Darwin in the Genome

Paul: You don't have to be a rocket scientist to work out what the NDT requires in the way of "random" mutations. It was even mentioned in this thread, but it still seems to be beyond you.PB: I invited you to explain it to the board. This is another nonanswer.PK2: I asked YOU to explain it because YOU brought up the issue. And you haven't - instead you expect me to explain it. It is your duty to back up your assertions - and you;ve been running away from this one for months. Calling my response a "nonanswer" is pure hypocrisy since you are the one refusing to answer MY query.(And I have explained it and told you where to find another explanation - but you don't listen).Paul:
If you were REALLY any sort of scientist at all - or even had a PhD it wouldn;t be difficult for you to discuss such a simple basic point. So either you know full well that you are wrong and are just evading the issue or you are misrepresenting your qualfications.PB: The mocking and scoffing starts here, I guess. Not impressive.PK2: You were the one who said that it wasn't scientific to refuse to explain criticisms. All I am asking you to do is to back up your own claimed refutation of NDT. And you keep on and on evading the issue. You may find my comments "mocking" you may not be impressed by them - but they remain true and remain a major indictment of your arguments.- or rather your unargued assertionsAnd no, I'm not impressed by your scoffing and mockery either.Paul: You don;t have to be that bright to notice that I did deal with your point about Darwins alleged extrapolations by pointing out that it was false.PB: No, you didn't such thing. If so, make a link. Proof your claims.PK2: When I asked you to do the same thing all you offered was links to threads. But here you go http://EvC Forum: Darwin in the Genome -->EvC Forum: Darwin in the Genome
i.e. message 47 in this very thread. And you claim that I don't read your posts.Paul: It doesn't take much brain to say that your reference to "Darwinian tale telling" is simply a random insult with no reference to the actual discussion.PB: I offered you to demonstrate the references, you didn't respond. For obviousl reasons.PK2 : I did respond by pointing out that you had none. After all you've been claiming that since the start and never produced any argument - so why should we believe that you've suddenly found something now ?
And I note that you offer no substantive justification of your use of the phrase "Darwinian tale-telling" thus confirming my point.Paul: And you have no references from _Darwin in the Genome_ that demonstrate NDT to be wrong. We both know that..PB: I will spell out the references later, haven't the book here.PK2: And since I do have the book I will point out the truth. So don't waste your time quote-mining.PK: We both know that Dr. Caporales findings are a bigger problem for your views than for NDT.PB: I explained why they are a bigger problem for DNT and evolutionism in general. Now YOU are going to explain. Simply claiming is all you do. EXPLAIN PLEASE. IN DETAIL, like I do all the time.PK2; EVERY time I have asked you to explain how one of them fitted into your theory you refused to go into detail I even pointed out how hypermutation went against your theory . You only need to go back a few posts to see me explictly ask about hairpin deletions - and no answer from you.An example of one of your ACTUAL answers is - I quote -"I will fit them in. The are part of the GUToB and will find their place in the MPG" Is THAT an "IN DETAIL" explanation ?Paul: Your assertions about the MPG are not supported by the evidence.PB: Get real, PK. That all the info for variation is in the genome is what Caporale demonstrated. That is the MPG I have been discussing for ages, now. Close your eyes, put your fingers in your ears and hummmmmmmmmmmm.PK2: Hypermutation alone refutes that claim. So does lateral transfer. So does duplication and diversification. Three examples discussed by Dr. Caporale. For someoen who claims to have read the book, you seem to have a very limited knowledge of its contents.Paul: And misrepresenting Darwin's reasoning - as you so repeatedly do here is just a contemptible debate tactic.PB: Okay, another excellent opportunity to explain how Dawrin got his dangerous idea. (Next, I will obliterate it.)PK2 : As I pointed out at the time it was mainly based on taxonomy and biogeography - likewise for Wallace. You even seemed to agree! But that didn't stop you going back to the same old distortions.Paul: But keep on evading and backpedalling, Peter. It shows that your view doesn't have a leg to stand on.PB: The Page attitude?PK2: No, just am observation. If you can't even explain a point that you claim to have refuted, if something your arguments insist is a vital part of the theory turns out to be - from your own claims - an assumption that can easily be dispensed with then you really don't know wnough for your opinion to count with any rational person.Well, if this is all evo's can put forward I consider evolutionism RIP. Long live the GUToB!!PK2: Obviously you have your personal opinion while we have proof that you don't know what you are talking about. Naturally in your mind your opinion wins.

