molecular genetic proof against random mutation (1)

Mutational hotspots are hotspots for very simple reasons. It has to do with the sequence. Certain stretches of DNA are prone to exposure to mutagens, for instance.It is all very simple chemistry, but the creationist will always try to make sand castles out of single grains of sand.Creationists also seem to have odd ideas about randomness. One creationist insisted that because there is enzymatic control of the insertion of some retrotransposons that the entire process is non-random, despite the fact that there is no control over WHERE these elements get inserted.You simply cannot make headway talking to a wall.

I notice peter B. has yet to provide any citations for 'directed evolution' or 'directed mutations.'I, on the other, can provide evidence to the contrary:"The flurry of studies ultimately revealed that Cairns's original proposal was untenable, and the community, including Cairns, now at the Radcliffe Infirmary in Oxford, United Kingdom, discarded it." 2002. Science.: **********************************
: EMBO J 1997 Jun 2;16(11):3303-11
: Genome-wide hypermutation in a subpopulation of stationary-phase cells underlies recombination-dependent adaptive mutation.
: Torkelson J, Harris RS, Lombardo MJ, Nagendran J, Thulin C, Rosenberg SM: Stationary-phase mutation in microbes can produce selected ('adaptive') mutants preferentially. In one system, this occurs via a distinct, recombination-dependent mechanism. Two points of controversy have surrounded these adaptive reversions of an Escherichia coli lac mutation. First, are the mutations directed preferentially to the selected gene in a Lamarckian manner?
: Second, is the adaptive mutation mechanism specific to the F plasmid replicon carrying lac? We report that lac adaptive mutations are associated with hypermutation in unselected genes, in all replicons in the cell. The associated mutations have a similar sequence spectrum to the adaptive reversions. Thus, the adaptive mutagenesis mechanism is not directed to the lac genes, in a Lamarckian manner,nor to the F' replicon carrying lac. Hypermutation was not found in non-revertants exposed to selection. Therefore, the genome-wide hypermutation underlying adaptive mutation occurs in a differentiated subpopulation. The existence of mutable subpopulations in non-growing cells is important in bacterial evolution and could be relevant to the somatic mutations that give rise to cancers in multicellular organisms.: ******************************
: "Researchers first noticed this happening in 1988 when John Cairns, then at Harvard University, showed that mutation rates in the bacterium Escherichia coli increased when the microbes needed to evolve new capabilities in order to survive changes in their environment.
: At the time, it seemed that only those genes directly involved with the adaptation changed,and this idea of adapative or directed evolution caused quite a stir.: But then last year, molecular geneticist Susan Rosenberg at Baylor College of Medicine in Houston and her colleagues showed that mutation rates increase throughout the genome, although only in a subset of the population. Another group also found that more than just the relevant genes changed." (How the Genome Readies Itself for Evolution, Elizabeth Pennisi, Science, vol 281,
: Number 5380, Issue of 21 Aug 1998, p1131-1134)
: *******************************: Imagine that.:
: *******************************
: Mutat Res 1999 Jul;437(1):51-60
: Mismatch repair is diminished during stationary-phase mutation.
: Harris RS, Feng G, Ross KJ, Sidhu R, Thulin C, Longerich S, Szigety SK, Hastings PJ, Winkler ME,Rosenberg SM.
: Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.
: This paper is an invited Response to a recent Commentary [P.L. Foster, Rev. Mut. Res. 436 (1999) 179-184] entitled "Are adaptive mutations due to a decline in mismatch repair? The evidence is lacking". The Commentary argues that no evidence exists supporting the idea that mismatch repair is limiting specifically during stationary-phase mutation. A primary concern of the author is to question the method that we used previously to measure growth-dependent mutation. In this method, mutation rates are calculated using counts of mutant colonies taken at times when those colonies arise, rather than at a predetermined, fixed time. Here we show further data that illustrate why this must be done to ensure accurate mutation measurements. Such accuracy was necessary for our published determination that mismatch repair proteins are not limiting during growth-dependent mutation, but become so during stationary-phase mutation. We review the evidence supporting the idea that stationary-phase reversion of a lac frameshift mutation occurs in an environment of decreased mismatch repair capacity. Those data are substantial. The data presented in the Commentary, in apparent contradiction to this idea, do not justify the conclusion presented there. Copyright 1999 Elsevier Science B.V.
: **********************
: Ann N Y Acad Sci 1999 May 18;870:275-89
: Mechanisms of genome-wide hypermutation in stationary phase.
: Lombardo MJ, Torkelson J, Bull HJ, McKenzie GJ, Rosenberg SM.
: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
: Stationary-phase mutation (a subset of which was previously called adaptive mutation) occurs in apparently nondividing, stationary-phase cells exposed to a nonlethal genetic selection. In one experimental system, stationary-phase reversion of an Escherichia coli F'-borne lac frameshift mutation occurs by a novel molecular mechanism that requires homologous recombination functions of the RecBCD system. Chromosomal mutations at multiple loci are detected more frequently in Lac+ stationary-phase revertants than in cells that were also exposed to selection but did not become Lac+. Thus, mutating cells represent a subpopulation that experiences hypermutation throughout the genome. This paper summarizes current knowledge regarding stationary-phase mutation in the lac system. Hypotheses for the mechanism of chromosomal hypermutation are discussed, and data are presented that exclude one hypothetical mechanism in which chromosomal mutations result from Hfr formation.
: ***************************
: Science 1998 Nov 6;282(5391):1133-5
: Evidence that gene amplification underlies adaptive mutability of the bacterial lac operon.
: Andersson DI, Slechta ES, Roth JR.
: Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.
: Adaptive mutability is the apparent alteration in specificity or rate of mutability seen in bacteria during stress. A model is proposed by which gene amplification during selective growth can give the appearance of adaptive mutability without requiring any change in mutability. The model is based on two assumptions, that a mutant lac locus with residual function allows growth if its copy number is increased, and that true reversion events are made more likely by replication of chromosomes with many copies of the locus. Apparent directed mutability, its recombination requirement, and its apparent independence of cell growth are all accounted for by the model. Evidence is provided for the required residual function and gene amplification.
: ***********************************: Mutat Res 2001 Jan 25;473(1):109-19
: Effect of endogenous carotenoids on "adaptive" mutation in Escherichia coli FC40.
: Bridges BA, Foster PL, Timms AR.
: MRC Cell Mutation Unit, University of Sussex, Falmer, BN1 9RR, Brighton, UK. b.a.bridges@sussex.ac.uk
: The appearance over many days of Lac(+) frameshift mutations in Escherichia coli strain FC40 incubated on lactose selection plates is a classic example of apparent "adaptive" mutation in an episomal gene. We show that endogenously overproduced carotenoids reduce adaptive mutation under selective conditions by a factor of around two. Carotenoids are known to scavenge singlet oxygen suggesting that the accumulation of oxidative base damage may be an integral part of the adaptive mutation phenomenon. If so, the lesion cannot be 7,8-dihydro-8-oxoguanine since adaptive mutation in FC40 is unaffected by mutM and mutY mutations. If active oxygen species such as singlet oxygen are involved in adaptive mutation then they should also induce frameshift mutations in FC40 under non-selective conditions. We show that such mutations can be induced under non-selective conditions by protoporphyrin photosensitisation and that this photodynamic induction is reduced by a factor of just over two when endogenous carotenoids are present. We argue that the involvement of oxidative damage would in no way be inconsistent with current understanding of the mechanism of adaptive mutation and the role of DNA polymerases. ****************************************I think I just falsified Peter's falsification....

