Dr Page's best example of common descent easily --and better-- explained by the GUToB

Dear All,
A couple of months ago Dr Page (aka SLPx) posted his ultimate proof for evolutionism at the molecular level, and I promised to have a look at it. I just did that and it turns out that his ultimate example that should have proven molecular evolution beyond doubt doesn’t even come close doing that. I was expecting Dr Page to draw my attention towards a study that demonstrates mono-interpretable results that would for ever demonstrate evolutionism to be right, and the GUToB (=grand unifying theory of biology = non-random mutations in a multipurpose genome) to be false. However, it turns out just the opposite. Dr Page posted clear-cut molecular biological evidence of non-random mutations in several species, and supports --rather than falsifies-- the GUToB. I will discuss the example in detail, that can be found here:http://www2.norwich.edu/spage/zfy1a.htmHow do we have to read the figure?
The rows demonstrate 10 homologue sequences of a not further specified stretch of DNA --but probably a protein coding gene-- of 10 distinct species. The species are presented at the left hand side and abbreviated to three letter codes (plus number): Hsy, Prt1, Prt2, etcetera. The first row demonstrates the nucleotides as found in Hsy, the second row the homologous sequence as found in Prt 1, the third row as found in Prt2, etcetera. The first block of 10 rows demonstrate the first part of the sequenced stretch of DNA in these species, the second block of 10 rows are the second part of the sequenced stretch of DNA, etcetera. Nucleotides are indicated as the letters A, C, G and T. Nucleotides in species that are shared with Hsy are indicated as dots (...), mutations are shown as letters (A, C, T, G). Hence, sequence homologies are dotted and point mutations can easily be observed.According to evolutionism the shared mutations are due to a mutation that occurred in a common ancestor and has been passed through into the species, thus being proof of common descent. On the other hand the GUToB holds that shared mutations are non-random mutations that have either been introduced on spots that are more prone to mutations --so called hotspot mutations--, while other shared mutations are due to a protein and/or RNA mediated mechanism. The latter is currently hard to proof, since the mechanism are still obscure (Although such mechanisms are present in bacteria as stress-induced error-prone redundant DNA polymerases, and evidence is also present in subspecies of D. melanogaster, e.g. in the 1G5 gene).A thorough look at the figure reveals that several spots in the homologues sequences demonstrate shared mutations: mutations on exactly the same spot in the DNA of several distinct organisms. Are these shared mutations due to common descent (as proposed by evolutionists) or due to a common mechanism (as proposed by Dr Borger)? Let’s find out.Firstly, let’s have a look at the first block of 10 rows. It is clear that the C on position 22 (from left) in Hsy (maybe Dr Page could provide the full names of the organisms) is variable throughout the presented species. In 6/10 we find a C-->T transition (C22-->T). It should be noted that this mutation does not proof common descent, since the mutation is occurring randomly throughout the species. For instance, while Lca, Hag and Ptr2 have a C in this position, all other sequences demonstrate a T. Thus, no consistent evolutionary pattern is observed.Secondly, we observe G88-->T (first block, left hand side) in 4/10 cases. Also no evolutionary pattern is observed. In other words, these point mutations do not proof molecular evolution at all. If they proof anything than it is the non-random character of these mutations. Apparently the mutations in the first block are non-random mutations and that is in accord with the GUToB. Evolutionist’s will have to claim that the aberrations exist because they have been introduced several times on the same spot, and therefore it is expected that we do not find a perfect alignment of mutations. I am sure, however, that Mark Pullen will object to such far-fetched explanations since he is wielding Occam’s razor. Besides, mutations introduced several times on the same spot also indicate the non-random character of these mutations.
Less obvious are the non-random mutational spots on position 49 and position 58 (from left hand side).The second block of 10 rows demonstrates similar findings. Position C9 and A60 in the Hsy sequences also seem to be non-random mutational hotspots unrelated to evolutionary descent. Position 89 from left hand side is very illustrative for a non-random-random mutational hospot: The non-random position is able to change at random with respect to nucleotide. This position demonstrates thus compelling evidence for the hypothesis of non-random mutations. It definitely is the end of evolutionary claims of common descent based upon sequence homology and shared mutations.The shared mutations in block 3 and block 4 may be explained accordingly.Best wishes, and have a nice contemplative day,
PeterThe ILLUSION is common descent, the FACT is non-random mutations.

Dear Dr Page,You write:"Goodness, me!
I skimmed through Borger the creationist's pap too quickly.I thought he was referring to this alignment:http://www2.norwich.edu/spage/alignmentgam.htmNow I see that he was referring only to the alignment of a partial exon form the ZFY gene.No wonder he comes to such bombastic and senseless conclusions.This makes his opening lines that much more based in bizarre fantasy.The credibility meter just went into the negative numbers...."PB: Thanks for your preliminary (I presume) response. Sorry for misrepresenting the figure. I was under the impression that you posted it to demonstate common descent at the molecular level. Next time please provide some more details in your mails, so I do not get confused.
However, my comments still stand as evidence for the GUToB. I am sure you don't agree and here is a nice challenge. Maybe you could respond point by point, and demonstrate where I go wrong with my interpretation. I would be grateful. Thanks in advance.best wishes,
Peter"Non-random mutation and selection? You better believe it!"