If you want a scientific discussion we can start with your explanation of how non-random mutations actually refute NDT - after all refusing to explain your criticisms is non-scientific as you said. But it seems that you do not want to discuss that.I also notice that providing the link to prove my claim - as you demanded seems to be considered a "non-answer".As is my list of examples which show that _Darwin in the Genome_ refutes your claim that information is never added to the genome (proving my point that the book is a greater problem for your views than for NDT).In short your idea of a "scientific" discussion means dropping the discussion because your errors are being revealed.Anyway to deal with your assertions.
1) p37-38 deal with the "hairpin" model. Since such models require that the existing sequence is similar they can only upset phylogenetic analysis at fine resolutions- which you apparently accept, unless you wish to claim each species is a seperate creation (which would then pose the question of why the sequences are similar enough to see such mutations). It poses no threat to the larger scale phylogenies which you seem to object to.2) Translocations - since these require that the material to be translocated is already present in the genome it would seem that your "related MPGs" are related by common descent. I thought your assertion was that MPGs were NOT related in that way. It seems to me that again translocations can only interfere with phylogenies at the fine resolution of individual branch points and can only do so because large scale evolution is correct.3) Your list is hardly exhaustive and so to suggest that these two factors alone account for all variation would be an obvious error. However unless you make that error your assertion is clearly unproven. I also note that you insist on repeating your false claim about Darwin, despite the fact that you know it to be untrue. The former is unscientific, the unscientific and dishonest.

