The Nature of Mutations

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Adaption is used quire widely. In the case of the article at U-M Web Hosting
it is clearly used to express the idea that this mutation is beneficial and no more:

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If the history of science has taught you anything, surely you know that science has been wrong on many occassions, and maintained that error ONLY because there was a vast number of scientists in that day and age who - based upon nothing more than emotional attatchment - kept the theory and ideals alive for their own agenda. Phlegistron (?) for example.Adaptation is not due to mutation.

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And am I right in thinking that you are a supporter of the ideas of Lee Spetner ? His followers tend to make the same errors as you in firstly misunderstanding the idea of "random mutations"

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I am not a supporter of anyone's "ideas", I am a supporter of the facts. And the facts dictate what is and what is not. A genetic change is not a mutation if it is mediated by the organism. Period.
A mutation (I have not yet looked over the entire site so I do not yet know what we have decided that your definition of a mutation is, so I will stick with mine until I get that far) is only a random copying error made during replication that mutation correcting enzymes failed to fix. Period.That is not my definition, that is the facts.Greetings!

Frog...

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You still haven't addressed what deleterious effect a gene duplication could have (particularly if its a duplication of a beneficial gene), given that they are, by your own admission, mutations...

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AFter giving this much thought, I guess that I would have to concede that there is a possibility of gene duplication mutations that could be totally beneficial, only with some conditions...First - does every gene duplication mutation carry with it only beneficial phenotypic effects?Second - I, personally, think that these should not simply be called "mutations" per say. Perhaps GDM's or something of the like, in order to distinguish them from single (or multiple) nucloetide substitutions, duplications or deletions...particularly since it is an entire gene that is being duplicated.But one thing does puzzle me about gene duplications, why and how are they copied without expression? Understand what I mean? In other words, once the RNA has pulled its copy from the DNA, why would it insert in into the DNA instead of beginning translation?To be honest, it doesn't make sense unless it is being mediated by the organism, and then if that is the case, then I go right back to my original stance, that it cannot be considered a mutation because it IS being mediated by the organism's genetic system.Anyone have an answer for this one? I am not being facetious, it is an honest question.Greetings!

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Perhaps you need to say what you mean by "variation". Most people assume that to mean "differences". Biologically it tends to refer to the phenomenon where individuals in a population tend not to be genetic clones of each other.

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I have not heard this before, and to be quite honest, it sounds like another play on words and phrases, just like calling evolution "change", period.Variation, as far as I have always read and understood it to be, is the difference between a valley goat and a mountain goat. They are both goats, but the valley specimen has small hooves and a short coat, while its mountain cousin sports larger and wider hooves and a longer coat to deal with the weather at the higher elevations, for example.That argument is a bogus one in my mind, for no one is an exact clone of another. As I have stated before, even "identical" twins have different fingerprints.Greetings!

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2nd, let’s say you are correct. A mutation that changes the original function of a gene is deleterious. If we traced the mutation of a bacteria through all of the generations to human beings, we would find one deleterious mutation after another (based on your definition), because each mutation would have changed the original purpose of the bacterial genes. So according to you, it is possible to get from a bacteria to a man with nothing but deleterious mutations.

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You are assuming evolution to be a fact, the very issue that we are discussing, therefore your entire argument presented here is null and void.Greetings!

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The differences in glyosylation which define blood types come from several well defined mutations.
mutations
Some of these changes in glycosylations, mutations within the glycosylating protein, can confer disease resistence
seminar on blood types
This is a well understood phenomina.

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I am not ignoring this, I have tried twice now to get access and there must be too many people on line right now, I have been waiting for a while. I am pressed for time and am trying to answer as many as possible. I will also answer this, but later when I have the time to look them up.By the way, thanks!Greetings!

That's not variation, per se - that's the results of variation after being acted on by natural selection.Variation would be whatever process would have resulted in one or more individuals having longer hair or wider hooves than their parents. We're arguing that mutation causes that.Certain variations, then, are acted on by natural selection, which selects for or against those traits, leading, over time, to their spread through the population of mountain goats. That's adaptation - the population adapts to its new environment. Sure, not all forms of variation are herediary. it is ony the hereditary variations that matter to natural selection because those are the only traits that are passed on to offspring and spread through populations.Variation between individuals can have many sources, most of them not genetic. heritable variation, on the other hand, is always genetic and it is that which natural selection is concerned.Hopefully this is making some sense to you. Also I think your definition of mutation is far too narrow. A mutation is simply a genetic variation that makes an offspring's genes different from the sum of its parents. In terms of population genetics we are concerned only with the mutations that occur in reproductive cells rather than mutations in somatic cells as these cannot be passed on.

