The Nature of Mutations

Hi Phospholipid, this statement is also inaccurate.

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I said that of the two catagories of mutations (neutral and deleterious, of which only the deleterious affect the phenotype), those which affect the phenotype damage whatever physiological character that incurs that mutation.

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They will always carry a deleterious affect,

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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.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

PG: The mutation is a deleterious mutation because it deminishes the original purpose of the protein. Period. This causes the protein to malfunction and not produce HDL up to standard levels. It is a deleterious mutation. I did not deny that it has a beneficial side-effect. But nice try.FK: As others have pointed out, you certainly have an odd way of looking at mutations. If there is a mutation to a gene such that the organism benefits, this is not a beneficial mutation if any portion of the initial function was lost. As Crashfrog pointed out, you are making some unwarranted assumptions as to the meaning of original function. But I will play your game. What are the deleterious effects of this mutation? It certainly wasn’t the decrease in HDL levels, since the mutated protein is more effective at its job. High HDL levels are not needed. To be a deleterious mutation, it has to have a deleterious effect. To say that HDL levels are diminished is meaningless in the context that their importance is diminished. I guess the bottom line is: Would you like to have this mutation?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.PG: As for the rest of your post, see the previous posts on transposons and adaptational variants. Single genetic pieces or entire sequences turning on and off gene expression.FK: In what way does that apply to the mosquito mutation, which happened via gene duplication and subsequent mutations?PG: As for the "major" creationist organizations, I don't know, I haven't talked to any of them. But I bet that if we got down to the nitty-gritty, they would be agreeing with me rather than you.FK: In the grand scheme of things, yes. But whether or not some mutations are beneficial, they will certainly disagree with you. The evidence is simply irrefutable. I have a suggestion. Write to AIG and ask them if it is true that there are no beneficial mutations. Their response will be that there are beneficial mutations, but they will claim that they don’t add information (another falsehood).FK

I'm afraid you did. Or at least that was what the following sentence seems to imply. Would you care to rephrase it to explain what you really meant, if this was not your intent?

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Yes, this is what I am saying, to the best of my knowledge. All supposed "mutations" that are considered purely beneficial are in fact not mutations at all, but simply genetic changes such as recombination. But recombination is not a mutation. (emphasis added)

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Please clarify.

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. With the approach of ancestral protein reconstruction, we here address the question of how a dramatically enhanced ribonucleolytic activity and the related antiviral activity evolved in a recently duplicated ribonuclease (eosinophil-derived neurotoxin) gene of higher primates. We show that the mother gene of the duplicated genes had already possessed a weak antiviral activity before duplication. After duplication, substitutions at two interacting sites (Arg-643Ser and Thr-1323Arg) resulted in a 13-fold enhancement of the ribonucleolytic activity of eosinophil-derived neurotoxin. These substitutions are also necessary for the potent antiviral activity, with contributions from additional amino acid changes at interacting sites. Our observation that a change in eosinophil-derived neurotoxin function occurs only when both interacting sites are altered indicates the importance of complementary substitutions in protein evolution.Thus, neutral substitutions are not simply ‘‘noises’’ in protein evolution, as many have thought. They may play constructive roles by setting the intramolecular microenvironment for further complementary advantageous substitutions, which can lead to improved or altered function. Overall, our study illustrates the power of the ‘‘paleomolecular biochemistry’’ approach in delineating the complex interplays of amino acid substitutions in evolution and in identifying the molecular basis of biological innovation.

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As to variation arising from mutation within a population, there are innumerable studies where this has been documented. One of my favorite examples is Orr HA, 1995, "The Population Genetics of Speciation: The Evolution of Hybrid Incompatibilities", Genetics 139 180.5-1813

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Speciation often results from the accumulation of complementary genes, i e . , from genes that, while having no deleterious effect within species, cause inviability or sterility when brought together with genes from another species. Here I model speciation as the accumulation of genic incompatibilities between
diverging populations. Several results are obtained. First, and most important, the number of genic incompatibilities between taxa increases much faster than linearly with time. In particular, the probability of speciation increases at least as fast as the square of the time since separation between two taxa. Second, as Muller realized, all hybrid incompatibilities must initially be asymmetric. Third, at loci that have diverged between taxa, evolutionarily derived alleles cause hybrid problems far more often than ancestral alleles. Last, it is easier to evolve complex hybrid incompatibilities requiring the simultaneous action of three or more loci than to evolve simple incompatibilities between pairs of genes. These results have several important implications for genetic analyses of speciation.