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Originally posted by peter borger:
Dear SLPx,

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Thanks for the references.

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They clearly demonstrate that the mutations are protein mediated. It remains to be established in what degree the environment directs the induction of these genes. But, as demonstrated by some of your references rec-enzymes are induced, so it does not falsify my assertions but rather provides further evidence for NON-RANDOM, protein directed mutations (in response to environmental change). Thanks, for the examples.
Maybe you could point out where ecactly these abtracts falsify NONRANDOM mechanisms. For instance, "genome wide" does not mean that it is random, rather that mutations can be found in several genes throughout the genome.

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I don't know whethyer I admire or am disgusted by this common quality in creatinists - taking something that is clearly evidence against their position and claiming that, in reality, it supports it. Strange...

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You really have to come up with better examples to claim falsification over mine (show me the sequences of a mutated gene in several subspecies of the organism after stationary phase).
Cheers,

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Peter

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Interesting - I have yet to see ANY 'falsifications' of anything form you. Wild extrapolations are not really evidence of anything.Better yet, since it is your claim that 'non-random mutations' exist and falsify NDT, and that this 'information' is pre-existing in the genome, maybe you can present some genetic analyses that demonstrate that some gene that is needed for survival but is not active exists in multicellular eukaryotes (provide the sequence of the genome), expose this multicellular eukaryote to some stressor, then demonstrate that the gene needed - and only the gene needed (i.e., not genome wide) is activated via a specific mutation.Syrely you can do this, since you claim to have falsified NDT.Your simplistic defintion of 'random' seems awfully out of place.

[QUOTE]Originally posted by wj:
[B][QUOTE]Originally posted by SLPx:Better yet, since it is your claim that 'non-random mutations' exist and falsify NDT, and that this 'information' is pre-existing in the genome, maybe you can present some genetic analyses that demonstrate that some gene that is needed for survival but is not active exists in multicellular eukaryotes (provide the sequence of the genome), expose this multicellular eukaryote to some stressor, then demonstrate that the gene needed - and only the gene needed (i.e., not genome wide) is activated via a specific mutation.Syrely you can do this, since you claim to have falsified NDT.Your simplistic defintion of 'random' seems awfully out of place.[/B][/QUOTE]Wouldn't the GLO pseudogene be a prime candidate for such a demonstration? There is strong evidence that it would be a fully functional gene with a few correcting mutations. Individuals can be stressed by removing dietary sources of vitamin C.Where is the evidence that such protein directed mutations have occurred? Are these only mutations within somatic cells or do they also occur in gamete cells?BTW, where is the evidence that members of nomadic tribes have functional GLO genes?[/B][/QUOTE]Good questions. I didn't follow the GLO opus, but it would seem that since we have the 'original' sequence, it would be easy enough to test the 'directed mutation' hypothesis.