PG: You are assuming evolution to be a fact, the very issue that we are discussing, therefore your entire argument presented here is null and void.FK: Ah, the old Fred Williams tactic of finding some minor nitpick and then trying to have the entire argument thrown out based on the nitpick.So let's rephrase just for you. IF evolution happened from single-celled organism to man, then based on your definitions it occurred primarily via deleterious mutations since the original functions of the genes would have been co-opted for other purposes. This should point out how silly your semantic argument is.Edited to add: The bottom line is that according to the way you have defined beneficial mutations, they are not required for evolution. Pretty much all evolution proceeds via deleterious mutations (based on your definition). This includes the line that would extend from single-celled organism to man.FK[This message has been edited by Fedmahn Kassad, 05-18-2003]

Hi Phospholipid,I politely refer you tothis post . It appears to have been lost in the fray.

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Phospho:
A genetic change is not a mutation if it is mediated by the organism. Period.
A mutation (I have not yet looked over the entire site so I do not yet know what we have decided that your definition of a mutation is, so I will stick with mine until I get that far) is only a random copying error made during replication that mutation correcting enzymes failed to fix. Period.

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That is not my definition, that is the facts.

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Can you please cite or direct me to some of the facts that indicate organisms can and do mediate their own genetic changes?Surely, you must have several sources handy. Thanks.

Phospho, you really should not make statements like

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And the facts dictate what is and what is not. A genetic change is not a mutation if it is mediated by the organism. Period.

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when you are unaware of the "facts". Organisms mediate their own mutations, albet unwittingly, all the time. Please look at some of the articels associated with this one
here.
I have copied one abstract below.

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Palindromic DNA and Genome Stability: Further Studiesa
SUSANNA LEWISb,d, ERCAN AKGNc and MARIA JASINc,e
bProgram in Genetics and Genomic Biology, Hospital for Sick Children Research Institute and Immunology Department, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, M5S 1A8 Canada
cCell Biology and Genetics Program, Sloan-Kettering Institute and Cornell University Graduate School of Medical Sciences, 1275 York Avenue, New York, NY 10021, USA

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This work was supported by a grant from the Medical Research Council of Canada and a Terry Fox grant from the National Cancer Institute of Canada (to S. L.) and a grant from the Pew Charitable Trusts (to M. Jasin). S. Lewis is a Research Scientist of the N.C.I.C.
dFax, 416/978-1938; phone, 416/978-4230; e-mail, lewis@immune.med.utoronto.ca
eFax, 212/717-3317; phone, 212/639-7438; e-mail, m-jasin@ski.mskcc.org

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Unusual DNA structures promote genetic instability. One such example is hairpin DNA, which can form from palindromic sequences and triplet repeats, and is also a characteristic intermediate in V(D)J recombination. We previously found that a large 15.3-kb palindrome that was introduced as a transgene into the mouse germline was highly unstable. Although it could be transmitted, the transgene was found to be rearranged in up to 56% of the progeny, and rearrangement events often involved deletion at the center of symmetry. Here, the fine structure of centrally deleted palindromes was sampled by analysis of recombinant junctions isolated from testes DNA, providing further evidence for a model, previously proposed, that accounts for such deletions on the basis of a hairpin-tip nicking activity. In addition to central deletions, gene conversion events were also elevated in the transgenic palindrome. We have now analyzed instability in two mouse sublines in which (as a result of inversion) the transgenic palindrome had been shortened to 4.2 kb. In these sublines, the transgene was still subject to both rearrangement and gene conversion events at a high frequency, similar to the original 15.3-kb palindrome. Recombination was not limited to the sequences constituting the inverted repeat, but was seen to include sequences lying outside the palindrome. As discussed, the salient feature in all of these observations, a high level of genetic change associated with palindromic DNA, underscores the significance of hairpin DNA and hairpin-tip nicking in genome stability.

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It essentially gives an example of organisms which have sequence mediated increases in copy errors, i.e. mutations. Many of the se mutations increase in times of stress to the organism which results in cellular stress and increased mutation. Most of this data is currently applicable to bacteria although there are many applications to multicellular and larger organisms also listed on this and other sites.And you never addressed my post in this thread re: blood type mutations and their beneficial effects, or are you calling a series of well defined mutations part of your variety which came pre-packaged by a diety who put the diseases in for the mutations to be beneficial for ?------------------
"Chance favors the prepared mind." L. Pasteur
Taz

By the way, PG, if you recall I pointed out that the major Creationist organizations would all disagree with you regarding beneficial mutations. Here is Jon Safarti, of AIG, writing on the matter:

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AiG has LONG pointed out that one should not deny beneficial mutations, but merely point out that evolution from goo to you via the zoo requires a HUGE number of information-GAINING mutations.

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The linkGo down to the post by "Socrates" about 2/3 down the page for the rest of the discussion. "Socrates" is Jon Sarfati.FK{Shortened display form of link, to restore page width to normal - Adminnemooseus}[This message has been edited by Adminnemooseus, 05-19-2003]

I am not a supporter of anyone's "ideas", I am a supporter of the facts. And the facts dictate what is and what is not. A genetic change is not a mutation if it is mediated by the organism. Period.M: Then please be so kind as to show the experimenteal evidence for this if you are a supporter of the facts....there are at least 3 people posting here with Ph.D.'s in molecular biology who do not agree with your so called definition of mutation and it is thus required of you to show the "factual" evidence that you are correct and we wrong...assertions are not evidence.

