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.

Well I see we are trotting this old horse back out again
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:
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. 2)Your claim is that this does not happen and that every mutation event must be a de novo error made by the polymerase. Since polymerase fidelity experiments have been done and never shown this phenomenon this also falsifies your claim. So simple genetics and simple biochemistry falsifieds the GUToB. 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:
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!!!!! 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. Where exactly will the next mutation occur in the sequences? If you can always a priori know then it is non-random...otherwise it is random.Your turn SLPx Have fun...

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?My interpretation would be that the changes represent a branch
of a tree, where some of the species are descended from others.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.It's all interpretation, there is not fact.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?

Just one quick comment for now - I have a meting shortly:

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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.

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Right off the bat, Borger the creationist launches into a bizarre hyperbole-ridden diatribe.I never wrote or implied that my dataset was the "ultimate proof for evolutionism at the molecular level."Borger is either 1. Lying to set us some sort of strawman argument or 2. is simply deluded enough that he actually recalls the series of posts in this way.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."Borger's opening statement will set the tone for my reply, whihc I hope to get to this afternoon.It will not be pretty.

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....

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

Hi SLPx!Creationists and evolutionists are fellow members of this site and should treat each other as respected colleagues. Disagreements should be expressed in a gentlemanly fashion as described in the forum guidelines. Extending help and assistance rather than ridicule and derision when a mistake or misstep is made would be welcomed by both sides I'm sure.--------------------EvC Forum Administrator

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: 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 sense 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.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. 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.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: 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?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: 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.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.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.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. 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? 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.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: 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 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...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.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? 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.cheers,
M

I've just read SLPx's reply (or one of them at least)
and have to ask the same question...That is, given the sequences how do you differentiate between
random and non-random mutations?In the segments given Hsy and Hag differ in only two locations,
and in one of these locations none of the other organisms show
a difference from Hsy.This would suggest that the differences are not the result of
any mechanism (directed or not) since they occur in only one
of the whole group.Likewise if the changes DON'T occur in the same place
across the whole group that would suggest that absence
of a mechanism.

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Originally posted by Admin:
Hi SLPx!

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Creationists and evolutionists are fellow members of this site and should treat each other as respected colleagues. Disagreements should be expressed in a gentlemanly fashion as described in the forum guidelines. Extending help and assistance rather than ridicule and derision when a mistake or misstep is made would be welcomed by both sides I'm sure.

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Sure, everyone makes mistakes.Certain individuals seem to not make mistakes and only later claim that they were to cover their tracks.

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.

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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!

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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.