PB: Thanks for your non-answers. Since you seem to hold scientific truth let's try again to start up a scientific debate on the topic. These are the points I have made and are still unsolved.PK3 Note that this drops the ongoing discussion.PK says:
If you want a scientific discussion we can start with your explanation of how non-random mutations actually refute NDT - after all refusing to explain your criticisms is non-scientific as you said. But itI also notice that providing the link to prove my claim - as you demanded seems to be considered a "non-answer".PB2: Your link is a non-answer for I already rebutted mail #47 in mail #48.PK3: No, you have not explained why the evidence of taxonomy, biogeography and the fossil record should be held to be irrelevant.PB (cont): And, since you keep repeating that I have to demonstrate NRM to refute NDT (what I did months ago, but apparently youdon't read my mails)PK3: Then provide a link to the post. If you can. Since we both know that you don;t understand this point we both know that all you'll ocme up wiht is assertions.PB cont :let's find out what Dr Caporale has to say about this in her excellent book that is a big thorn in the eye of the orthodox evolutionists. From Darwin in the Genome:"Once we learned about DNA, we saw that mistakes in copying generate mutations and so we've assumed that random mutation followed by selection underlies evolution. However, I have come to the conclusion that using our current knowledge to expand on Darwin's insights does not require that all mutations be random with respect to their potential effects on biological function". (page 42).PK3 : So Dr. Caporale clearly says that the randomness of mutations was only "assumed" and that the assumed randomness was "with respect to biological function" (as I have said - obviously you read neither my posts nor the book) and that such a view is "not required" for evolution. Thanks for providing a quote which so neatly illustrates your errors.Quotes cont:
"So, E coli cannot randomly try every possible change and then wait for selection to capture the very best one". (page72)."Randomly trying out mutations in each copy of each of many thousands of gene families could mean eons spent wandering lost through the broad mutation landscape, in spite of the fact that information could be could be available to help guide the journey. Still, most people assume that mutaions happen randomly throughout the duplicated genes, and that natural selection picks those that lead to a useful new function". (page 129).Which goes on to state that particular parts of the gene - the binding sites are more prone to mutation - and that is the limit of the "non-random" nature proposed. This is also consistent of Dr Caporales view that evolutionary theory must be expanded to include genomic strategies.Quotes continue:
"New levels of interaction and regulation rarely arise through letter by letter random mutations of random DNA sequences". (page 144).PK3: Which is only a problem for people - like Lee Spetner - who for some strange reason insist that evolution is limited to point mutations"The genomic landscape is huge. Random wandering through the landscape of possible mutations is no the most efficient strategy for long term survival. In our own case, random mutation would mean that any one of the more than 3 billion spots in our genome had the same probablity of each kind of change." (page 185).PK3 : And goes on to say "It does not mean all mutations are precisely targetted" And of course this does not refer to evolutionary theory which never seems to have cared much about the issue."Current evolutionary theory states that variation results from genetic changes that remain forever random, and that selection operates upon the results of this random genetic variation. It is time toincorporate the observations described in this book into evolutionary biology". (page 192).I completely agree and I already mentioned this in a mail in May 2002: NDT RIP. Then, it was firmly denied and now here we have Dr Caporale with exactly the same claim. You can of course deny her, too.PK3L I suggest you provide a link to this, too or I will assume that you are lying. But note that I do not deny it at all and have expressed ageement with it. It is you that has disagreed by insisting that instead of following the rourt proposed by Dr Caporale, evolution should be thrown out and replaced by your idle musings.PK (cont): As is my list of examples which show that _Darwin in the Genome_ refutes your claim that information is never added to the genome (proving my point that the book is a greater problem for your views than for NDT).PB: Apparently you didn't read the book properly. The mechanisms described are included in GUToB.PK3: Then the GUToB claims that information can be added to the genome. It seems that the GUToB is inconsistent.PK (cont): In short your idea of a "scientific" discussion means dropping the discussion because your errors are being revealed.PB: What a humbug. I've never dropped a discussion. As a matter of fact, I have won all my discussions with evo's. (Till now, Dr Douglas Theobald from the Talk-origin was the best defender of evolutionism, but not good enough. He couldn't defend the IL-1 beta incongruence).PK3: Since you did start this part of the discussion to stop a previous discussion, and given your habit of proclaiming victory even when you have lost (and noting your abject defeat on another thread currntly in progress) your statment is so obivously false I can only conclude that you are either a compulsive liar or deeply delusionalPB(cont) In response to:
PB: 1) Non-Random Mutations type 1 (NRM1). This type of NRM introduces mutations on the same positions and the position where they are introduced depends on the flanking DNA regions. NRM1 are also known as ‘positional NRM’. NRM1 have been also observed in the ZFY region and in mtDNA. NRM1 has been observed in T4 by Lynn Ripley and was described in Caporale’s book (page 37, 38). Implications: NRM1 will line up and give the illusion of common descent in phylogenetic analysis.
Since phylo-geneticists cannot exclude NRM1, this type of mutations invalidates the evolutionary conclusions that the alignment of genes and shared mutations is proof for common descent.PK says:
Anyway to deal with your assertions.
1) p37-38 deal with the "hairpin" model. Since such models require that the existing sequence is similar they can only upset phylogenetic analysis at fine resolutions- which you apparently accept,
unless you wish to claim each species is a seperate creation (which would then pose the question of why the sequences are similar enough to see such mutations). It poses no threat to the larger scale phylogenies which you seem to object to.PB2:
At present, the hairpin model is able to explain specific NRM in T4. There is no reason to assumethat additional mechanism are not operative in the genome. As mentioned several times before, since you cannot exclude NRM, evidence of common descent based upon shared mutations is a nonscientific conclusion. You have to exclude NRM in the assessed sequence. I have demonstrated NRM for the ZFY region and mtDNA on this board and that should have far reaching consequences for evolutionism (if it is science).PK3: Since your argument requires assuming mechanisms that have not been observed and for which there is no reason to even think that they plausibly might then I can only say that you have a strange view of science. I add that since the mechanism you did quote did not support your claims it seems that your best evidennce is wholly inadequate. And if you havve REALLY demonstrated NRM of the sort you assume for the regiosn you claim, provide a link to the relevant posts.PB(cont)
In response to: PB: 2) Non-Random Mutations type 2 (NRM2). This type of NRM is mediated by protein and/or RNA driven mechanism that translocate preexisting DNA elements, or vary nucleotides in genes in a
similar fashion as observed for immunoglobulins. NRM2 also plays a pivotal role in parasite-host interactions, and are likely to be abundant in other interactions between organisms where ‘evolutionary armsrace’ is ongoing. They have been demonstrated beyond any doubt for the 1G5gene in Drosophila. Implications: Alignment of mutations (‘shared mutations’) in related MPGs. Variation is preexisting.PK says:
2) Translocations - since these require that the material to be translocated is already present in the genome it would seem that your "related MPGs" are related by common descent. I thought your
assertion was that MPGs were NOT related in that way.PB2: Correct, there is only common descent within MPGs. Related MPGs have been created. Why would the Creator reinvent the wheel? It is illogic. A gene encoding cytochrome in chimp works as good as it works in human. So, if it mutates nonrandomly in human, also in chimp. What you observe is the illusion of common descent. I have provided evidence for this view in the ZFY region in primates.PK3: So far as is known all versions of cytochrome C work in anything which requires it. So why is yeast cytochrome-C so different from that in chimps ? Given that there are many alternative choices why did your hypothetical designer choose to produce a pattern consistent with common descent ?PK (cont): It seems to me that again translocations can only interfere with phylogenies at the fine resolution of individual branch points and can only do so because large scale evolution is correct.PB: Tranlocation of genetic elements may affect gene expression and thus induce variation within the MPG. That was my claim, not that they affect the illusion of common descent. It probably depends on the DNA sequences (docking sites, recognition sites) where the elements translocate to. If the MPG is similar probably such nonrandom translocation of DNA elements also line up. "Expect the unexpected"PK3 : Gene expression would affect the phenotype so it is not relevant to my argument which only deals with the genotype. Given that both the transposed element and the area it is transposed too must already be similar, if not identical, for there to be any problem the evidence for large scale evolution remains untouched because such mutations can never explain the initial similarity required for them to even be a possible problem.PB (cont)In response to:
3) NRM1 and NRM2 explain observed biological variation. It tells us that the mechanisms for biological variation are already preexistent in the genomes of organisms (=multipurpose genome) and can be activated upon the right triggers. Darwin was the first to discover the MPG, but his extrapolation of microbe-to-man evolution is completely, entirely unwarranted because the phenomena are unequal. (Unless you assume an uncommitted MPG of the original microbe we all evolved from). That Darwin’s extrapolation on variation in Galapagos finches to support
‘microbe-to-man-evolution’ is unwarranted is also demonstrated by observations that ‘his’ finches are still able to interbreed (Science, 26 April 2001). Thus, they are still the same MPG.PK says:
3) Your list is hardly exhaustive and so to suggest that these two factors alone account for all variation would be an obvious error. However unless you make that error your assertion is clearly unproven.PB: Of course there are many more preexisting/preprogrammed mechanism to induce variation in the MPG, but where does help that help you? Why would it unprove my assertion?PK3 : It helps me to point out the additional mechanisms exist because they contradict your claims. For instance lateral transfer is one of the biggest problems in working out phylogenies in bacteria - but it contradicts the GUToB claim that information cannot be added to the genome. It would also make your presentation of your assertion more honest which I would regard as an improvement, even if it undermines the assertion itself.PK (cont): I also note that you insist on repeating your false claim about Darwin, despite the fact that you know it to be untrue. The former is unscientific, the unscientific and dishonest.PB: None of these remarks relates to my claim that Darwin made an unwarranted extrapolation.Maybe you could point it out. I mean how is your answer related to my claim? I almost have to believe that you agree with me on Darwin's unwarranted extrapolation.PK3; They directly relate to precisely that claim which I regard as an outright lie.PB (cont) Since you were unable to rebut my claims, evolutionism still stands refuted. But at least you gave it a try.PK3: A good example of your tendancy to claim victory when in fact your have been defeated.PB(cont) Finally, I owe you the Dr Caporales vision on Junk DNA:
"Now that our genome is available, we will be able to connect these slippery DNA regions to their-finetuning-knob role, if they have one. But we will be able to do this only if we look into our genome with
some respect, seeking to learn. We will not find them if we dismiss boring repetitive sequences asjunk DNA". (page 69)."Transposons are found among the many repetitive sequences in the genome that have been called 'junk DNA'. They are by no stretch of imagination useless junk, however." (page 149).PK3: I note that these deal with only a small fracton of "junk" DNA. Most "junk" DNA stilll seems to be no more than "junk"PB: Dawkins is out.PK3: And the reason for indulging your petty personal hatreds is ?