[QUOTE]Originally posted by peter borger:
[B]Dear SLPx,In response to pointing out the scientific evidence for me you reply:"I don't know whethyer I admire or am disgusted by this common quality in creatinists - taking something that is clearly evidence against their position and claiming that, in reality, it supports it. Strange..."There can only be two reasons for not responding to my question:1) You do not know the content of your refernces,
2) You do not understand the content of your references.If this is the case, do not hesitate to ask.Best wishes,
Peter[/quote]Ah - the ever present creationist condescension.No, Pete, I know and understand. What I do not understand is how you can manipulate it to make it appear to support your claims.Wishful thinking.Oh - what questions were those?[/B][/QUOTE]

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Originally posted by peter borger:
Dear SLPx,

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I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations.

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You mean the ones that you had already claimed in fact support your version of non-random mutations? You hadn't even read them yet, but were claiming them as support for your position?I'm shocked!

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One of the guys in field of hypermutations says in the article that you refer to says:

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"Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal.""

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If I understand his last sentence properly, he says: "All regions are not equal"

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In my opinion not equal means that a mechanism (=non-random) is involved, isn't it?

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If by mnechanism you mean some guiding force, I say LOL!If by mechanism (ahh - I love the sound of a semantics game coming!) you mean a tendency to do one thing over another, than of course., However, as has explained to you repeatedly on this board, there are simple physicochemical reasons for mutations occurring in some areas over others.Water tends to collect in low areas rather than high ones.Are you going to suggest that some Ubermensch plays a role in that, too?

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Originally posted by peter borger:
Dear SLPx,
I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations.

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You mean the ones that you had already claimed in fact support your version of non-random mutations? You hadn't even read them yet, but were claiming them as support for your position?

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I'm shocked!

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Guess I hit that nail on the head, eh "Peter"?

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One of the guys in field of hypermutations says in the article that you refer to says:
"Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal.""

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If I understand his last sentence properly, he says: "All regions are not equal"

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In my opinion not equal means that a mechanism (=non-random) is involved, isn't it?

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If by mnechanism you mean some guiding force, I say LOL!

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I say:
The driving force could be the environment that induces certain proteins (e.g. polymerases) that carry out the mutations.

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And how does your 'conclusion' of non-random mutation falsifying NDT follow from that? In your selective readings of the papers I cited, di dyou not notice that the mutations were not centered - directed - specifically to the genes 'needed'?
Or did that slip by your razor-keen scientific insight?

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You say:
If by mechanism (ahh - I love the sound of a semantics game coming!) you mean a tendency to do one thing over another, than of course., However, as has explained to you repeatedly on this board, there are simple physicochemical reasons for mutations occurring in some areas over others.

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I say:
"Molecular mechanism in biology usually involve proteins and/or RNA molecules. If so, all necessities are present in the genome"

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LOL! Yeah, I guess those "kinds" must have been jammy-packed with all sorts of genes that they didn't need and that are, dammit, no longer present in their in-kind descendants...

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You say:
Water tends to collect in low areas rather than high ones.

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Are you going to suggest that some Ubermensch plays a role in that, too?

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I say:
You use similar faulty analogies as Mark24. You cannot compare gravity and protein mediated mechanism. I know you have to use such analogies, since you need naturalistic explanations for NDT. However, if all things are in the genome to respond to environmental change, a naturalistic explanations is untenable."

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My "analogy" was not to NDT, rather it was to demonstrate that there are perfectly natural reasons for apparently 'specified' outcomes. As is so often the case, the creationist eads too much into posts and tries to make much of their shallow comprehensive skills.
I am still waiting for your unequivocal evidence that these unused but maybe someday necessary genes are in the genomes of all creatures, just waiting for that one lucky mutation - in the right conditions, of course - to be turned on.Your silly (and typically overconfident) position simply supports something I have believed for some time now - evolutionists base their thoughts on what is known, creaetionists base theirs on what is not.

[QUOTE]Originally posted by peter borger:I say:
"Read something on neutral evolution (NT). You will find out that according to NT genetic change is expected on third positions in AA codons (due to redundancy in the genetic code). They are not present for the major part of protein coding genes. I think that's a bit peculiar in the light that it took these organsims millions of years to evolve."best wishes
Peter[/B][/QUOTE]Hi Peter,I was hoping that you could point out where in Kimura's works he explains that genetic change is expected on third positions in AA codons. I think what the creationist is doing is engaging in a classic cart-before-the-horse misrepresentation here.But, please, Peter, prove me wrong. I possess a collection of Kimura's works, and I am fairly certain that I will have the paper(s) you cite.

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Originally posted by peter borger:

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Furthermore, Rosenberg says that "[adaptive mutations] provides the molecular basis for a potential path for the rapid evolution of new traits". This clearly indicates that all necessities for 'evolution' (=variation induction) are present in the genome and may be activated in response to the environment. If so, NDT RIP.

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I was wondering - did/do any of these papers deal with multicellular eukaryotes?

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In conclusion, I do not see how this article supports your vision. Could you please explain?