Dear Dr Page,You write (as if I am your worst enemy):Dr Page: Just one quick comment for now - I have a meting shortly:quote:
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Originally posted by peter borger:
Dear All,
A couple of months ago Dr Page (aka SLPx) posted his ultimate proof for evolutionism at the molecular level, and I promised to have a look at it. I just did that and it turns out that his ultimate example that should have proven molecular evolution beyond doubt doesn’t even come close doing that.
--------------------------------------------------------------------------------Dr Page: Right off the bat, Borger the creationist launches into a bizarre hyperbole-ridden diatribe.Dr Borger: Better provide some extra information next time you send in your stuff. Or do I have to smell this is the ZFY region?Dr Page: I never wrote or implied that my dataset was the "ultimate proof for evolutionism at the molecular level."Dr Borger: Better provide some extra information next time you send in your stuff. Why did you present these data? They nicely demonstrate non-random mutations.Dr Page: Borger is either 1. Lying to set us some sort of strawman argumentDr Borger: Listen Dr Page, I am trying to discuss the topic of evolution in a scientific way. If you are not able to do that I am wasting my time with you. I am not setting up a strawman argument, I simply wanna know how you see these sequences, since you presented them as something that advocates evolutionism.Dr Page: or 2. is simply deluded enough that he actually recalls the series of posts in this way.Dr Borger: The way you post your stuff is indeed very deluding. You are the one who mailed this link, no additional information added. You let me guess what I have to do with it. I looked at it carefully, and I present my comments. Now it is your turm to repsond in a scientific way. You can do that, isn't it? Or did you find your bulla in a cereal box? Dr Page: In REALITY, I had presented the link to Borger the creationist so that he could tell us all which of the genetic changes are due to 'natural' mechanisms and which are "directed."Dr Borger: Your example demonstrates non-randomness of mutations that give the illusion of common descent. It is clearcut evidence of the GUToB.Dr Page: Borger's opening statement will set the tone for my reply, whihc I hope to get to this afternoon.It will not be pretty.Dr Borger: Pathetic little evolutionist. Best wishes,
Peter

dear Peter,P: I had prepared a point-by-point response to this, but instead
I will ask a question and then suggest my interpretation
(and your post was, after all, just your interpretation of that
data in a manner suited to your theory).
Question:: What makes you think the genetic changes happened
more than once?PB: I do not think this, I advocate non-random mutations. To explain the data evolutionary it has to be inferred, though.P: My interpretation would be that the changes represent a branch
of a tree, where some of the species are descended from others.PB: The data do not demonstrate that. Point it out.P: I am probably moulding the data to what I expect happened, but
building up an inheritance seems much more likely than
independtly mutating in the same way at the same spot.PB: yes, it seemed to me too. However, looking at the data this is unlikely. A similar non-random mechanism operable in all species is more likely.P: It's all interpretation, there is not fact.PB: At least you get it. I prefer the interpretation with the less assumptions (Occam's razor, you know).P: On the other hand, if we build a tree from this data, and then
are told what the organisms are ... and they appear to be
in the right place from an evolutionary perspective whose
interpretation is supported?PB: That's why I asked Dr page to provide the full names for the organisms. I think that I already know what the results are. A careful look at the Ptr1 and Ptr2 (probable two subspecies) is very suggestive. Let's wait for Dr page's reply.best wishes,
Peter"Non-random mutations & selection? You better believe it!"

dear Mammuthus,M: Well I see we are trotting this old horse back out againPB: Actually this horse is fairly new. I introduced it only a couple of moths ago, backed it up with scientific papers, and now I try to get it from the ground as a new scientific view on shared mutations. It won't go without resistence from orthodox evolutionists. I am aware of that.M: I am sure SLPx will be along soon to spank this post out into orbit for the silliness that it is but I will put in my two cents.PB: Compared to your reponse he put in close to zero cents.PB:
According to evolutionism the shared mutations are due to a mutation that occurred in a common ancestor and has been passed through into the species, thus being proof of common descent. On the other hand the GUToB holds that shared mutations are non-random mutations that have either been introduced on spots that are more prone to mutations --so called hotspot mutations--, while other shared mutations are due to a protein and/or RNA mediated mechanism.M: 1)Your average high school student can do genetic experiments to show transmission of traits from parent to offspring. Thus identity by descent is a fact. Mutations are passed from parent to offspring.PB: Yep, what's your point with respect to Dr Page's example?2)Your claim is that this does not happen and that every mutation event must be a de novo error made by the polymerase.PB: No, it does not have to involve such polymerases. It may be due to physicochemical properties of the nucleotides (=mechanism).M: Since polymerase fidelity experiments have been done and never shown this phenomenon this also falsifies your claim.PB: The experimenets that would yield compelling ecidence have not been preformed. I mean, there has never been a study into several related species with respect to non-random muations. Although, the mtDNA experiments come close.M: So simple genetics and simple biochemistry falsifieds the GUToB.PB: This can hardly be an objection. Since evolutionism has been so many times falsified, so why bother.
Seriously, it only demonstrates that the GUToB should be fine-tuned. What do you expect from a new theory? That it is perfect at once?M: It hardly figures Peter that every mutation found among a group is a de novo mutation i.e. even single gene diseases that are transmitted in some families are not de novo mutations but inherited.PB: Mutations can be transmitted within species (kinds if you like), that's not the question. The question is whether muations are always introduced at the same spots. Apparently they are. Such non-random muations create the illusion of comment descent. Yes, dear Mammuthus, at last we have something that is created by mutations. It won't help evolutonism, though. On the contrary.PB:
The second block of 10 rows demonstrates similar findings. Position C9 and A60 in the Hsy sequences also seem to be non-random mutational hotspots unrelated to evolutionary descent. Position 89 from left hand side is very illustrative for a non-random-random mutational hospot: The non-random position is able to change at random with respect to nucleotide. This position demonstrates thus compelling evidence for the hypothesis of non-random mutations. It definitely is the end of evolutionary claims of common descent based upon sequence homology and shared mutations.M: Seem to be non-random? Compelling evidence? Or how about this little gem "The non-random position is able to change at random with respect to nucleotide"..so the non random position changes at random so it is non-random? LOL!!!!!PB: Non-random with respect to postion, (semi)random with respect to nucleotide. I spelled this out several times before. Apparently it is hard to get. However, this position does NOT advocate common descent, it rather proofs the GUToB.M: And looking after the fact at where a mutation occurs and claiming you knew it would happen there is hardly compelling evidence for non-random mutation.PB: Such mutations mean the end of molecular evidence of common descent. That suffices.M: Where exactly will the next mutation occur in the sequences?PB: I don't care. You are not longer able to use shared muations as evidence for common descent. That's quite a defeat for evolutionism.M: If you can always a priori know then it is non-random...otherwise it is random.
Your turn SLPx Have fun...PB: What are you? Masochist? Best wishes,
Peter

