA | | TCA | ||
| CTA | | CTA | ||
| CCA | | CCA | ||
| CGT | | CGT | ||
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and | and | ||
{{cquote|We see then that the mutation reduces the specificity of the ribosome protein and that means a loss of genetic information. ... Rather than saying the bacterium gained [[antibiotic resistance|resistance to the antibiotic]], it is more correct to say that is lost sensitivity to it. ... All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.}}[http://en.wikipedia.org/wiki/Lee_Spetner] | {{cquote|We see then that the mutation reduces the specificity of the ribosome protein and that means a loss of genetic information. ... Rather than saying the bacterium gained [[antibiotic resistance|resistance to the antibiotic]], it is more correct to say that is lost sensitivity to it. ... All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.}}<ref>Wikipedia contributors. [http://en.wikipedia.org/wiki/Lee_Spetner Lee Spetner.] English Wikipedia.</ref> | ||
Georgia Purdom from AiG, Ph.D. of molecular genetics, has stated, | Georgia Purdom from AiG, Ph.D. of molecular genetics, has stated, | ||
{{cquote|Mutations only alter current genetic information; they have never, ''ever'' been observed to add genetic information; they can only change what is there. I have a lot of papers come across my desk of supposedly mutations that have added genetic information, and I've read them all, and I've looked at them all, and never, ''once'' have I seen one that has added genetic information; they just don't do that.}} [http://www.answersingenesis.org/home/area/bios/g_purdom.asp][http://www.youtube.com/watch?v=W6WFUCJNu2w] | {{cquote|Mutations only alter current genetic information; they have never, ''ever'' been observed to add genetic information; they can only change what is there. I have a lot of papers come across my desk of supposedly mutations that have added genetic information, and I've read them all, and I've looked at them all, and never, ''once'' have I seen one that has added genetic information; they just don't do that.}} <ref>Answers in Genesis. [http://www.answersingenesis.org/home/area/bios/g_purdom.asp Dr. Georgia Purdom: Molecular Geneticist, Speaker, Author, Researcher.]</ref><ref>Purdom, Georgia. [http://www.youtube.com/watch?v=W6WFUCJNu2w "Beneficial" Mutations: Big Fairy Tale!] Via YouTube.</ref> | ||
== Mathematical challenge == | == Mathematical challenge == | ||
Mutations either beneficial, negative or neutral are rare instances. They happen on average about once in every 10 million duplications of the DNA molecule (10<sup>7</sup>, a one followed by 7 zeroes). For evolution to progress, organisms require a series of related mutations to occur. The odds of getting two mutations that are related to one another is the product of their separate probabilities. If every 10<sup>7</sup> duplications of DNA a mutation occurs the equation would start to look like this; 10<sup>7</sup> x 10<sup>7</sup> or 10<sup>14</sup>. a one followed by 14 zeroes, a hundred trillion. Mutations which are related or not would barely change finch beak sizes due to drought, or change the shape of a fly wing. | Mutations either beneficial, negative or neutral are rare instances. They happen on average about once in every 10 million duplications of the DNA molecule (10<sup>7</sup>, a one followed by 7 zeroes). For evolution to progress, organisms require a series of related mutations to occur. The odds of getting two mutations that are related to one another is the product of their separate probabilities. If every 10<sup>7</sup> duplications of DNA a mutation occurs the equation would start to look like this; 10<sup>7</sup> x 10<sup>7</sup> or 10<sup>14</sup>. a one followed by 14 zeroes, a hundred trillion. Mutations which are related or not would barely change finch beak sizes due to drought, or change the shape of a fly wing. | ||
What are the odds of getting three related mutations? That is, again taking into account the mutation rate of duplicated DNA, one in a billion trillion or 10<sup>21</sup>. Suddenly the [[ocean]] isn't big enough to hold enough bacteria to make that chance very likely. You can quickly tell that at just three related mutations, evolution via related, dependent mutational change through [[natural selection]] as its mechanism to produce truly novel information or molecule-to-man change is woefully inadequate. <ref>[http://www.sciencemag.org/cgi/content/citation/160/3826/408 Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution] By Paul S. Moorhead, Martin M. Kaplan; Wistar Institute Symposium; ''Science'' Vol. 160. no. 3826, p. 408, 1967</ref> <ref>Dr. Gary Parker. ''Creation: Facts of Life'' [http://www.answersingenesis.org/home/area/cfol/ch2-mutations.asp] </ref> | What are the odds of getting three related mutations? That is, again taking into account the mutation rate of duplicated DNA, one in a billion trillion or 10<sup>21</sup>. Suddenly the [[ocean]] isn't big enough to hold enough bacteria to make that chance very likely. You can quickly tell that at just three related mutations, evolution via related, dependent mutational change through [[natural selection]] as its mechanism to produce truly novel information or molecule-to-man change is woefully inadequate.<ref>[http://www.sciencemag.org/cgi/content/citation/160/3826/408 Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution] By Paul S. Moorhead, Martin M. Kaplan; Wistar Institute Symposium; ''Science'' Vol. 160. no. 3826, p. 408, 1967</ref><ref>Dr. Gary Parker. ''Creation: Facts of Life'' [http://www.answersingenesis.org/home/area/cfol/ch2-mutations.asp Mutations, Yes; Evolution, No.]</ref> | ||