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best wishes,
Peter

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I already have a couple of times, but again - the mutations are not 'directed' at specific regions of the genome, therefore, they are not non-random in the way that you want them to be. You have focused - as do all creationists that try to use this flawed 'logic' - on the fact that some regions of the genome are more prone to mutation than others I am unaware of any evidence indicating that the regions that are more likely to receive mutations are those that would help the prokaryotic bacteria to adapt to its new environment.Indeed, in the papers I cited, which you have apparently finally read (long after claiming that they supported your position) it is pointed out that only a subset of the bacteria were able to survive. Clearly, if there were some "direction" mechanism, we should be able to see near;y 100% survivability. I mean, if the needed genes and apparatus are already in the genome, and there is this non-random mechanism, it should be a bit more efficient, don't you think?What you appear to be doing in Woodmorrapping - claiming that a set of anomalies indicate that the opposite position is correct.Bad logic, bad science, good zealotry.[This message has been edited by SLPx, 09-17-2002]

Hi "Peter B",I was wondering if you had planned to address my posts 133 and 134?

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Originally posted by peter borger:
Originally posted by peter borger:
Dear SLPx,
I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations.
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You mean the ones that you had already claimed in fact support your version of non-random mutations? You hadn't even read them yet, but were claiming them as support for your position?

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I'm shocked!

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Guess I hit that nail on the head, eh "Peter"?

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I say:
Why reiterate this, while I already explained to you that the article you referred to was in a mail to Fred Williams not a message addressed to me, so I missed it (look it up, if you like, it was a Science paper in a mailing to Fred. But anyway, it is nit-picking)

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I have no need to look it up. It is right here:http://EvC Forum: molecular genetic proof against random mutation (1) -->EvC Forum: molecular genetic proof against random mutation (1)Message 96. I DIRECTLY address you in reply to a request from you. You replied in Message 97 that these citations support your position. As is so common with creationists, you then actually went on condescendingly how I must not understand the content of the papers (message 102, Aug.22) and such.Yet it was not until SEPTEMBER 12 that you actually even read the papers! (YOUR message 123 in the linked thread).So, "Peter B", your 'memory' is a bit clouded. You have: 1)Tried to misrepresent the situation by claiming that I was writing to Williams, not you. That is demonstably false. 2) You arrogantly and overconfidently implied that it was I that had not read the papers or could not understand them when in reality it took you nearly a month to get around to looking at them DESPITE the fact that you had previously proclaimed them supportinve of your claims, and then still ignored the fact that not of them even comes close to supporting the notion of 'directed mutation' as you describe it.Nitpicking, indeed...

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One of the guys in field of hypermutations says in the article that you refer to says:
"Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal.""
If I understand his last sentence properly, he says: "All regions are not equal"

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In my opinion not equal means that a mechanism (=non-random) is involved, isn't it?

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If by mechanism you mean some guiding force, I say LOL!

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I say:
The driving force could be the environment that induces certain proteins (e.g. polymerases) that carry out the mutations.

​

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And how does your 'conclusion' of non-random mutation falsifying NDT follow from that? In your selective readings of the papers I cited, did you not notice that the mutations were not centered - directed - specifically to the genes 'needed'?
Or did that slip by your razor-keen scientific insight?

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I say:
Probably prokaryotes differ from eukaryotes in this respect (although they have lots of redundant genes too). In comparison, it was long thought that prokaryotes do not have introns, but now we know that some have. So, a mechanism not optimal/fully present in prokaryotes may be fully operative in eukaryotes.

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Just so stories form the creationist. You have learned well from creationist Spetner, who also had no actual supportive evidence for his fairy tales occurring in multicellular eukaryotes.

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you quote:
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You say:
If by mechanism (ahh - I love the sound of a semantics game coming!) you mean a tendency to do one thing over another, than of course., However, as has explained to you repeatedly on this board, there are simple physicochemical reasons for mutations occurring in some areas over others.

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I say:
"Molecular mechanism in biology usually involve proteins and/or RNA molecules. If so, all necessities are present in the genome"

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LOL! Yeah, I guess those "kinds" must have been jammy-packed with all sorts of genes that they didn't need and that are, dammit, no longer present in their in-kind descendants...

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I say:
Loss of genes is a common mechanism in evolutionism[sic] to explain observations. There is even a discipline in evolutionism that postulates utter hypothetical gene additions and gene deletions to reconcile gene trees with species tree.

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Please expand on this. Please provide citations, as well. Also, please explain why it is that you believe that all gene trees should be exactly the same.

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You say:
Water tends to collect in low areas rather than high ones.
Are you going to suggest that some Ubermensch plays a role in that, too?

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I say:
You use similar faulty analogies as Mark24. You cannot compare gravity and protein mediated mechanism. I know you have to use such analogies, since you need naturalistic explanations for NDT. However, if all things are in the genome to respond to environmental change, a naturalistic explanations is untenable."

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You say:
My "analogy" was not to NDT, rather it was to demonstrate that there are perfectly natural reasons for apparently 'specified' outcomes. As is so often the case, the creationist eads too much into posts and tries to make much of their shallow comprehensive skills.