Dear Dr Page,quote:
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Originally posted by Mammuthus:
PB: That's why I asked Dr page to provide the full names for the organisms. I think that I already know what the results are. A careful look at the Ptr1 and Ptr2 (probable two subspecies) is very suggestive. Let's wait for Dr page's reply.
M: Unlikely Peter...Ptr1 and Ptr2 given that Page is a primatologist are probably Pan troglodytes 1 and 2..or two common chimps as opposed to Pan paniscus or bonobos...oops I inferred that so it must be wrong and another example of non-random mutation..LOL!--------------------------------------------------------------------------------Dr Page: Considering that fact that Borger has - or claims to have - the paper from which the sequences were obtained, I find it odd that he would not be able to figure out which species were which.Dr Borger: Brilliant reply again. However, where do I claim that I have the paper? All I did is respond to your example of evolutionism that turns out to have nothing in common with common descent. As I predicted in a previous letter, the ZFY region can only be understood by assuming non-random mutations. Now it turns out that my prediction holds true. I didn't even know that the sequences you provided in mailing #12 in the thread "sad what creationism can do to a mind (2)" is part of this region. Since I wasn't aware of this, I unintendedly (blindly) did my assertions on non-randomness of mutations in this region and they turn out to be right. What else does a theory require to proof its validity? Sceptical scientists should be convinced of the predictive power of the GUToB by now.Best wishes,Peter
"Non-random mutations & selection? Better believe it!"

Dear Dr Page,quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
However, where do I claim that I have the paper?
--------------------------------------------------------------------------------Dr Page: [b]Are you now claiming that you have not read the Kim et al. paper? The paper that YOU presented as "proof" that "non-random" mutations occur and therefore evolution is false? Have you at least read it? Or do you just search the lit for a certain phrase and run with it?Dr Borger: Whether I have or don't have the paper is not the issue, here. Why don't you start to repond in detail, and beat my interpretation of the data.Dr Page: And Percy wonders why I have no respect for you...Dr Borger: You're pretty intolerant towards people with different opinions.Best wishes,
Peter

PB: That's why I asked Dr page to provide the full names for the organisms. I think that I already know what the results are. A careful look at the Ptr1 and Ptr2 (probable two subspecies) is very suggestive. Let's wait for Dr page's reply.M: Unlikely Peter...Ptr1 and Ptr2 given that Page is a primatologist are probably Pan troglodytes 1 and 2..or two common chimps as opposed to Pan paniscus or bonobos...oops I inferred that so it must be wrong and another example of non-random mutation..LOL!PB:
Yeah, I figured that out myself already. Hsa isn't that hard too. Since when is Page a primatologist? In a previous letter he proclaimed himself as an "anatomist by education".Best wishes,
Peter