Lateral transfers - if they are to have any effect at all - must add information to the genome (in the sense that the genome has information).Quoting Dr Caporale "In one bacterial genome, the gene encoding an enzyme that digests a carbohydrate was pieced together out of DNA from two different species" p79Don't forget the links - you wouldn't want us to think you were lying about those posts, would you ?

Lateral transfer is where DNA froum OUTSIDE the genome is incorporated INTO the genome. Therefore lateral transfer adds information not previously in the genome. Isn't that obvious ?PK: Quoting Dr Caporale "In one bacterial genome, the gene encoding an enzyme that digests a carbohydrate was pieced together out of DNA from two different species" p79PB: ever heard of recombination?PK2: Yes. It does not take genes out of OTHER SPECIES. Did you actually READ the quote ?PK: Don't forget the links - you wouldn't want us to think you were lying about those posts, would you ?PB: You already have all necessary links in message #48. Probably you didn't read them yet.PK2: If the links to the messages I asked for are there then it should be easy for you to identify which link links to which message. If on the other hand then it is not the case that you have provided the links. All I am doing is asking you to back up your statements in the same way you demanded of me.And since at least four people other than you are reading this thread, and will have noticed that you demanded a link - not a list of LONG threads one of which might contain one of the messages somewhere - my use of "us" is entirely reasonable.[This message has been edited by PaulK, 02-14-2003]