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I say:
Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude.

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You may recall that I was not the one claiming that articles that I had not read support my position. THAT is overconfidence. Also, I was not the one that 'explained' that perhaps I didn't understand what was in the articles... the ones that you hadn't yet read...
The analogy was clear, and it fulfilled its purpose. That you could not understand it has nothing to do with anyone's overconfidence, real or imagined.

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Challenge me and I will falsify common descent beyond doubt. I will open a new thread, if you like.

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Consider this a challenge. Similar to the other challenge that you suggested, discussing gene trees and such.
I think I will find your beyond-doubt falsification most informative, and will gingerly forward it to the appropriate authorities such that we can immediately informa those thousands of scientists that utilize evolutionary theory in their research that they are going about their work all wrong.

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And concerning the Uebermensch: you were the one that introduced space-aliens to explain genes in humans not present in apes. I can think of several better 'scientific' non-testable explanations.

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I did no such thing. Please stop misrepresenting me and trying to erect strawman arguments.

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You say:
I am still waiting for your unequivocal evidence that these unused but maybe someday necessary genes are in the genomes of all creatures......

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(Creatures? When did you become a creationist? )

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When did you become such a moron?

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....just waiting for that one lucky mutation - in the right conditions, of course - to be turned on.

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I say:
Redundant genes are 'non per niente' in the genome. Yes, my hypothesis of "(non-)random mutation in a multipurpose genome" is ALMOST as incredible as evolutionism. Probably we have to wait for another decade and we will know. At least if the appropriate experiments are carried out. That is: the comparison of subspecies with related species. That is not: the comparison of individuals of distinct species.

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How do you propose this comparison be done?

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You say:
Your silly (and typically overconfident) position simply supports something I have believed for some time now - evolutionists base their thoughts on what is known, creationists base theirs on what is not.

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I say:
The real silly thing is that even the major part of the tiny bit that we know from the genome does NOT point in the direction of evolution.

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And there is the gem - that nugget of creationist stupidity that pops its head out once in a while.I wonder what your more knowledgible and rational colleagues would think if they knew that you were writing - and apparently believe - something so asinine?
I guess you didn't realize that all those duplicated genes actually fit quite well within an evolutionary framework? Nah - you are a creationist, and your personal opinions are the REALLY important things! facts be damned!

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(ever heard of the second DNA associated code of transcription? And there may even be a third code involved in coactivation of transcription. Firstly, there is NO evolutionary explanation for the first code. And now we find that the first code gives rise to a second code through possible another code. So you better present a pretty good story to explain this by a random mechanism).

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Frankly, no, I have not heard of this. Please provide some verifiable documentation that I can check to see if your depiction of this is accurate.

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BTW, I already gave an alternative explanation for all observations in the genome. Yes, it is a HYPOTHESIS --just like evolutionism is-- and it should be tested.

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test away. You're the expert scientist, right?
Oh - where is this hypothessis again?

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And in regard to "overconfident": All I did was demonstrating that evolution is NOT a fact. Present it as a hypothesis and I don't have a problem, and I wouldn't even have registered to this board. Present it "overconfidently" as FACT and I will blow it up! No problem, just show the right examples.

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Whatever you say, Petey....Whatever you say....

Wow...This is just getting boring....The creationist's fusilade of slime is nearing completion.1. Claim not to be a creationist.
2. Claim to have refuted/falsified evolution
3. refuse to support said falsification with anything other than assertion
4. claim that evolutionists are wrong, deluded, ignorant, etc.
5. Make false accusations against opponants
6. try to weasel out of uncomfortable situations by ignoring them or blaming them on 'the medium' or by projecting
7. say that you will get back to something, but never do
8. start a new thread on something else
9 re-claim falsification of evolution
10. stop posting, but claim victory on last series of posts
11. go to another board, do it all over againI'm just wondering when 10 and 11 show up...

Peter the false witness boy:"BTW, I discussed this already with Dr page himself and he couldn't address it beyong 'maybe it isn't properly rooted'."This is entirely untrue. I have mentioned that I would like ot discuss this, but PB never has, not with me anyway. I have never made such a reply.Peter B has taken the route of the desparate creationist, putting words in the mouth of his opponant (see especially his last post to me!) and engaging in dishgonesty.We should all be wary of this.

Please not the sections in bold:

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Originally posted by peter borger:
Dear SLPx,

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You wrote in a previous mail I didn't see yet:

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"------------------------------------------------------------------
quote:
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Originally posted by peter borger:
I say:
"Read something on neutral evolution (NT). You will find out that according to NT genetic change is expected on third positions in AA codons (due to redundancy in the genetic code). They are not present for the major part of protein coding genes. I think that's a bit peculiar in the light that it took these organsims millions of years to evolve."

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best wishes
Peter
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Hi Peter,

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I was hoping that you could point out where in Kimura's works he explains that genetic change is expected on third positions in AA codons. I think what the creationist is doing is engaging in a classic cart-before-the-horse misrepresentation here.

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But, please, Peter, prove me wrong. I possess a collection of Kimura's works, and I am fairly certain that I will have the paper(s) you cite."