Dear Mammuthus,PB: Actually this horse is fairly new. I introduced it only a couple of moths ago, backed it up with scientific papers, and now I try to get it from the ground as a new scientific view on shared mutations. It won't go without resistence from orthodox evolutionists. I am aware of that.M: No, it is old...pseudoscience backed up with hyperbole and falsified by genetics, population biology, ecology, paleontology, zoology, and common sensePB: No, I backed it up by several publications.PB: Compared to your reponse he put in close to zero cents.M: Oh well, my prediction failed. Maybe he will do a point by point today. On the other hand, he said he was off to a meeting so I guess he did not have time to respond.PB: I am still waiting for his point-by-point reply.M: 1)Your average high school student can do genetic experiments to show transmission of traits from parent to offspring. Thus identity by descent is a fact. Mutations are passed from parent to offspring.PB: Yep, what's your point with respect to Dr Page's example?M: It refutes your non-random mutation arguement. You state that shared mutations are due to INDEPENDENT mutation events in exactly the same place with exactly the same substitution and thus two people could be genetically identical and it would be to non-random mutation rather than identitiy by descent. There is no positive evidence for such a mechanism and it is falsified by everything we know about polymerases and transmission genetics.PB: If you would have a careful look at the presented sequences than it is will become clear that for instance the the mutations in Ptr 1 that are not present in Ptr2 can aslo be found ON EXACTLY THE SAME SPOT in Lca and Str. I call that NON-RANDOM mutations.M: As to Page's example, it means that if primate A and primate B share a mutation it is because of common ancestry and not some non existent magic polymerase that just be pure dumb luck makes organisms that in every other characteristic would be joined together as a related group magically genetically similar as well.PB: I know the evolutionary explanantion. It doesn't explain the presented sequences. The GUToB explains these sequences better.2)Your claim is that this does not happen and that every mutation event must be a de novo error made by the polymerase.PB: Yes, or due an alternative mechanism and afterwards the mutations are inherited within species. Mutations on the same spot are interpreted as proof for common descent while they aren't. Have another close look at the sequences. Block 1: Ptr1, Ptr2, Lca and Str. Ptr1 is more related to Str than to Ptr2. Common descent? No, common mechanism.PB: No, it does not have to involve such polymerases. It may be due to physicochemical properties of the nucleotides (=mechanism).M: However, transition and transversion mechanisms have been well studied and their characteristics well described. In addition, the mutation dynamics of most polymerases are known and yet nobody has ever seen what you are describing...but random introduced mutations are known from just about every polymerase...ever wonder why people spend loads of cash to by high fidelity Taq polymerase instead of the plain jane type?PB: In vitro experiment may not be representative for in vivo situations. That is elementary. You know that. The sequenceing data in sub populations are very revealing in this, as demonstrated previously for the 1G5 gene in Drosophila.M: Since polymerase fidelity experiments have been done and never shown this phenomenon this also falsifies your claim.PB: Nope, it has been recently described that certain mutations are always introduced in vivo at the same spot due to the properties of the surrounding DNA sequences and the physicochemical properties of DNA. (References are somewhere on this site in a discussion with Quetzal).PB: The experiments that would yield compelling ecidence have not been preformed. I mean, there has never been a study into several related species with respect to non-random muations. Although, the mtDNA experiments come close.M: Nuclear and mtDNA studies have been done in abundance between and among species and unless you were living under a rock it would be hard to miss them. And as mentioned above, the polymerases that replicate DNA, transcribe RNA, etc have been characterized and do not show the properties required to falsify genetics much less evolution. But I guess you will continue to believe that a child gets Huntingtons disease from its parent not because of descent but because of a magic enzyme that just happens to cause exactly the same mutation and disease to segregate in the family...wow, what a compelling idea.PB: We already disussed the non-random character of mtDNA mutations that also give the impression of common descent (common ancestor of human and chimp around 150kya, though). It is your interpretations against mine. I prefer mine, since it makes more scientific sense.M: So simple genetics and simple biochemistry falsifieds the GUToB.PB: This can hardly be an objection. Since evolutionism has been so many times falsified, so why bother.
