Dear Paul,
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.
PB3: There is nothing in taxonomy, biogegraphy and fossil record that cannot be explained alternatively. It certainly doesn't unequivaocal evidence for evolution from microbe to man. It even better supports GUToB.
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.
PB3: I already did that in message #103.
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.
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).
PK3: 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.
PB3: Yep, and is the end of NDT.
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.
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.
(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?
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.
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 delusional
PB3: 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.
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?
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.
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).
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.
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?
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.
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.
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).
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.
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 ?
PB: Good riddance to atheistic nihilism. (nothing personal, though)
Best wishes,
Peter
[This message has been edited by peter borger, 02-14-2003]
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