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I say:
It is known that the redundancy in the genetic code leads to neutral positions on the third positions of codons. For instance, the aminoacid leucine can be coded by 6 different codons including CUU, CUC, CUA, CUG. A look at these 4 codons reveals that the third letter of the code is unimportant for determining the aminoacid. This is known as "wobble in the anticodon". The same accounts for the aminoacids valine, serine, proline, threonine, alanine, arginine, and glycine. So, these positions are not under selective constraint (neutral positions) and are expected to behave accordingly. I don't know whether Kimura also had these positions in mind, but I do.

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Why is it that I have come to expect this sort of thing from Peter B, creationist?Oh, I know - its the whole creationist thing...

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Originally posted by peter borger:
Dear SLPx:
THIS IS WHAT YOU WROTE. MY RESPONSE IS IN CAPITAL LETTERS< SO YOU WILL NOT GET CONFUSED.

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Thanks, Pete. I do find your posts most confusing.

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Originally posted by peter borger:
Dear SLPx,
I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations.
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SLPx:You mean the ones that you had already claimed in fact support your version of non-random mutations? You hadn't even read them yet, but were claiming them as support for your position?
I'm shocked!

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Guess I hit that nail on the head, eh "Peter"?

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I say:
Why reiterate this, while I already explained to you that the article you referred to was in a mail to Fred Williams not a message addressed to me, so I missed it (look it up, if you like, it was a Science paper in a mailing to Fred. But anyway, it is nit-picking)

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SLPx:
I have no need to look it up. It is right here:

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http://EvC Forum: molecular genetic proof against random mutation (1) -->EvC Forum: molecular genetic proof against random mutation (1)

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Message 96. I DIRECTLY address you in reply to a request from you. You replied in Message 97 that these citations support your position. As is so common with creationists, you then actually went on condescendingly how I must not understand the content of the papers (message 102, Aug.22) and such.

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Yet it was not until SEPTEMBER 12 that you actually even read the papers! (YOUR message 123 in the linked thread).

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So, "Peter B", your 'memory' is a bit clouded.

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MY RESPONSE:
THE ONLY ONE HERE TO MISREPRESENT THINGS IS YOU. iF YOU GO BACK IN THE THREAD THAN YOU WILL FIND OUT THAT I REFFERRED TO THE SCIENCE PAPER IN YOUR MAIL TO FRED. THIS MAIL CAN BE FOUND IN THIS THREAD #52, THE CAIRNS EXCERPT. SO NEXT TIME BEFORE YOU START TO BLAME ME READ BACK AND PREPARE PROPERLY.

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You know, it is the strangest thing. Looking at my post #52, I did indeed post a reply to Williams with a link to a Science article containing information on Cairns. But if one looks at the links to replies in the bottom of that post, one sees that you did not respond to it until post #123. This of course is well after I had already reposted a quote from that source and supplied several abstracts to papers that provide direct evidence against 'directed' mutations - the ones you claimed were in fact evidence for them.While I see that I was in error in so far as interpreting your post #123 and #126, I maintain that you did not read, or perhaps understand, the implications of the abstracts I posted in #96. One has to be a dogmatist extraordinaire to believe that papers explaining how mutations occurred genome-wide really indicate a non-random mechanism.

quote:

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You have: 1)Tried to misrepresent the situation by claiming that I was writing to Williams, not you. That is demonstably false. 2) You arrogantly and overconfidently implied that it was I that had not read the papers or could not understand them when in reality it took you nearly a month to get around to looking at them DESPITE the fact that you had previously proclaimed them supportinve of your claims, and then still ignored the fact that not of them even comes close to supporting the notion of 'directed mutation' as you describe it.

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Nitpicking, indeed...

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One of the guys in field of hypermutations says in the article that you refer to says:
"Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal.""
If I understand his last sentence properly, he says: "All regions are not equal"

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MY RESPONSE:
THIS CAN BE FOUND IN MAIL #52 TO FRED, THE CAIRNS EXCERPT. NOT IN A MAIL TO ME.

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Yes, I see that now. My sincere apologies. However, again, I quoted from that article in a message directed to you, to which you responded immediately with some nonsense about the articles really supporting non-random mutation. And again we see that the creationist hangs his hat on what might be, rather than what is.

quote:

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In my opinion not equal means that a mechanism (=non-random) is involved, isn't it?

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If by mechanism you mean some guiding force, I say LOL!

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I say:
The driving force could be the environment that induces certain proteins (e.g. polymerases) that carry out the mutations.

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And how does your 'conclusion' of non-random mutation falsifying NDT follow from that? In your selective readings of the papers I cited, did you not notice that the mutations were not centered - directed - specifically to the genes 'needed'?
Or did that slip by your razor-keen scientific insight?

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I say:
Probably prokaryotes differ from eukaryotes in this respect (although they have lots of redundant genes too). In comparison, it was long thought that prokaryotes do not have introns, but now we know that some have. So, a mechanism not optimal/fully present in prokaryotes may be fully operative in eukaryotes.

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Just so stories form the creationist. You have learned well from creationist Spetner, who also had no actual supportive evidence for his fairy tales occurring in multicellular eukaryotes.

