Talk:Mutation
From Conservapedia
Is there a reason why the TOE paragraph is at the top instead of the paragraph explaining what mutations are?--TimS 22:27, 8 May 2007 (EDT)
There are some serious mistakes in this article. First off, RNA is not found in the nucleus of the cell unless its mRNA, and in that case would not be mutated or affect the genetic makeup of the organism in question. mRNA is copied from the DNA structure itself and thus cannot alter DNA. Second, ribosomes are not responsible for correcting the DNA structure, they are responsible for protein synthesis and production of tRNA. It should also be mentioned that most mutations have no effect on the codons read to synthesis proteins due to similar 3 base codes. —The preceding unsigned comment was added by Biology (talk) June 2007
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Gain-of-Function Mutations
Sickle hemoglobin is a gain of function mutation Conservative.--TimS 17:05, 5 September 2007 (EDT)
I have to ask, after reading this article and having much background knowledge of Sicklic hemoglobin, why anyone one would label it as a gain or a loss of function mutation? Heterozygous carriers of the Sicklic hemoglobin trait have hemoglobin that binds O2 just as regular hemoglobin does the only difference is in low O2 environments where the sicklic hemoglobin changes to a sicklic shape, otherwise it functions just like normal hemoglobin. I am not a biologist so I do not know how this relates to functional mutation grouping but I am a biochemist and I know for a fact that the sicklic hemoglobin is caused by a point mutation, where there is a change in the beta subunit to the amino acid valine at position 6 instead of the glutamic acid that is found in normal hemoglobin. As for homozygous carriers it has been found that the degree of anemia varies widely between patients. In general, patients with sickle cell disease have hematocrits that are roughly half the normal value (e.g., about 25% compared to about 40-45% normally). Patients with hemoglobin SC disease (where one of the beta globin genes codes for hemoglobin S and the other for the variant, hemoglobin C) have higher hematocrits than do those with homozygous Hb SS disease. The hematocrits of patients with Hb SC disease run in low- to mid-thirties. The hematocrit is normal for people with sickle cell trait. So depending on the variant of the disease caused by the homozygous carriers the disease does not have to be life threatening.
If anything I believe that a good example of a gain of function mutation would be found in HIV. SIV Vpu is not a viroporin, HIV-1 O Vpu is not a viroporin, however HIV-1 M Vpu is a viroporin (gated cation channel specific to Na+). This is a new activity that evolved in HIV after the split from SIV over a 10 year timeframe and is part of the reason that the HIV-1 M clade is the most common type of HIV in the world. This cation channel is gated and therefore more complicated than just a simple ion channel, considering that this is a new viral component found only in the HIV-1 M clade it is a safe conjecture to say that this is an example of a gain of function mutation considering that the HIV clades before HIV-1 M did not contain a gated cation channel specific to Na+.
Apolipoprotein AI is another example of what I believe would classify as a gain of function mutation. The Apolipoprotein AI Milano allele is the mutated allele. In an experiment where reconstituted HDL particles made of Apolipoprotein AI were infused into arteriosclerotic rabbits, the rabbits had fewer and less extensive plaques. There was decreased aortic cholesterol, and decreased cell proliferation (both of which improve cell wall flexibility. These experiments all point to the Apolipoprotein AI as a lipid-binding protein that is a major component of High Density Lipoprotein particles, and therefore play an important role in removing cholesterol from cells. Subsequent detailed research of the Apolipoprotein AI mutation has demonstrated that it has improved biological function that directly contributes to lowering the incidence of cardiovascular disease in the individuals carrying it.
Perhaps the two examples I listed above should be placed into the article since they are well researched in the scientific community due to the amount of press heart disease and HIV both get.--Able806 15:40, 12 November 2007 (EST)
- Feel free to add them, although keep in mind the target audience.
- The sickle hemoglobin is sometimes used as evidence for evolution (as opposed to creation), and I suspect that is why it was included in this article. However, leading creationists only dispute information-gaining mutations, and accept that there are information-losing mutations, such as apoliproprotein AI, which result in a gain of function or a benefit in some circumstances.[1]
- Philip J. Rayment 20:54, 12 November 2007 (EST)
- I will look into the APO-AIM but for now if it does not meet the standards then it should be left out. The HIV example though I know meets because it also increased the size of the genome of HIV. So I will add it in.--Able806 09:59, 15 November 2007 (EST)
No new genetic info?
The statement that "mutations that create new genetic information have never been observed" is simply false, unless you're using some unusual definition of genetic information, in which case that should be explained. Dadsnagem2 21:55, 7 January 2008 (EST)
- No, it's not false, and I would consider it a usual use of "information", although not the meaningless (literally) definition that evolutionists often use (i.e. any change (except perhaps a deletion) is by definition new information). However, I do take your point that the definition wasn't explained. As a partial answer to that, I've linked "information", and although that article doesn't specifically mention genetic information, it's better than nothing. Philip J. Rayment 04:24, 8 January 2008 (EST)
According to Molecular Pathology
There are three main classes of mutation with several subclasses.
Deletions
Deletions of DNA ranging from 1 bp to megabases.
Insertions
Insertions of DNA including duplications.
Single base substitutions
Missense Mutations
Replacement of one amino acid with another in the gene product.
Nonsense Mutations
Replacement of an amino acid codon with a stop codon.
Splice Site Mutations
Create or destroy signals for exon-intron splicing
Within these main classes a mutation can be consided a loss of function or gain of function. There are also Frameshifts and Dynamic Mutations. Since I did not start this article I want to know if anyone would object if I made these corrections as well as provide some background information about what exactly these mutations trully are?--Able806 09:07, 12 February 2008 (EST)