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That'll do for you to go on. Your turn. You have stated numerous times that your assertions have been "demonstrated" (such as in this quote: To date, you have failed to provide any references in support of any of your assertions. Please do so.[This message has been edited by Quetzal, 05-03-2003]

Hi PLG,I am assuming you have access to some of these articles..please indicate if you do not.PLG: First, where is there any evidence that mutation gives rise to variation? There is none. Provide that which you call evidence, and I will demonstrate that it is only transposon-activated genes that before hand were dormant and non-expressed.M: cases where transposons activate genes or influence their transcription is relatively rare. If you have references to the contrary please post them. The last one in particular negates your position as they deal with adaptation via point mutation in a study encompassing 20,000 generations of bacterial evolution.mutation is the only way of giving rise to genetic variation...note, this list is extremely limited and meant only as an example...one could probably jam the server posting all the literature on genetic mutation research even excluding that involving transposable elements.Enard W, Przeworski M, Fisher SE, Lai CS, Wiebe V, Kitano T, Monaco AP, Paabo S.
Molecular evolution of FOXP2, a gene involved in speech and language.
Nature. 2002 Aug 22;418(6900):869-72.Britten RJ, Rowen L, Williams J, Cameron RA.
Majority of divergence between closely related DNA samples is due to indels.
Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4661-5.Britten RJ.
Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels.
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13633-5.Lenski RE, Winkworth CL, Riley MA.
Rates of DNA Sequence Evolution in Experimental Populations of Escherichia coli During 20,000 Generations.
J Mol Evol. 2003 Apr;56(4):498-508.

Hi PLG,
I don't think your messages have been rude or out of line so no problem from my point of view...the thread has been pretty interesting.As to epigenetics, it is a reasonable question and someone else asked what it was a few days ago.Below is a review containing the abstract...I don't think it fits with what you are trying to get across. Methylation is a reversible process that shuts down or turns on genes for example in female mammals the one of the two X chromosomes is inactivated to compensate for the dose of genes relative to males who have one X chromosome. There are autosomal genes where one allele is shut down by methylation so called imprinted genes. This is a consistent form of gene regulation, not a mutation. It is also largely a stochastically driven process i.e. 50:50 chance which X chromosome is inactivated in a given cell. This is not a deterministic mutation mechanism for driving evolution as you seem to be defining mutation. Nor are transposable elements relevant to epigenetics as you have described.Electrophoresis 2001 Aug;22(14):2838-43
DNA methylation and mammalian epigenetics.Reik W, Dean W.Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge, UK. wolf.reik@bbsrc.ac.ukEpigenetic modifications of DNA such as methylation are important for genome function during development and in adults. DNA methylation has central importance for genomic imprinting and other aspects of epigenetic control of gene expression, and during development methylation patterns are largely maintained in somatic lineages. The mammalian genome undergoes major reprogramming of methylation patterns in the germ cells and in the early embryo. Some of the factors that are involved both in maintenance and in reprogramming, such as methyltransferases, are being identified. Epigenetic changes are likely to be important in animal cloning, and influence the occurrence of epimutations and of epigenetic inheritance. Environmental factors can alter epigenetic modifications and may thus have long lasting effects on phenotype. Epigenetic engineering is likely to play an important role in medicine in the future.

Hi PLG..An even better review of epigenetics and evolution...unfortunately Nature Reviews Genetics requires a subscription...but you can get it in most university libraries with a bio department.Nature Reviews Genetics 4, 359-368 (2003)WHAT GOOD IS GENOMIC IMPRINTING: THE FUNCTION OF PARENT-SPECIFIC GENE EXPRESSIONJon F. Wilkins, & David Haig1 Society of Fellows, 7 Divinity Avenue, Harvard University, Cambridge, Massachusetts 02138, USA.
2 Bauer Center for Genomics Research, 7 Divinity Avenue, Harvard University, Cambridge, Massachusetts 02138, USA.
3 Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA.correspondence to: Jon F. Wilkins jwilkins@cgr.harvard.eduParent-specific gene expression (genomic imprinting) is an evolutionary puzzle because it forgoes an important advantage of diploidy protection against the effects of deleterious recessive mutations. Three hypotheses claim to have found a countervailing selective advantage of parent-specific expression. Imprinting is proposed to have evolved because it enhances evolvability in a changing environment, protects females against the ravages of invasive trophoblast, or because natural selection acts differently on genes of maternal and paternal origin in interactions among kin. The last hypothesis has received the most extensive theoretical development and seems the best supported by the properties of known imprinted genes. However, the hypothesis is yet to provide a compelling explanation for many examples of imprinting.