Lets cut this short. First there is no respose to my point that the ongoing discussion was dropped. Therefore it is clear that your claim that you never drop discussions was made to deny the fact that you DID drop one in this thred.Which of them explains how NRM contradicts evolutionary theory ? [QUOTE] PB cont :let's find out what Dr Caporale has to say about this in her excellent book that is a big thorn in the eye of the orthodox evolutionists. From Darwin in the Genome:"Once we learned about DNA, we saw that mistakes in copying generate mutations and so we've assumed that random mutation followed by selection underlies evolution. However, I have come to the conclusion that using our current knowledge to expand on Darwin's insights does not require that all mutations be random with respect to their potential effects on biological function". (page 42).PK3 : So Dr. Caporale clearly says that the randomness of mutations was only "assumed" and that the assumed randomness was "with respect to biological function" (as I have said - obviously you read neither my posts nor the book) and that such a view is "not required" for evolution. Thanks for providing a quote which so neatly illustrates your errors.PB3: evolution unequals NDT. I claimed to overthrow NDT and that is what I did. Caporale's quotes back me up. That you think Caporale's book is entirely consistent with evolutionism is your believe. Problem is now you have to explain Caporale's observation from NDT. That there is selection for such mechanism is not the question. But the origin of such mechanism from scratch is the question. And that unique proteins are involved NRM has been demonstraed in mammals. They have a unique protein to carry out recombinations in the germline of immunoglobulins.[\QUOTE]Ah! more backpedalling. As you well know - IF you have read the book - Dr Caporale believes that these mechanisms evolved. So in fact your claim that the book refutes NDT has been shown to be a lie.So with your argument crumbling around your ears you still try to claim victory !
These are the quotes you produced to try to refute NDT - and NOT ONE OF THEM DOES - your best evidence turns out to be no evidence at all. [QUOTE] Quotes continue:
"New levels of interaction and regulation rarely arise through letter by letter random mutations of random DNA sequences". (page 144).PK3: Which is only a problem for people - like Lee Spetner - who for some strange reason insist that evolution is limited to point mutations.PB3: Spetner -at least- thought thoroughly on the issue evo's try to address, that's for sure. Building a living cell from scratch, which requires at least 1000-2000 regulated and expressed genes, through an utter random mechanism is not-to-discuss nonsense. People who think it is possible are like medieval alchemists trying to make gold from lead. They didn't understand the laws of nature. It has proven to be a waste of time.[\QUOTE]Spetner - like you - didn’t bother to find out about the theory he was trying to refute. And my experience of his writing indicates that he doesn;t think deeply at all - shallow sophistry is more typical of his work. No wonder you have to resort to rather pathetic stramwne in an attempt to make him look good. [QUOTE] quotes (cont):
"The genomic landscape is huge. Random wandering through the landscape of possible mutations is no the most efficient strategy for long term survival. In our own case, random mutation would mean that any one of the more than 3 billion spots in our genome had the same probablity of each kind of change." (page 185).PK3 : And goes on to say "It does not mean all mutations are precisely targetted" And of course this does not refer to evolutionary theory which never seems to have cared much about the issue.PB3: Still, not all mutations are random.[\QUOTE]Hardly a problem for evolutionary theory. [QUOTE] (cont)
"Current evolutionary theory states that variation results from genetic changes that remain forever random, and that selection operates upon the results of this random genetic variation. It is time toincorporate the observations described in this book into evolutionary biology". (page 192).PB: I completely agree and I already mentioned this in a mail in May 2002: NDT RIP. Then, it was firmly denied and now here we have Dr Caporale with exactly the same claim. You can of course deny her, too.PK3: I suggest you provide a link to this, too or I will assume that you are lying. But note that I do not deny it at all and have expressed ageement with it. It is you that has disagreed by insisting that instead of following the rourt proposed by Dr Caporale, evolution should be thrown out and replaced by your idle musings.PB: Lying about what. That Caporale's examples are the end of NDT?[\QUOTE]Lying that you agree with Dr Caporales statement - since you certainly do not. (The end of NDT ? What a laugh! - you can;t even work out how NRM affects NDT !). [QUOTE] PK (cont): As is my list of examples which show that _Darwin in the Genome_ refutes your claim that information is never added to the genome (proving my point that the book is a greater problem for your views than for NDT).PB: Apparently you didn't read the book properly. The mechanisms described are included in GUToB.PK3: Then the GUToB claims that information can be added to the genome. It seems that the GUToB is inconsistent.PB3: The GUToB claims that 'novel' genes are always related to preexisting DNA elements.[\QUOTE]So GUToB says the same as NDT on that matter. Excpet of course fotr the fact that lateral transfer completely messes up the MPGs which are supposedly part of GUToB. So GUToB is inconsistent, as I said. [QUOTE] PK (cont): In short your idea of a "scientific" discussion means dropping the discussion because your errors are being revealed.PB: What a humbug. I've never dropped a discussion. As a matter of fact, I have won all my discussions with evo's. (Till now, Dr Douglas Theobald from the Talk-origin was the best defender of evolutionism, but not good enough. He couldn't defend the IL-1 beta incongruence).PK3: Since you did start this part of the discussion to stop a previous discussion, and given your habit of proclaiming victory even when you have lost (and noting your abject defeat on another thread currntly in progress) your statment is so obivously false I can only conclude that you are either a compulsive liar or deeply delusionalPB3: I dragged it back in focus. This thread is about NRM as described in Dr Caporale's book. I summarised the 2 types of NRM and what they mean for evolutionism.[\QUOTE]ANd in case 1 on finding that it did NOT show what you claimed you retreated to claiming that there were unkown mechanisms which DID support your claim - but with no reason beyond the fact that your argument needed them. [QUOTE] PB(cont) In response to:
PB: 1) Non-Random Mutations type 1 (NRM1). This type of NRM introduces mutations on the same positions and the position where they are introduced depends on the flanking DNA regions. NRM1 are also known as ‘positional NRM’. NRM1 have been also observed in the ZFY region and in mtDNA. NRM1 has been observed in T4 by Lynn Ripley and was described in Caporale’s book (page 37, 38). Implications: NRM1 will line up and give the illusion of common descent in phylogenetic analysis.
Since phylo-geneticists cannot exclude NRM1, this type of mutations invalidates the evolutionary conclusions that the alignment of genes and shared mutations is proof for common descent.PK says:
Anyway to deal with your assertions.
1) p37-38 deal with the "hairpin" model. Since such models require that the existing sequence is similar they can only upset phylogenetic analysis at fine resolutions- which you apparently accept,
unless you wish to claim each species is a seperate creation (which would then pose the question of why the sequences are similar enough to see such mutations). It poses no threat to the larger scale phylogenies which you seem to object to.PB2:
At present, the hairpin model is able to explain specific NRM in T4. There is no reason to assumethat additional mechanism are not operative in the genome. As mentioned several times before, since you cannot exclude NRM, evidence of common descent based upon shared mutations is a nonscientific conclusion. You have to exclude NRM in the assessed sequence. I have demonstrated NRM for the ZFY region and mtDNA on this board and that should have far reaching consequences for evolutionism (if it is science).PK3: Since your argument requires assuming mechanisms that have not been observed and for which there is no reason to even think that they plausibly might then I can only say that you have a strange view of science.PB3: What's the big deal? Evolutionism relies also on mechanism that have never been observed. Ever observed the evolution from microbe to man? I didn't, neither did you. It is all inference.