Seriously, it only demonstrates that the GUToB should be fine-tuned. What do you expect from a new theory? That it is perfect at once?M: I expect from a theory..well in your case it is hypothesis...that it is not in direct conflict with all the data from the outset and falisified by the data itself. I don't propose a hypothesis that storks bring babies just because I have never directly witnessed a conception event and did not see the birth of every person in the world personally either...but I think you must believe that hypothesis as well since you deny that parents can pass their genes to their offspring.PB: I also expect this for a hypothesis. The hype of evolutionism is renowned for not having predictive power, while the GUToB already predicted several things that are indeed observed. I rest my case.M: It hardly figures Peter that every mutation found among a group is a de novo mutation i.e. even single gene diseases that are transmitted in some families are not de novo mutations but inherited.PB: True. However, I know of several examples that demonstrate the same mutations independent of a family history on the same spots. Hint: leukemia's.PB: Mutations can be transmitted within species (kinds if you like), that's not the question. The question is whether mutations are always introduced at the same spots. Apparently they are. Such non-random muations create the illusion of comment descent. Yes, dear Mammuthus, at last we have something that is created by mutations. It won't help evolutonism, though. On the contrary.M: This paragraph is nonesense. Your claim is akin to mutations are transmitted from parent to offspring on Tuesdays but the rest of the week it is all a non observed non random mutation process.PB: You response is hard to follow. Please explain how it relates to my reply.M: Considering all species transmit their genes from parent to offspring..even a clone tranmits a copy of its genes to its clone...what evidence have you that this process stops between species?PB: All the biological evidence we have. You infer common descent from shared mutations. You simply leave out the possibility that shared mutations may be due to a common mechanism. It is the usual evo debate: Evolution is true so all data have to be interpreted accordingly. That is no science. That's the other way around.M: The fact that organisms transmit their genes and mutations from parent to offspring is why the observed mutation patterns are due to identity by descent and not by a sudden stoppage of genetics in all species, a new mechanism that is refuted by polymerase biochem anyway, and then back to normal again.PB: You simply never considered that other possibilites --apart from common descent and evolutionism-- might be found that are more likely and more explanatory.M: Seem to be non-random? Compelling evidence? Or how about this little gem "The non-random position is able to change at random with respect to nucleotide"..so the non random position changes at random so it is non-random? LOL!!!!!PB: Non-random with respect to position, (semi)random with respect to nucleotide. I spelled this out several times before. Apparently it is hard to get. However, this position does NOT advocate common descent, it rather proofs the GUToB.M: LOL!!!!!!!! This just keeps getting better and better Pete...now it is semi-random? How about the non-reciprocal-semi-sweet-non-decaffeinated-mutations? And I have said many times before, it is still random even if their is a higher probability of a site mutating. It would only be non-random if you could a priori determine where the mutations will occur. That you say it will probably occur there or there shows that it is not predeterminant but random....but you will continue to repeat your false mantra endlessly is my testable hypothesis and the prediction based on itPB: I consider this a NON-ANSWER. You simply don't want to get my point. Although I explained it over and over, you keep misrepresenting it.M: And looking after the fact at where a mutation occurs and claiming you knew it would happen there is hardly compelling evidence for non-random mutation.PB: Such mutations mean the end of molecular evidence of common descent. That suffices.M: LOL! You should go to ego-mania modification classes. I saw you comparing yourself to Einstein in another thread to. This demonstrates that you really are immune to science if you think that your little post hoc conclusion is evidence of anything beyond your lack of critical thinking skills. It would only be evidence if you could say BEFOREHAND EXACTLY where the next mutation is going to occur EVERY time...PB: Sometimes an idea is brought forward by a single person. Although I was standing on the shoulders of giants. M: Where exactly will the next mutation occur in the sequences?PB: I don't care. You are not longer able to use shared muations as evidence for common descent. That's quite a defeat for evolutionism.M: Poor Peter, if you cannot answer my question and don't care you are not going to get anywhere with your little pet hypothesis. It is clear that you do not care to substantiate your claims. Just repeating that it is evidence for anything you are saying has certainly not impressed anyone thus far.PB: It is clear that you are unable to think beyond your own truths. However, with 'I don't care' I meant 'it is irrelevant'. If such non-random mutations exists --and they do as demonstrated-- they introduce the end of the best molecular evidence of common descent. And THAT is quite a defeat for evolutionism. And THAT is why you deny them.M: If you can always a priori know then it is non-random...otherwise it is random.PB: I already explained several times that the NON-RANDOMNESS is with respect to position, and usually with repect to nucleotide. As soon as I find out the exact mecahnism I will call it "Borger's rule". Your turn SLPx Have fun...PB: What are you? Masochist?M: Nope, I am just here for the profound comedy that you provide..since I cannot get the Simpsons here I need something to replace the silliness that it used to provide for me..your ideas make Homer's gaffes pale in comparison.Have a nice holiday, (If you plan to visit Australia you know where to find me and we could discuss the topic while drinking beer in the sun)Best wishes,
Peter[This message has been edited by peter borger, 12-20-2002]

