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If even one of the [[nucleotides]] in a [[gene]] is changed to another, then a new variation of the [[allele]] has been added to the population, and a different amino acid may be assembled into the [[protein]] during [[gene expression]].
If even one of the [[nucleotides]] in a [[gene]] is changed to another, then a new variation of the [[allele]] has been added to the population, and a different amino acid may be assembled into the [[protein]] during [[gene expression]].


== Types of Mutations ==
== Types ==
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.
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== Mutations and Evolution ==
== Evolution ==
It is clear that new [[gene]] [[alleles]] are accumulating in populations today, but there are two possible sources for these changes; mutations, and intentional changes introduced by [[genetic recombination]]. The [[theory of evolution]] attributes the continued production of genetic diversity to mutations, but [[evolutionists]] overlook the fact that the [[cell]] was [[intelligent design|intelligently designed]]. The cellular machinery was programmed to perform a level of self genetic engineering, and is editing genes systematically so that organisms can [[adaptation|adapt]] to a wide variety of environmental conditions.  
It is clear that new [[gene]] [[alleles]] are accumulating in populations today, but there are two possible sources for these changes; mutations, and intentional changes introduced by [[genetic recombination]]. The [[theory of evolution]] attributes the continued production of genetic diversity to mutations, but [[evolutionists]] overlook the fact that the [[cell]] was [[intelligent design|intelligently designed]]. The cellular machinery was programmed to perform a level of self genetic engineering, and is editing genes systematically so that organisms can [[adaptation|adapt]] to a wide variety of environmental conditions.  


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Despite the few examples of genetic mutations that increase the information in the genome, it is unrealistic to assume that this information would assemble in the first place because there would be no genetic information for mutations to act upon. New beneficial types of structures and functions not already resident in the gene pool of the [[species]] are highly unlikely through the process of mutation. This is to say that mutations are not a reasonable means of producing cascading morphological change and to suggest that the evidence would support the neodarwinian mechanism is unfounded.
Despite the few examples of genetic mutations that increase the information in the genome, it is unrealistic to assume that this information would assemble in the first place because there would be no genetic information for mutations to act upon. New beneficial types of structures and functions not already resident in the gene pool of the [[species]] are highly unlikely through the process of mutation. This is to say that mutations are not a reasonable means of producing cascading morphological change and to suggest that the evidence would support the neodarwinian mechanism is unfounded.


=== Mutations reduce rather then increase information ===
=== Mutations reduce information ===
Obviously mutations can indeed cause dramatic changes. Many experiments have been performed on fruit flies (Drosophila) where poisons and radiation induced mutations. However, the problem is that they are always deleterious. The Drosophila experiments showed an extra pair of wings on a fly, but these were a hindrance to flying because there are no accompanying muscles. Therefore, these flies would be eliminated by natural selection. Even in the case of mutations which can change the amount of DNA possessed by an organism, an increase in the amount of DNA does not result in increased function. Biophysicist Dr. [[Lee Spetner]] in his book, ''[http://store.nwcreation.net/notbychshmot.html Not by Chance: Shattering the Modern Theory of Evolution]'', analyzed examples of mutational changes that evolutionists claimed were increases in information, and demonstrated that they were actually examples of loss of specificity, meaning loss of information.
Obviously mutations can indeed cause dramatic changes. Many experiments have been performed on fruit flies (Drosophila) where poisons and radiation induced mutations. However, the problem is that they are always deleterious. The Drosophila experiments showed an extra pair of wings on a fly, but these were a hindrance to flying because there are no accompanying muscles. Therefore, these flies would be eliminated by natural selection. Even in the case of mutations which can change the amount of DNA possessed by an organism, an increase in the amount of DNA does not result in increased function. Biophysicist Dr. [[Lee Spetner]] in his book, ''[http://store.nwcreation.net/notbychshmot.html Not by Chance: Shattering the Modern Theory of Evolution]'', analyzed examples of mutational changes that evolutionists claimed were increases in information, and demonstrated that they were actually examples of loss of specificity, meaning loss of information.


{{cquote|In all the reading I've done in the life-sciences literature, I've never found a mutation that added information. … All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it." - Spetner}}
{{cquote|In all the reading I've done in the life-sciences literature, I've never found a mutation that added information. … All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it." - Spetner}}
===Beneficial effect of mutations is dangerous===
This is not to invalidate beneficial mutations by any means, what is merely trying to be emphasized is the essence of mutational change is degradation of the genome as time goes on. Recently as of April of 2007, such findings have been clearly observed in many instances. The ''Proceedings of the National Academy of Sciences'' (PNAS) had published within it an online paper. The definate conclusion implied is that when beneficial mutations begin to accumulate, natural selection takes hold and accelerates the mutation rate. Since benefits to fitness are being produced they begin to establish themselves in a population, eventually however there is, "increased deleterious load," because the findings show natural selection as inevitably short-sided.
The paper released titled, ''Complete genetic linkage can subvert natural selection'' states that:
{{cquote|'''How Genetic Linkage Can Subvert Natural Selection.''' There is almost certainly no physiological barrier to such an effect in most organisms: the genomic mutation rate in organisms from viruses to eukaryotes is a quantitative trait affected by many mutations whose effects can readily cumulate to intolerable levels of error. In what follows, we show that there need not be a selective barrier to this process either: because the full fitness effect of increased deleterious mutation takes some time to accumulate after a higher mutation rate has evolved, it is theoretically possible for a population to evolve a critically high mutation rate and subsequently go extinct.
...
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> }}


=== Mathematical challenges ===
=== Mathematical challenges ===
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====Protein folds====
====Protein folds====
Calculations have been done and research published in the ''Journal of Molecular Biology'' by Douglas Axe, a [[protein]] scientist. He shows just how exceptionally rare the chance of getting certain working protein sequences can be let alone whole genomic structure evolution from fish to man as ultimately predicted. In other words, as Dr. Axe wrote regarding the probability it is, "''less than one in a trillion trillion trillion trillion trillion trillion.''" <ref>D.D. Axe, “''Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds'',” Journal of Molecular Biology, 341(5) (2004):1295–1315</ref>
Calculations have been done and research published in the ''Journal of Molecular Biology'' by Douglas Axe, a [[protein]] scientist. He shows just how exceptionally rare the chance of getting certain working protein sequences can be let alone whole genomic structure evolution from fish to man as ultimately predicted. In other words, as Dr. Axe wrote regarding the probability it is, "''less than one in a trillion trillion trillion trillion trillion trillion.''" <ref>D.D. Axe, “''Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds'',” Journal of Molecular Biology, 341(5) (2004):1295–1315</ref>
===Mutation load===
Although beneficial mutations are theoretically possible, [[natural selection]] does not act at the molecular level, but rather it operates only at the level of the [[organism]]. It selects only those mutations that produce a physiological change, which alters the survival or reproductive rate of the organism. As such, for every rare beneficial mutation that might occur, countless numbers of harmful mutations are accumulating within the genome of the organism - producing what is known as a "mutation load".
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
</ref> }}


== References ==
== References ==
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