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MY RESPONSE:
YOU ARE WRONG. WHEN SPETNER WROTE HIS BOOK (BEFORE 1997) THESE EXPERIMENTS HAD RECENTLY BEEN PUBLISHED, SO SPETNER WAS PRETTY UP TO DATE WITH HIS BOOK.

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I am wrong? Well, then, Peter B., please supply us with the documentation for non-random mutations occurring in multicellular eukaryotes that result in phenotypic change. The best he could do was some pap about sea gull wings... Which of course had no genetic analysis in its support...
Spetner the creationist could not do this then, and he has not done it yet.
Help him out.

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THAT THE MECHANISM IS NOT EXACTLY AS HE (AND CAIRNS) THOUGHT IT WAS, IS NOT SURPRISING SINCE NOTHING IN BIOLOGY IS AS WE EXPECT IT TO BE.

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So he was wrong then. Good to hear you say that.

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FURTHERMORE, THE CAIRNS INTERPRETATION IS ONLY A MINOR POINT IN SPETNER'S BOOK SO YOU CANNOT REJECT HIS ENTIRE BOOK ON CAIRN'S PARTIAL RECANTATION.

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I didn't. Indeed, the Cairn's bit was mentioned in regards to "non-random mutation" in general, not to anyone's vanity press book targeting a lay audience.

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BETTER READ HIS BOOK INSTEAD OF ONLY HIS OPPONENTS. AND WHY DO YOU THINK THERE HAVE BEEN CARRIED OUT SO MANY EXPERIMENTS TO FALSIFY CAIRNS INTERPRETATION?

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In reality, so many experiments were carried out to see if he was right (he wasn't), not to try to disprove him.

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THE NDT WOULD HAVE FALLEN, AND THAT IS EXACTLY WHY YOU OBJECT/DENY THE NON-RANDOMNESS OF MUTATION IN THE 1G5 GENE. AND THAT'S WHY NDT BLOCKS SCIENTIFIC PROGRESS.

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What progress would be made by accepting a fringe idea on non-random mutation? I object/deny it because as I have repeatedly explained and supplied references for, the idea of non-randomness is not what it is made out to be by folks like you.

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you quote:
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You say:
If by mechanism (ahh - I love the sound of a semantics game coming!) you mean a tendency to do one thing over another, than of course., However, as has explained to you repeatedly on this board, there are simple physicochemical reasons for mutations occurring in some areas over others.

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I say:
"Molecular mechanism in biology usually involve proteins and/or RNA molecules. If so, all necessities are present in the genome"

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LOL! Yeah, I guess those "kinds" must have been jammy-packed with all sorts of genes that they didn't need and that are, dammit, no longer present in their in-kind descendants...

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I say:
Loss of genes is a common mechanism in evolutionism[sic] to explain observations. There is even a discipline in evolutionism that postulates utter hypothetical gene additions and gene deletions to reconcile gene trees with species tree.

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Please expand on this. Please provide citations, as well. Also, please explain why it is that you believe that all gene trees should be exactly the same.

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MY RESPONSE:
ANY RECENT BOOK ON MOLECULAR EVOLUTION HAS A CHAPTER CONCERNING ‘RECONCILIATION OF GENE TREES WITH SPECIES TREES'.

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They do? Examples please.

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ACCORDING TO EVOLUTIONARY BIOLOGISTS, GENE TREES HAVE TO BE IN AGREEMENT WITH SPECIES TREES.

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This is a major misrepresentation on your part, Peter B. It is outright false.
Your credibility - what little you may have once had here - is now completely gone.

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WHY? OTHERWISE ALL GENES LYING OUT PROVIDE FALSIFICATIONS OF COMMON DESCENT.

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This is just asinine, and indicative of your dogmatic ignorance. Any text on molecular evolution not only explains why discrepencies exist, they actually predict that more will be found.

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YOU CAN FIND THIS HIGHLY DISPUTABLE MATHEMATHICAL TRICK FOR INSTANCE IN 'MOLECULAR EVOLUTION, A PHYLOGENTIC APPROACH by R. PAGE'. WHAT EVO’S DO IS THE OTHER WAY AROUND REASONING. THEY CLAIM THAT SINCE EVOLUTION IS TRUE, THE EVIDENCE FOR PUTATIVE DUPLICATIONS IS SIMPLY THE INCONGRUENCE BETWEEN THE GENE AND THE SPECIES TREE. I OBJECT TO SUCH SIMPLISICISM.

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I object to your idiocy, but it won't get me anywhere. Is it a 'trick'? That sounds awfully inflammatory, Peter B. Perhaps you don't understand statistics? Or maybe the workings of genomes? Well, either way, your claims are getting more and more bizarre and more and more desparate.

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FOR EXAMPLES: (http://taxonomy.zoology.gla.ac.uk/rod/papers/page97mpe.pdf).