Dr Page says:
And Percy wonders why I have no respect for you...Dr Borger says:
Still waiting for your point-by-point reply.Best wishes,
Peter

Dear dr Page,Dr Page says:
And Percy wonders why I have no respect for you...Dr Borger says:
Still waiting for your point-by-point reply.Best wishes,
Peter

Dear Dr Page,PB: I presume this is your scientific response.quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
Dear All,
A couple of months ago Dr Page (aka SLPx) posted his ultimate proof for evolutionism at the molecular level, and I promised to have a look at it.
--------------------------------------------------------------------------------Page: I have already exposed this hyperbolic nonsense as being completely fabricated. Strawman, confabulation, nonsense.P: And I already responded to this. Next time include more information if you sent in your stuff.quote:
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I just did that and it turns out that his ultimate example that should have proven molecular evolution beyond doubt doesn't even come close doing that.
-------------------------------------------------------------------------------Page: Continuing evidence that Borger, while having earned a doctorate, is utterly unaware of how science actually works and progresses.PB: Actually I was under the impression that hypotheses have to be tested for its validity. Taking a hypothesis as fact is NO science. Verification of a hypothesis and ignorance of falsifications is also NO science.quote:
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I was expecting Dr Page to draw my attention towards a study that demonstrates mono-interpretable results that would for ever demonstrate evolutionism to be right, and the GUToB (=grand unifying theory of biology = non-random mutations in a multipurpose genome) to be false.
--------------------------------------------------------------------------------Page: Megalomania is treatable, Pete.PB: Since when is postulating a theory associated with megalomania? I also provided scientific evidence for the GUToB, so better watch your words. All you did till now is present me with poly-interpretable data, discussed subject to your pet theory.Page: Of course, it should have been obvious - both from the context of my announcing post - and the NAME OF THE LINK for christ's sake - that it was an alignment of data from a paper that YOU had been hawking for some time.PB: As obvious as the Non-random mutations in the ZFY region, I guess?Page: Your delusional narrative is entertaining, to say the least. But wait - the best is yet to come...PB: You are not very consistent in your opinions. In another letter you referred to my vision as "interesting at the least"quote:
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However, it turns out just the opposite. Dr Page posted clear-cut molecular biological evidence of non-random mutations in several species, and supports --rather than falsifies-- the GUToB.
--------------------------------------------------------------------------------Page: Just a preview - in order for non-random mutations to be demonstrated, we would need a baseline. That is, we would need to know the sequence prior to the mutation, we would need to know what the pressures were, and we would need to then observe the mutations occur (after the fact, of course). We do not see that at all.PB: Maybe you need such base line sequence. I don't. Any of the shown ZFY sequences could function as such base line to detect positional non-random mutations (= mutations that are always introduced at the same spot in the sequence, a mutational hotspot). Such positional mutations will line up, as reiterated before, and give the illusion of common descent. In fact your experiments have already been carried out in the follow up of mutations in HIV. A region of gp120 (3 loop) has been followed for 6 years. After 3 years 2 amino acid (AA) changes were observed (E-->D and H-->P), while after 6 years 9 aminoacid changed (the initial 2 AA were again involved, now D-->Q, and P-->G (the same AA mutated almost every year, demonstrating the non-random character of this mutation). (From: The evolution explosion, page 114, by SR Palumbi, ISBN 0-393-32338-2 pbk).Page: Furthermore, I eagerly await Borger's explanation as for why not all the primates in the study did not experience the same mutations. Could it be that the 'non-random mutations' acted in a random way? (or am I laughing too soon?)PB: If you had read al my letters, you would have noticed that I proposed two types of mutations operating at the same moment: 1) Non-random mutations, and 2) random mutations. The first show up as alignments the second are scattered throughout the sequences.quote:
--------------------------------------------------------------------------------I will discuss the example in detail, that can be found here:http://www2.norwich.edu/spage/zfy1a.htm--------------------------------------------------------------------------------Page: Hmmm... look at that link title - zfy1a
Could it pertain to the ZFY region that Borger has been referring to all along? Why, yes!PB: Yeah, I could have figured out for myself that you posted the ZFY region in the "sad what evolutionists can do to a mind (2)". It just dropped out of thin air.quote:
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How do we have to read the figure?
The rows demonstrate 10 homologue sequences of a not further specified stretch of DNA --but probably a protein coding gene-- of 10 distinct species.
--------------------------------------------------------------------------------Error 1.Ptr1 and Ptr2 are 2 individuals of the same species.
Pan troglodytes, common chimpanzee.PB: Thanks for clearing that up. Of course it was obvious. Maybe I should have said: (sub)species. So now we have 9 species and 1 subspecies of one of them.quote:
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The species are presented at the left hand side and abbreviated to three letter codes (plus number): Hsy, Prt1, Prt2, etcetera. The first row demonstrates the nucleotides as found in Hsy, the second row the homologous sequence as found in Prt 1, the third row as found in Prt2, etcetera. The first block of 10 rows demonstrate the first part of the sequenced stretch of DNA in these species, the second block of 10 rows are the second part of the sequenced stretch of DNA, etcetera. Nucleotides are indicated as the letters A, C, G and T. Nucleotides in species that are shared with Hsy are indicated as dots (...), mutations are shown as letters (A, C, T, G). Hence, sequence homologies are dotted and point mutations can easily be observed.
--------------------------------------------------------------------------------Page: Very good. I guess you read my primer here:http://www2.norwich.edu/spage/alignment1.htm
Perhaps you can find all the non-random GUToB proof in that alignment, too?PB: I skimmed it. The non-random mutations are easy to spot. Later more about the NRM.quote:
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According to evolutionism[sic] the shared mutations are due to a mutation that occurred in a common ancestor and has been passed through into the species, thus being proof of common descent.
--------------------------------------------------------------------------------Error 2 (hey - I am being generous).
It is strong evidence for common descent, not proof.PB: I concur that it can be interpreted as evidence pointing in the direction of common descent. But than non-random mutations have to be scientifically excluded and the issue is that I provided evidence for non-random mutations. So, it will always be my interpretation against your interpretation. My goal was to bring doubt upon evolutionism in a scientific way. I just did that.quote:
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On the other hand the GUToB holds that shared mutations are non-random mutations that have either been introduced on spots that are more prone to mutations --so called hotspot mutations--, while other shared mutations are due to a protein and/or RNA mediated mechanism.
--------------------------------------------------------------------------------Page: Amazing.... Funny thing is, evilutionists (IS THIS A JOKE, read the spelling) accept that there are non-random mutations. At least according to your benign definitions given above. Of course there are regions of the genome more prone to experiencing mutations. This has long been recognized. Unless you published this amazing insight decades ago, it would appear that your GUToB is just post-hoc gibberish - at least the reality based stuff.PB: Apparently, these mutations have severe consequences for molecular evidence of common descent. That is new, and the news will not be spread by evolutionists, I guess.Page: There is one problem already - if your take on non-random mutations were correct, why do we not see all species with said hot-spots etc. exhibiting the exact same pattern of mutation?PB: Since DNA/protein complex in cells is not linear but rather 3D. The 3D structure of DNA may differentially affect the positions of the non-random mutations. Probably dependent on the class of organisms.Page: Since this is not the case, the rational logical conclusion is that, in fact, despite the non-random influences on some mutations, they are indeed random.PB: Let me rephrase: Since YOU assume this is not the case. I pointed out that the shared mutations that line up in comparison studies that you take as evidence of common descent, might as very well be these mutations. I thought that was this discussion about.quote:
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The latter is currently hard to proof, since the mechanism are still obscure (Although such mechanisms are present in bacteria as stress-induced error-prone redundant DNA polymerases, and evidence is also present in subspecies of D. melanogaster, e.g. in the 1G5 gene).
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Page: Yes - more evidence of the co-option of evidence against non-random mutations as evidence for it. Incredible. Oxidative stress induced genome wide mutation. Some mutations are selected for. Borger claims 'non-random!' Everyone else claims 'selection working on random mutations!'PB: That is exactly what I expect from oxidative stress induced mutations. Who claimed that the mutations that line up in the IG5 gene are induced by oxidative stress? Or the non-random mutations in your ZFY region? And, by know you should know that I don't care what everybody else says. It's a worthless argument.quote:
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A thorough look at the figure reveals that several spots in the homologues sequences demonstrate shared mutations: mutations on exactly the same spot in the DNA of several distinct organisms. Are these shared mutations due to common descent (as proposed by evolutionists) or due to a common mechanism (as proposed by Dr Borger)? Let's find out.
--------------------------------------------------------------------------------Page: Amazingly, evolutionists believe that there are common mechanisms in mutation as well! They just do not ascribe some magical phenomenon as the cause (creatons... LOL!). Of course, Borger is missing the big picture: The pattern of the shared mutations.PB: Strawman. I don't need the creatons in this matter. You know that, and everybody else who read my mails knows that.Page: Now, the alignment in question is but a small locus (part of one exon of one gene), so one should not necessarily expect to find a great deal of phylogenetic information in it. Looking at larger alignemts - such as those I have supplied Borger with links for on several occasions - show distinct patterns. Patterns that are consistent not with 'non-random' (as per PB) distributions, but with distributions that are readily, logically, and statistically explained via descent.PB: Many small loci make a big locus. Probably all your evidence for common descent may comprise non-random hotspots. I will have a close look at your ultimate molecular evidence for common descent soon. I already spotted some interesting things. And I agree with you that a superficial look would convince the layman. Therefore, I will have a careful look. I am not that gullible.quote:
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Firstly, lets have a look at the first block of 10 rows. It is clear that the C on position 22 (from left) in Hsy (maybe Dr Page could provide the full names of the organisms)
--------------------------------------------------------------------------------Page: Don't you know? These species came form the Kim paper that you have been hawking. Hylobates syndactylus. The preferred phylogeny is actually Ssy - Symphalangus syndactylus.PB: You mean the paper that demonstrate complete stability of the ZFY region? No neutral mutations for 30My. You weren't able to provide an satisfactory answer to this observation. Yes, I remember.quote:
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is variable throughout the presented species.
--------------------------------------------------------------------------------Page: And?PB: And? Is that all you can think of? Dr Page there is NO sign of common descent!quote:
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In 6/10 we find a C-->T transition (C22-->T). It should be noted that this mutation does not proof common descent, since the mutation is occurring randomly throughout the species.
--------------------------------------------------------------------------------Page: Since no evolutionist would ever be so stupid to try to claim that a single mutation proofs anything, I fail to see why an expert molecular biologist such as yourself would even mention it.PB: A bunch of single mutations make a lot. If this were the only mutations I wouldn't be bothered. But these non-random mutations show up every time I study DNA sequences in detail. It makes me rather suspicious about the so called random character of mutations.quote:
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For instance, while Lca, Hag and Ptr2 have a C in this position, all other sequences demonstrate a T. Thus, no consistent evolutionary pattern is observed.
--------------------------------------------------------------------------------Page: Actually, Ptr2 does not have a C there. Hag is the other gibbon, so, in fact, Hag and Hsy both have a C there. Lca, ring tailed lemur, also has a C there. What that indicates is that T was probably the ancestral state, and the ancestor for the gibbons experienced a mutation there as did the lemur's. Of course, again, trying to support or falsify anything based on a single nucleotide locus is ridiculous.PB: It is more of the same. If it were only this one I wouldn't be bothered. But I am starting to detect a pattern: non-random mutations. Glad you admitted.quote:
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Secondly, we observe G88-->T (first block, left hand side) in 4/10 cases. Also no evolutionary pattern is observed. In other words, these point mutations do not proof molecular evolution at all.
--------------------------------------------------------------------------------Page: And you think this proofs what? They are, after all, individual point mutations, and frankly, I cannot find what you are refeering to. Woodmorappe-like, you seem to be using a coding/counting system unique to you alone.PB: See above. I am beginning to see a pattern: non-random mutations. What/who is Woodmorappe?quote:
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If they proof anything than it is the non-random character of these mutations.