Dear Mammuthus,AS far as I was aware the most widely accepted theory behind the evolution of imprinting was the parental conflict hypothesis. Do you have any references for this differential NS driven theory or is it just the parental conflict hypothesis by another name, your description certainly doesnt make it seem so.cheers,wounded

Hi Wounded,
It is just the parental conflict hypothesis with a different name..I don't know why they did not refer to it as such in the abstract as in the text they do.."and the kinship theory proposes that imprinting has evolved because of an evolutionary conflict in individuals between maternally and paternally derived alleles8."Reference 8 on kinship theory is
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Haig, D. Genomic Imprinting and Kinship (Rutgers Univ. Press, New Brunswick, 2002).
A collection of papers that trace the development of the kinship theory, with retrospective commentaries.cheers,
M

Hello? PPG?Maybe we're overwhelming him with posts. Tell ya what, PPG, since a great many posters on this board are supremely more qualified to discuss this than I, I won't expect you to respond to any of my posts. I'll continue posting where I think I have something to add but don't feel like you have to respond unless you are particularly moved to do so.It's just that I'm quite interested to hear your rebuttals to the evidence of purely beneficial mutation that has been presented so far (as well as the specific example of the mosquitos, which by your own definition is a purely beneficial mutation, since duplications are mutations, by your own admission.) I'd hate for you to use all your time addressing my amaturish posts and ignoring the better arguments being levied your way.

This is the Glossary entry for "Adaption" from Mark Ridley's _Evolution_(2nd Edition) - one of the leading undergraduate texts."Feature of an organism enabling it to survive and reproduce in its natural environment better than if it lacked the feature"So any beneficial mutaiton would be an adaption.

Yes, I do have a life, thank you. And a very exciting and rewarding one, at that. Anyways...the only weaseling that has been done was already done. That by evolutionary theorists is playing word games with the definitions of the word mutation, which is what I am trying to get set straight for the debate.This is only my first post today, so I will refrain from further rattling until I can get to some other posts and see what ya'lls definition has come up to be.Hasta...

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Unfortunately, it looks like PG lit out of here once he figured out that the beneficial mutations argument was one he couldn't win.

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Again, you must be misunderstanding what my whole argument is. I have not stated that there were no mutations that, in certain environments, may provide some amount, however small, of a beneficial side-affect to its bearer.My argument is this: There is no such thing as a catagory of mutations in and of themselves that can be purely beneficial; that is, not having also a negative, deleterious affect directly upon the molecular machinery in which it occurs.And it is not this argument that I cannot win, it is yours.Greetings!

Well, part of the problem is linguistic: words describe meaning, they don't contain it. Words are fuzzy in that regard. If you try to pin down their meaning you wind up restricting meanings you didn't mean to restrict - as you can see from the thread, we tried to choose a definition that was sufficiently specific without leaving things out. It's pretty hard, which is why I don't care much for dictionary games in debates. While there's an argument for defining terms before you argue about them, one has to realize that true, absolute agreement on meaning is never possible between speakers.

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After all, the objective is to come up with a definition that covers the wide range of possible mutations while at the same time restricting things to something that the creationist can't weasel out of...

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Interesting, "Q". Therefore, you are not interested here in debating what the facts are of the debate, all you want to do is corner me and try to make me look like I do not know what I am talking about. Poor sportsmanship, very poor. You show your true colors, and they have nothing to do with science.

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If that's so, I wish he could have posted something like "Blah blah blah I'm done wasting my time with you people" like other people who give up seem to do, that way we wouldn't be wasting our time coming up with definitions we're not going to use.

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And even more interesting, Frog. If this really is your entire goal, "coming up with definitions" that your "not going to use" in a debate, why even come here?Honestly, I thought that I would meet people on this board that would be interested in sitting down and talking about the facts, not coming here to play games. I am not like your "run-of-the-mill" anti-evolutionist. At one time I believed, but after having a desire to actually know what all the fuss was about, I left my bias at the front door and began to actively search for the facts on the subject, and only the facts.There are a huge amount of assumptions at play in the theory of evolution, far too many to make it tenable to a thinking person interested in finding out what the truth is. I am not here promoting God, I am here saying that evolutionary theory doesn't cut it. Looking at it from a forensic science point of view, there are too many holes in the story to make me believe that "evolution did it".Please, if your only time here is to play games with me, then go home and let me talk to someone who has a real interest in what I say. I may be wrong in some things, but that is another reason why I am here, to talk to people who are worth talking to and to learn some more things that I do not already know. Thanks.Greetings!