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The abstract:"The processes of gene duplication, loss, and lineage
sorting can result in incongruence between the phylogenies
of genes and those of species. This incongruence
complicates the task of inferring the latter from the
former. We describe the use of reconciled trees to
reconstruct the history of a gene tree with respect to a
species tree. Reconciled trees allow the history of the
gene tree to be visualized and also quantify the relationship
between the two trees. The cost of a reconciled
tree is the total number of duplications and gene losses
required to reconcile a gene tree with its species tree.
We describe the use of heuristic searches to find the
species tree which yields the reconciled tree with the
lowest cost. This method can be used to infer species
trees from one or more gene trees."Whats your point?I am constantly amazed at how the creationist interprets 'explanations' as 'excuses' and the like. Pitiful, really.

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You say:
Water tends to collect in low areas rather than high ones.
Are you going to suggest that some Ubermensch plays a role in that, too?
I say:
You use similar faulty analogies as Mark24. You cannot compare gravity and protein mediated mechanism. I know you have to use such analogies, since you need naturalistic explanations for NDT. However, if all things are in the genome to respond to environmental change, a naturalistic explanations is untenable."

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You say:
My "analogy" was not to NDT, rather it was to demonstrate that there are perfectly natural reasons for apparently 'specified' outcomes. As is so often the case, the creationist Reads too much into posts and tries to make much of their shallow comprehensive skills.

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I say:
Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude.

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No, it is a valid conclusion.

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You may recall that I was not the one claiming that articles that I had not read support my position. THAT is overconfidence. Also, I was not the one that 'explained' that perhaps I didn't understand what was in the articles... the ones that you hadn't yet read...
The analogy was clear, and it fulfilled its purpose. That you could not understand it has nothing to do with anyone's overconfidence, real or imagined.

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Challenge me and I will falsify common descent beyond doubt. I will open a new thread, if you like.
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Consider this a challenge. Similar to the other challenge that you suggested, discussing gene trees and such.
I think I will find your beyond-doubt falsification most informative, and will gingerly forward it to the appropriate authorities such that we can immediately informa those thousands of scientists that utilize evolutionary theory in their research that they are going about their work all wrong.

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MY RESPONSE:
THE MOLECULAR GENAEOLGY OF INTERLEUKIN-1-beta demonstrates an aberration from the species tree.

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So?

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And concerning the Uebermensch: you were the one that introduced space-aliens to explain genes in humans not present in apes. I can think of several better 'scientific' non-testable explanations.
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I did no such thing. Please stop misrepresenting me and trying to erect straw man arguments.

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MY RESPONSE;
YES, YOU DID. IN RESPONSE TO THE GENES PRESENT IN HUMAN NOT PRSENT IN MAN.

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What genes might be present in humans but not in man, I wonder...

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You say:
I am still waiting for your unequivocal evidence that these unused but maybe someday necessary genes are in the genomes of all creatures......
(Creatures? When did you become a creationist? )

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When did you become such a moron?

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MY RESPONSE:
JUST KIDDING.

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I see...

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....just waiting for that one lucky mutation - in the right conditions, of course - to be turned on.

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I say:
Redundant genes are 'non per niente' in the genome. Yes, my hypothesis of "(non-)random mutation in a multipurpose genome" is ALMOST as incredible as evolutionism. Probably we have to wait for another decade and we will know. At least if the appropriate experiments are carried out. That is: the comparison of subspecies with related species. That is not: the comparison of individuals of distinct species.

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How do you propose this comparison be done?

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MY RESPONSE:
AS DEMONSTRATED FOR THE 1G5 GENES IN A LARGE AMOUNT OF SUBPOPULATIONS.

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What do you mean sub-population?

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I AM INTERESTED IN THE SEQUENCES OF ONE PARTICULARE GENE (SAY HEMOGLOBIN OR CYTOCHROME C) THROUGHOUT THE DIFFERENT HUMAN SUBPOPULATIONS. I WONDER WHETHER THESE DATA ARE PRESENT INLITERATURE?

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I don't know about that particular gene, but Paabo's group has done an extensive study on the mitochondrial genome and, why, it must be a mere coincidence, the findings fit wquite nicely with evolutionary hypotheses.

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You say:
Your silly (and typically overconfident) position simply supports something I have believed for some time now - evolutionists base their thoughts on what is known, creationists base theirs on what is not.

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I say:
The real silly thing is that even the major part of the tiny bit that we know from the genome does NOT point in the direction of evolution.

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And there is the gem - that nugget of creationist stupidity that pops its head out once in a while.

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I wonder what your more knowledgible and rational colleagues would think if they knew that you were writing - and apparently believe - something so asinine?
I guess you didn't realize that all those duplicated genes actually fit quite well within an evolutionary framework? Nah - you are a creationist, and your personal opinions are the REALLY important things! facts be damned!

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(ever heard of the second DNA associated code of transcription? And there may even be a third code involved in coactivation of transcription. Firstly, there is NO evolutionary explanation for the first code. And now we find that the first code gives rise to a second code through possible another code. So you better present a pretty good story to explain this by a random mechanism).
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Frankly, no, I have not heard of this. Please provide some verifiable documentation that I can check to see if your depiction of this is accurate.

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MY RESPONSE:
I ALREADY GAVE THE REFERENCES. I AM WAITING FOR A REPONSE.

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I am still waiting for your hypothesis...
A response to what? Let me guess - that falsifies evolution too?