--------------------------------------------------------------------------------Page: Are you really trying to claim that descent is falsified via two single nucleotide loci in one part of one exon of one gene in a genome of 3 billion nucleotides?
the reader can come to their own conclusions about that...PB: The two single nucleotide in this small stretch of DNA can be used to support my assertion that the other alignments may have a similar origin: non-random mutations.quote:
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Apparently the mutations in the first block are non-random mutations and that is in accord with the GUToB.
--------------------------------------------------------------------------------Page: What utter poppycock. In a 110 site block of nucleotides, PB observes a few areas in which there is a relative 'split' between the nucloetide at a particular locus. Big deal. Why does not PB mention the clearly random SNPs?PB: Because we are discussing non-random mutations, of course! And how to detect them. And how they give the illusion of common descent. The random mutations are irrelevant.Page: Those in one of the two common chimps? That not all common chimps demonstrate the exact pattern of nucloetide change seems to contradict GUToB, does it not?
PB: Even if this was true, the observation also contradicts the evolutionary vision of common descent. However, simply assuming a non-ranom spot that again mutated is more in accord with these observations. It is GUToB.quote:
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Evolutionist's will have to claim that the aberrations exist because they have been introduced several times on the same spot, and therefore it is expected that we do not find a perfect alignment of mutations.
--------------------------------------------------------------------------------Page: "Several times" is not a necessary claim at all. Strawman.PB: If not, please explain what happens to this position molecular genetically.quote:
--------------------------------------------------------------------------------I am sure, however, that Mark Pullen will object to such far-fetched explanations since he is wielding Occam's razor. Besides, mutations introduced several times on the same spot also indicate the non-random character of these mutations.
--------------------------------------------------------------------------------Page: Since this "several times" schtick is a non-sequitur and a strawman, there is no need to induce any logical concpept at all.PB: HERE THE THEORY OF EVOLUTION THROUGH RANDOM MUTATION AND SELECTION ENDS. IT FALLS AGAIN. It is not valid at the molecular level! QED.quote:
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Less obvious are the non-random mutational spots on position 49 and position 58 (from left hand side).
--------------------------------------------------------------------------------Page: Again, your counting scheme seems off. Are you referring to the C possessed by Lca and Str? Str is the outgroup, that it and Lca possess it indicates it is the ancestral state, as lemurs branched off well before the OWMs and gibboins did. You may have noticed that that particular change is in a poly-T spot, yes, a known 'hot spot.' No big surprise - I would think - to a moleuclar biologist of paradigm-smashing status such as yourself.PB: A known hot spot? Than we only have to wait till we have knowledge about the other hotspots. As long as we don't have this knowledge you are free to claim them as common descent. I know they're
not.quote:
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The second block of 10 rows demonstrates similar findings. Position C9 and A60 in the Hsy sequences also seem to be non-random mutational hotspots unrelated to evolutionary descent. Position 89 from left hand side is very illustrative for a non-random-random mutational hospot: The non-random position is able to change at random with respect to nucleotide.
--------------------------------------------------------------------------------Page: I will use my most professional and logical answer here - at least that this assertion deserves:Page: ROTFLMAO!!!PB: Yeah, your old scientific arguments again:Page: The non-random position changes at random!Page: Are you for real!!!???Page: This is pure comedy.Page: So non-random, it is random. I have got to remember that one...quote:
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This position demonstrates thus compelling evidence for the hypothesis of non-random mutations. It definitely is the end of evolutionary claims of common descent based upon sequence homology and shared mutations.The shared mutations in block 3 and block 4 may be explained accordingly.Best wishes, and have a nice contemplative day,
Peter
--------------------------------------------------------------------------------Page: I contemplated your infantile nonsense, and found it most entertaining, to say the least.PB: You are too kind! (You like to repeat yourself, isn't it)Page: I do hope - and this is a sincere hope - that you have not written any of this down and presented it to your colleagues or tried to submit it anywhere.PB: I am always so grateful for your concern about my colleagues and carreer!Page: Of course, it is all stored on my hard drive. And it is available on
here.PB: If I see some day a paper on non-radom mutations and how to detect them with your name on it, I know where you got it from Page:I have written some things that I regret, made some mistakes, etc.,...PB: Pretty obvious. Better look before you leap. I, on the contrary, do not regret any of my mailings.Page: ...but man, Peter, this is just career-ending nonsense. You would do yourself a favor by keeping this to yourself.PB: I see, it is not allowed in the evolutionary community to postulate some new ideas. In my discipline it is welcomed to have new insights. However, what else would one expect from an static outdated vision of life. I do not look for a career in evolutionary biology, since I do not find it intellectual satisfying to keep up a paradigm that isn't explanatory.Page: So non-randomit is random...PB: Hard to get isn't it? This non-random position --position says something about location (where)-- demonstrates randomness with respect to nucleotide. The same position is over and over and over involved. It is a NON-random POSITION. Therefore, the other positions might as well be NON-RANDOM positions and might also be non-random with respect to nucleotide.Page: CLASSIC!PB: Thanks for the acknowledgement.Best wishes, and thanks for your thoughts,
Peter[This message has been edited by peter borger, 12-23-2002]

Dr Page, you've done it again! After reading your stuff, I literally laughed my pants off! You've chosen the wrong job. You could be a comediant. More (obliterative comments) soon.Best wishes and a happy NY,
Peter

Dear Peter,I will soon eleborate on the mechanisms involved in non-random mutations, but that will take a bit of time. The hotspot mutations in p53 mentioned earlier on this board were already hinting in the right direction. If you wanna know all ins and outs of non-random mutations, I recommend you to read Lynn Caporale's book "Darwin in the genome". I've read it over the weekend and it is more compelling evidence for non-random mutations. Her book also provides molecular mechanisms that explain these particular type of mutations and can even explain recurring indel-mutations. As I claimed before, it is also possible to predict non-random mutations. That is, the position where they are going to be introduced, and the nucleotides involved. It is definitely the end of the NDT era. Also, they have far reaching consequences for molecular phylogeny. Orthodox evolutionists will not like it (and that's an euphemism).Best wishes,
Peter

Dear Page,Page: I was especially tickled by the fact that you don't seem to know that humans and chimps are in the same Class....PB: I recall somebody (Goodman?) claiming them to be the same species.best wishes,
Peter