Variation, as far as I have always read and understood it to be, is the difference between a valley goat and a mountain goat. They are both goats, but the valley specimen has small hooves and a short coat, while its mountain cousin sports larger and wider hooves and a longer coat to deal with the weather at the higher elevations, for example.M: That is phenotypic variation. However, genetic variation is more akin to things likeNature 2000 Dec 7;408(6813):708-13Erratum in:
Nature 2001 Mar 29;410(6828):611Comment in:
Nature. 2000 Dec 7;408(6813):652-3.Mitochondrial genome variation and the origin of modern humans.Ingman M, Kaessmann H, Paabo S, Gyllensten U.Department of Genetics and Pathology, Section of Medical Genetics, University of Uppsala, Sweden.The analysis of mitochondrial DNA (mtDNA) has been a potent tool in our understanding of human evolution, owing to characteristics such as high copy number, apparent lack of recombination, high substitution rate and maternal mode of inheritance. However, almost all studies of human evolution based on mtDNA sequencing have been confined to the control region, which constitutes less than 7% of the mitochondrial genome. These studies are complicated by the extreme variation in substitution rate between sites, and the consequence of parallel mutations causing difficulties in the estimation of genetic distance and making phylogenetic inferences questionable. Most comprehensive studies of the human mitochondrial molecule have been carried out through restriction-fragment length polymorphism analysis, providing data that are ill suited to estimations of mutation rate and therefore the timing of evolutionary events. Here, to improve the information obtained from the mitochondrial molecule for studies of human evolution, we describe the global mtDNA diversity in humans based on analyses of the complete mtDNA sequence of 53 humans of diverse origins. Our mtDNA data, in comparison with those of a parallel study of the Xq13.3 region in the same individuals, provide a concurrent view on human evolution with respect to the age of modern humans.Can you please demonstrate which of these mutations were mediated by the organism? And all of this variation is due to mutation. Please note, the frequency of these haplotypes vary among populations and vary over time as some human haplotypes have become extinct:Proc Natl Acad Sci U S A 2001 Jan 16;98(2):537-42 Related Articles, LinksErratum in:
Proc Natl Acad Sci U S A 2002 Jan 8;99(1):541Comment in:
Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):390-1.Mitochondrial DNA sequences in ancient Australians: Implications for modern human origins.Adcock GJ, Dennis ES, Easteal S, Huttley GA, Jermiin LS, Peacock WJ, Thorne A.Research School of Pacific and Asian Studies and John Curtin School of Medical Research, Australian National University, Canberra ACT 0200, Australia.DNA from ancient human remains provides perspectives on the origin of our species and the relationship between molecular and morphological variation. We report analysis of mtDNA from the remains of 10 ancient Australians. These include the morphologically gracile Lake Mungo 3 [ approximately 60 thousand years (ka) before present] and three other gracile individuals from Holocene deposits at Willandra Lakes (

Sorry Nosy....I missed your post.Basically, you have a loss of function of one component COX8H preceded by accelerated mutation in another componenet COX8L. This allows for the loss of COX8H in a specific group as the COX8L function compensates for the loss and in addition, allows for adaptive change in a specific phenotypic trait. The accelerated rate of COX8L evolution (i.e. higher mutation rate) was a source of beneficial mutations.

From "Q"...

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Your attention invited to the reference provided in my post #90 of this thread. In addition, in an earlier post I referenced an article by Zhang and Rosenberg which also referenced this question. I will quote the abstract here:
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An improved understanding of the evolution of gene function at the molecular level may provide significant insights into the origin of biological novelty and adaptation.

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This is my fault. This may sound like a line, but it is not. I have been arguing from the standpoint that, in my mind, evolutionary theory has not been demonstrated, but is kept alive via misguided terminology and under certain assumptions that have yet to be demonstrated. The grand assumption in particular - that evolution has been in fact proven as reality.When I approach this board, this is the attitude I come with. Saying this, I basically am looking for someone to demonstrate from the facts (with no assumptions of the so-called "truth" of evolution) that evolution is a possibility. Only now have I realized that I have not made this clear to ya'll.This may put a damper on the discussion on your part, I don't know. Basically, when "Q" quotes the above, the author assuming the truth of evolution, I must take out all references and "matter-of-fact" statements out of the quote. Then I get a different understanding of the paragraph than what "Q" is trying to get across. Why? Because the author believes that evolution has been proven (because he has been unwittingly duped into the bogus terminology and word-games that evolutionary theorists dish out), it is not his fault, he just got caght up into it. Does this make any sense to you?Basically what I am here for is for someone to demonstrate that my original assertion of mutations is incorrect - while ignoring all references to the fact of evolution...because it is not a fact yet, and I doubt that it ever will be.Greetings!