==Mutation load== | ==Mutation load== | ||
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April of 2007 paper by the ''Proceedings of the National Academy of Sciences'' (PNAS) states that: | April of 2007 paper by the ''Proceedings of the National Academy of Sciences'' (PNAS) states that: | ||
{{cquote|Our theoretical findings indicate that mutator hitchhiking can set in motion a self-reinforcing loss of replication fidelity, but the question of how a process as robust as natural selection could allow this to happen remains. The key fact is that natural selection, although eminently robust, is a short-sighted process that favors traits with immediate fitness benefits. The fitness cost of mutator hitchhiking is generally not anticipated because of the slow accumulation of deleterious load. When a mutator hitchhikes with a new beneficial mutation, a simple model shows that the increased deleterious load due to the mutator is in fact suppressed during the spread of the beneficial mutation. Indeed, the full fitness cost of the mutator is only realized well after the beneficial mutation has stopped spreading (''SI Text''). A mutator may therefore enjoy the immediate benefit of producing a new beneficial mutation without anticipating the eventual increase in deleterious load. Because of this delay in the accumulation of deleterious load, natural selection can drive mutation rate up to the point of no return, where fM<sup>m</sup>M<sup>u</sup><sup>2</sup> becomes the dominant term ([http://www.pnas.org/content/vol104/issue15/images/large/zpq0130757960004.jpeg Fig. 4A]); even if the increase in deleterious load is lethal, it is not anticipated ([http://www.pnas.org/content/vol104/issue15/images/large/zpq0130757960004.jpeg Fig. 4B]). At the population level, this failure to anticipate the establishment of a lethal deleterious load is partly due to the sharpness of the threshold separating lethal from viable mutation rates ([http://www.pnas.org/cgi/content/full/104/15/6266#B22 22, 24]), such that there is no slow fitness decrease to "warn" of impending extinction. <ref>[http://www.pnas.org/cgi/content/abstract/0607280104v1 ''Complete genetic linkage can subvert natural selection''] by Philip J. Gerrish, Alexandre Colato, Alan S. Perelson, and Paul D. Sniegowski, ''Proceedings of the National Academy of Sciences'' USA, published online before print April 3, 2007 | {{cquote|Our theoretical findings indicate that mutator hitchhiking can set in motion a self-reinforcing loss of replication fidelity, but the question of how a process as robust as natural selection could allow this to happen remains. The key fact is that natural selection, although eminently robust, is a short-sighted process that favors traits with immediate fitness benefits. The fitness cost of mutator hitchhiking is generally not anticipated because of the slow accumulation of deleterious load. When a mutator hitchhikes with a new beneficial mutation, a simple model shows that the increased deleterious load due to the mutator is in fact suppressed during the spread of the beneficial mutation. Indeed, the full fitness cost of the mutator is only realized well after the beneficial mutation has stopped spreading (''SI Text''). A mutator may therefore enjoy the immediate benefit of producing a new beneficial mutation without anticipating the eventual increase in deleterious load. Because of this delay in the accumulation of deleterious load, natural selection can drive mutation rate up to the point of no return, where fM<sup>m</sup>M<sup>u</sup><sup>2</sup> becomes the dominant term ([http://www.pnas.org/content/vol104/issue15/images/large/zpq0130757960004.jpeg Fig. 4A]); even if the increase in deleterious load is lethal, it is not anticipated ([http://www.pnas.org/content/vol104/issue15/images/large/zpq0130757960004.jpeg Fig. 4B]). At the population level, this failure to anticipate the establishment of a lethal deleterious load is partly due to the sharpness of the threshold separating lethal from viable mutation rates ([http://www.pnas.org/cgi/content/full/104/15/6266#B22 22, 24]), such that there is no slow fitness decrease to "warn" of impending extinction.<ref>[http://www.pnas.org/cgi/content/abstract/0607280104v1 ''Complete genetic linkage can subvert natural selection''] by Philip J. Gerrish, Alexandre Colato, Alan S. Perelson, and Paul D. Sniegowski, ''Proceedings of the National Academy of Sciences'' USA, published online before print April 3, 2007 | ||
</ref> }} | </ref> }} | ||