Also, ever observed a graviton?[\QUOTE]Gravitons are to the best of my klnowledge still hypothetical - and microbe ot man evolytuion is not a mechanism. Therefore my objection - which was specifically directed at unobserved MECHANISMS still holds. Also ithere IS good reason to think that gravitons exist and that mnicrobes to man evoution occurred- which is more than you have for your mechanisms My criticism stnads, oyur argument is unscientific and irrational. [QUOTE] PK3 (cont): I add that since the mechanism you did quote did not support your claims it seems that your best evidennce is wholly inadequate. And if you havve REALLY demonstrated NRM of the sort you assume for the regiosn you claim, provide a link to the relevant posts.PB3: links to be found in message #103.[\QUOTE]
More when I have had time to examine them. I am already unimpressed with the drosophilia example. [QUOTE] PB(cont):
In response to: PB: 2) Non-Random Mutations type 2 (NRM2). This type of NRM is mediated by protein and/or RNA driven mechanism that translocate preexisting DNA elements, or vary nucleotides in genes in a similar fashion as observed for immunoglobulins. NRM2 also plays a pivotal role in parasite-host interactions, and are likely to be abundant in other interactions between organisms where ‘evolutionary armsrace’ is ongoing. They have been demonstrated beyond any doubt for the 1G5gene in Drosophila. Implications: Alignment of mutations (‘shared mutations’) in related MPGs. Variation is preexisting.PK says:
2) Translocations - since these require that the material to be translocated is already present in the genome it would seem that your "related MPGs" are related by common descent. I thought your
assertion was that MPGs were NOT related in that way.PB2: Correct, there is only common descent within MPGs. Related MPGs have been created. Why would the Creator reinvent the wheel? It is illogic. A gene encoding cytochrome in chimp works as good as it works in human. So, if it mutates nonrandomly in human, also in chimp. What you observe is the illusion of common descent. I have provided evidence for this view in the ZFY region in primates.PK3: So far as is known all versions of cytochrome C work in anything which requires it. So why is yeast cytochrome-C so different from that in chimps ? Given that there are many alternative choices why did your hypothetical designer choose to produce a pattern consistent with common descent?PB3: I am not so sure whether or not Cyt C can be interchanged between organisms without any effect. Does is imply that you can also interchange all other proteins without effect? Than, it would suggest that proteins are not relevant in specifiying the species. Probably there are not so many alternatives. And the pattern is probably not consistent with common descent (Zhang and Chinappa, Mol Biol Evol 1994, 11:365).[\QUOTE]It seems that you do not even knwo that cytochrom-C is highly conserved and perform the same function in a very great many organisms. ANd I very mcuh doubt that you claimed reference supports you claim - not least because you have a habit of misrepresenting your sources. [QUOTE] PK (cont): It seems to me that again translocations can only interfere with phylogenies at the fine resolution of individual branch points and can only do so because large scale evolution is correct.PB3: Translocations usually take place at exacly the same spot. As observed for several types of leukemia that are due to translocation. Translocation that are neutral are usually not observed, but might be present in the same spot too.[\QUOTE]Which means that there must BE an exact same spot. Thanks for supporting my point., [QUOTE] PB: Translocation of genetic elements may affect gene expression and thus induce variation within the MPG. That was my claim, not that they affect the illusion of common descent. It probably depends on the DNA sequences (docking sites, recognition sites) where the elements translocate to. If the MPG is similar probably such nonrandom translocation of DNA elements also line up. "Expect the unexpected"PK3 : Gene expression would affect the phenotype so it is not relevant to my argument which only deals with the genotype.PB3: Since when is the phenotype irrelevant to evolution?[\QUOTE]Since we are only dealing with the subject of deriving phylogenies from genotypes the phenotype is irrelevant. YOu seem to be unable to even understand the point being discussed. IS that really the case or are you simply using a debate tactic of throwing up any objection you can think of regardless of relevance ? [QUOTE] PK3 (cont): Given that both the transposed element and the area it is transposed too must already be similar, if not identical, for there to be any problem the evidence for large scale evolution remains untouched because such mutations can never explain the initial similarity required for them to even be a possible problem.PB3: depends on the DNA region/chromosome you study.[\QUOTE]That seems to be obviously false. How can looking at a differnbt region change the fact that the initial similarity must still be there ? [QUOTE] PB (cont): In response to:
3) NRM1 and NRM2 explain observed biological variation. It tells us that the mechanisms for biological variation are already preexistent in the genomes of organisms (=multipurpose genome) and can be activated upon the right triggers. Darwin was the first to discover the MPG, but his extrapolation of microbe-to-man evolution is completely, entirely unwarranted because the phenomena are unequal. (Unless you assume an uncommitted MPG of the original microbe we all evolved from). That Darwin’s extrapolation on variation in Galapagos finches to support
‘microbe-to-man-evolution’ is unwarranted is also demonstrated by observations that ‘his’ finches are still able to interbreed (Science, 26 April 2001). Thus, they are still the same MPG.PK says:
3) Your list is hardly exhaustive and so to suggest that these two factors alone account for all variation would be an obvious error. However unless you make that error your assertion is clearly unproven.PB: Of course there are many more preexisting/preprogrammed mechanism to induce variation in the MPG, but where does help that help you? Why would it unprove my assertion?PK3 : It helps me to point out the additional mechanisms exist because they contradict your claims. For instance lateral transfer is one of the biggest problems in working out phylogenies in bacteria - but it contradicts the GUToB claim that information cannot be added to the genome. It would also make your presentation of your assertion more honest which I would regard as an improvement, even if it undermines the assertion itself.PB3: Where does this help you rebutting point 3? It doesn't.[\QUOTE]On the contrary, it proves the point - lateral DNA transfer goes against your point since it is NOT produced by mechanisms within the genome receiving it. [QUOTE] PK (cont): I also note that you insist on repeating your false claim about Darwin, despite the fact that you know it to be untrue. The former is unscientific, the unscientific and dishonest.PB: None of these remarks relates to my claim that Darwin made an unwarranted extrapolation.Maybe you could point it out. I mean how is your answer related to my claim? I almost have to believe that you agree with me on Darwin's unwarranted extrapolation.PK3; They directly relate to precisely that claim which I regard as an outright lie.PB3: Even if Darwin had more such examples (e.g. mockingbirds, pigeons, cats, dogs, etc) they don't go beyond his finches. It is all MPG (=GUToB).[\QUOTE]So you won’t even defend your lie. And your reference to MPGs is speculation only. THe evidence still supportes evolution,[\QUOTE]PB (cont) Since you were unable to rebut my claims, evolutionism still stands refuted. But at least you gave it a try.PK3: A good example of your tendancy to claim victory when in fact your have been defeated.PB3: You didn't rebut claim 3. Or maybe I missed it. Point it out, please.[\QUOTE]So why are you trying to argue against something that - according to you - was never written ? [QUOTE] PB: Dawkins is out.PK3: And the reason for indulging your petty personal hatreds is ?PB: Good riddance to atheistic nihilism. (nothing personal, though)[\QUOTE]Dawkisn isn’t a nihilist.

