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Mutation: Difference between revisions
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{{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 | ||
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Regarding the inevitable continuous degredation of the human genome by the high rate of accruing mutation, Alexey S. Kondrashov, a leading researcher in the field of evolutionary genetics, has stated, | |||
{{cquote|Despite all of the elaborate mechanisms that a cell employs to handle its DNA with the utmost care, a newborn human carries about 100 new mutations, originated in their parents, about 10 of which are deleterious. A mutation replacing just one of the more than three billion nucleotides in the human genome may lead to synthesis of a dysfunctional protein, and this can be inconsistent with life or cause a tragic disease. Several percent of even young people suffer from diseases that are caused, exclusively or primarily, by preexisting and new mutations in their genomes, including both a wide variety of genetically simple Mendelian diseases and diverse complex diseases such as birth anomalies, diabetes, and schizophrenia. Milder, but still substantial, negative effects of mutations are even more pervasive. As of now, we possess no means of reducing the rate at which mutations appear spontaneously. However, the recent flood of genomic data made possible by next-generation methods of DNA sequencing, enabled scientists to explore the impacts of deleterious mutations on humans with previously unattainable precision and begin to develop approaches to managing them.<ref>[https://onlinelibrary.wiley.com/doi/book/10.1002/9781118952146 ''Crumbling Genome: The Impact of Deleterious Mutations on Humans''] by Alexey S. Kondrashov, ''Proceedings of the National Academy of Sciences'' USA, published online before print April 3, 2007</ref> }}}} | |||
== References == | == References == | ||