Well where does population genetics appear in the "definition" - and why rely on a physicist to give a definition ? Especially a physicist who appears to be on the whole hostile to evolution and who relies heavily on anti-evolutionary sources ?But all this is irrelevant. You have failed to answer the pquestion of IN WHAT SENSE mutations are expected to be random in NDT - because oyu knwo full well that your claims would fail if you did so. That is why you tried to drop that discussion, and probably why you are trying to deny dropping that discussion - although why you think that telling an obvious lie will help you, I have no idea.

Let me put it simp

Look Peter, you have no arguments to back up you fantasies.Your assertions have all been answered and it is clear that you don't know what you are talking about. I am now convinced that you do not possess a PhD in any science.And just to point it out I find the Zhang and Chinappa paper on the web. It does NOT refute the use of cytochrome-C to establish phylogenies. Instead it just points out 2 anomalies (plants which apparently have cytochrome-C closer to fungi) and proposes possible explanations. The fact that these ARE anomalies and that the cytochrome-C data in general strongly supports common descent provide further evidence against you.

While you seem quite happy to accuse your opponents of ignoring arguments that you have yet to actually make the fact is that you lack rational argument and much of your case depends on misrepresenting the words of others. We are STILL waiting for an ARGUMENT to back up your claim that _Darwin in the Genome_ refutes NDT instead of vague ramblings. After all the pages this thread has gone through it is rather clear that you do not have one.The second part of your post simply demonstrates your lack of reasoning ability. I never claimed that anomolies were evidence FOR evolution - nor is it necessary for me to do so. What I did point out is that your claim that the anomolies invalidated the use of cytochrome-C in phylogeny was false - a claim that you did not even bother to argue for instead referring to the paper as if it were the conclusion of the authors - which it was not. The anomolies do not change the fact that a general pattern exists and is best explained by common descent. That is my argument but of course you find it easier to deal with a strawman of your own invention.ANd I don;t know why you think it funny that your behaviour here makes it clear that you are incapable of the rational thought required to achieve a PhD in any science. Unless of vcourse your "PhD" were awareded by an institution similar to the one awarding a "PhD" to Kent Hovind.

If I remember correctly he didn't actually acknowledge that he WAS the asthma researcher. He certainly didn't volunteer the information, and I very much doubt that "our" "Peter Borger" (if that is his real name) has any real scientific qualifications. After all a medical researcher would probably have to know enough statistics to understand the importance of sample size, which this Peter Borger seems not to grasp at all.

Face the REAL facts Peter - if that IS your nameYou don't have a scientific theory. You have a collection of opinions largely invented ad hocNDT is doing just fine and science is not about to throw it out on the say-so of some crank who can't even accurately represent his sources or even from a coherent argument.I have looked at the links and I have to say my opinon is unchangedTHe deviations do not call common descent into serious question because the evidence is still overwhelmingly in favour of common descent. Common design has serious problems not least that a designer must be assumed, although we have no evidence as such (violating parsimony) and that common design does not explain the evidence as well - since it does NOT explain why the evidence is so strongly consistent with common decent. A scientist would uinderstand these points.And no you are not a stoic. Your last comment reveals that your position is based on religious hate propaganda.And why do you spend time here when all you do is make yourself look bad ? After all it is obivous that you don't even know what the theory you claim to have refuted is !

I an sorry, but Peter Borger is an arrogant liar who substitutes imagination for knowledge. It is really hard to answer such a person without making highly critical remarks concerning his conduct.What can you say about someone who claims to "love" everyone yet feels the need to insert gratuitous slanders into his posts ?[This message has been edited by PaulK, 02-19-2003]

The full article is available online for subscribers at Genome Biology | Home page.An obvious oversight in Peter's argument is that both genes would be accumulating mutations, reducing the time needed to 75 million years,Another question is his use of the term "purifying selection" which usually refers to the elimination of harmful mutations.There is also the obvious question of the situation in other species which is certainly relevant but not discussed at all.

Well the alpha-actinin-3 puzzle turned out to be quite simple.There are two possibilities that need to be considered that have not been dealt with.Firstly alpha-actinin-3 may confer some benefit even if the loss does not have serious consequences.http://web1.tch.harvard.edu/...arch/mrrc/investigators/beggs
"Although absence of ACTN3 is not associated with any obvious clinical
phenotype, it remains possible that this mutation acts as a genetic
modifier, either of other neuromuscular disease, or possibly accounting for some of the natural variability in human athletic performance. "But there is more. According to a document produced by the Institute for Neuromuscylar Research (download from Forbidden!) this is in fact the case "We have collaborated with the Australian Institute of Sport to study the a-actinin-3 gene in elite athletes . We now have evidence that the presence of a-actinin - 3 is associated with elite performance in sprinting sports". Even though there seems to be a benefit associated with the absence of alpha-actin-3 in endurance sports this is still enough to raise serious doubts about the claim that the disabling mutation is selectively neutral.The other possibility is that the redundancy is a relatively new development - perhaps restricted to humans. And the evidence supports this view, too:http://hmg.oupjournals.org/cgi/content/abstract/10/13/1335"Murine Actn2 and Actn3 are differentially expressed, spatially and
temporally, during embryonic development and, in contrast to humans,
-actinin-2 expression does not completely overlap -actinin-3 in postnatal skeletal muscle, suggesting independent function. Furthermore, sequence comparison of human, mouse and chicken -actinin genes demonstrates that ACTN3 has been conserved over a long period of evolutionary time, implying a constraint on evolutionary rate imposed by continued function of the gene."
(the cut-and-paste lost the 'alpha' character. I have not replaced it)The INMR report cited earlier claims that "We have also studied the a-actinin-3 gene throughout evolution and have demonstrated it appears to be essential in all other species — including mice, chickens, baboons and chimpanzees."[This message has been edited by PaulK, 02-19-2003]