Well, maybe just a few points...
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Originally posted by peter borger:
Dear Dr Page,
PB: I presume this is your scientific response.
As I found little scientific to respond to, your impliation is appropriate.
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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.
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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.
Or, better yet, you can simply not append your fantasy-driven baggage to the posts of others?
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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.
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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.
Lithium run out again?
You prattled on about "proof beyond doubt".
My statement stands, and you have falsified nothing.
Hyperbolic assertion and confabulation are not falsifications.
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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.
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Page: Megalomania is treatable, Pete.
PB: Since when is postulating a theory associated with megalomania?
When the one postulating said "theory" ignores falsifications of foundational concepts and concocts magical particles and processes to prop up said "theory".
Thats when.
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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.
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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.
So you are omniscient as well as a paradigm-busting genius? Allow me to grovel in your presence...
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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).
Yup. Just like looking at the flames of a fire tells us exactly how the fire started...
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Such positional mutations will line up, as reiterated before, and give the illusion of common descent.
Perhaps it is the shared via descent mutations that produce the illusion of GUToB?
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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).
I guess the fact that other AAs changed in addition to the original ones can just be ignored. You have a paradigm to bust!
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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.
How convenient...
But how do you tell the difference?
Are you saying that non-random mutational loci can also mutate randomly?
How absurd and ad hoc does this new theory of biology get?
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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.
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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.
WHy would you say that?
They are not subspecies, at least not according to the GENBANK information.
They are members of the same species.
Or does that put a kink in your interpretation and so must be ignored?
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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.
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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.
Yes, they must be easy to spot when you simply co-opt the evidence for descent.
I eagerly await your ... evidence... that the indicated loci represent non-random mutations. I will be especially interested to read how you explain the shared indels...
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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.
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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.
No, you just look at the synapomorphies and say "Look, directed mutation."
In a similar fashion, creationists like to look at the fossil record and proclaim that it presents evidence not for evolution, but for a single world wide flood. Simply presenting an interpretation does not make it correct. One needs corroboration and foundational support. It is demonstrable that mutations can be passed on via descent. Therefore, it is logical to conclude that patterns of such mutation are demonstrative of descent.
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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.
No, you have brought doubt upon your competence in areas outside of asthma research.
My interpretation, as alluded to above, is premised on verifiable concepts. Yours is premised on "creatons" and already falsified concepts (directed mutations), and you just won't give up.
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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.
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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.
Please start making sense. Repeating how important you think your "discoveries" are just solidifies my belief that you have some sort of neurosis. That is not an ad hominem, that is based on what I have read.
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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.
What utter nonsense.
Primates are all of the same class. Even members of the same species exhibit mutations that you cannot 'explain' with your 'theory'!
This is archive stuff...
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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.
Yeah - me and every evolutionary biologist.
Just-so stories hold less water than interpretations with proof-of-concept support:
Science 1991 Oct 25;254(5031):554-8
Gene trees and the origins of inbred strains of mice.
Atchley WR, Fitch WM.
Department of Genetics, North Carolina State University, Raleigh 27695.
Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.
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Science 1992 Jan 31;255(5044):589-92
Experimental phylogenetics: generation of a known phylogeny.
Hillis DM, Bull JJ, White ME, Badgett MR, Molineux IJ.
Department of Zoology, University of Texas, Austin 78712.
Although methods of phylogenetic estimation are used routinely in comparative biology, direct tests of these methods are hampered by the lack of known phylogenies. Here a system based on serial propagation of bacteriophage T7 in the presence of a mutagen was used to create the first completely known phylogeny. Restriction-site maps of the terminal lineages were used to infer the evolutionary history of the experimental lines for comparison to the known history and actual ancestors. The five methods used to reconstruct branching pattern all predicted the correct topology but varied in their predictions of branch lengths; one method also predicts ancestral restriction maps and was found to be greater than 98 percent accurate.
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Science 1994 Apr 29;264(5159):671-7 Application and accuracy of molecular phylogenies.
Hillis DM, Huelsenbeck JP, Cunningham CW.
Department of Zoology, University of Texas, Austin 78712.
Molecular investigations of evolutionary history are being used to study subjects as diverse as the epidemiology of acquired immune deficiency syndrome and the origin of life. These studies depend on accurate estimates of phylogeny. The performance of methods of phylogenetic analysis can be assessed by numerical simulation studies and by the experimental evolution of organisms in controlled laboratory situations. Both kinds of assessment indicate that existing methods are effective at estimating phylogenies over a wide range of evolutionary conditions, especially if information about substitution bias is used to provide differential weightings for character transformations.
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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.
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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.
Creatons do not exist, yet they are part of your 'theory.' I do not know where you posit the intervention of these magical non-existent particles, and do not care. Just as I do not care where unicorns live.
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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.
Again with the misrepresenation.
Funny how creationists so readily embrace their unethical practices.
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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.
No comment...
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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)
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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.
I (and others) did. That you ignored/dismissed them is a given.
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is variable throughout the presented species.
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Page: And?
PB: And? Is that all you can think of? Dr Page there is NO sign of common descent!
Amazing - a piece of one exon of one gene, representing a whopping 0.000125% of the genome, does not exhibit clear unambiguous phylogenetic signal and we are expected to accept the 'falsification'
of evolution.
I found nothing else to think of...
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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.
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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.
And what DNA sequences have you studied?
It must be comforting to look at all those sequences and just see all that evidence for YOUR theory, despite the fact that everyone else with a passing knowledge of the subject sees it as evidence for evolution.
How does it feel to know that every other person - scientist and layman alike - is just plain wrong and you are right but unrecognized?
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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.
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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?
I see a pattern, too. I see a creationist consistently ignoring their errors and proclaiming that things exist that do not. You counted wrong, Borger. try again.
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If they proof anything than it is the non-random character of these mutations.
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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.
Please take another look. Look at the overall paterns. Frankly, only a zealot would see "non-random mutation" when looking at the big picture.
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Apparently the mutations in the first block are non-random mutations and that is in accord with the GUToB.
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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.
LOL!
Yes, that is right. Random mutations are irrelevant when trying to prove the existense of non-random ones!
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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.
NO, it demosntrates that individuals can experience mutations that not all members of the population do. Pretty simple stuff.
I really do like your alternative explanation - a non-random locus simply mutated again. Randomly. Classic...
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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.
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Page: "Several times" is not a necessary claim at all. Strawman.
PB: If not, please explain what happens to this position molecular genetically.
There is nothing to explain. Your "several times" claim is spurious.
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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.
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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.
HERE BORGER EXPERIENCES A SCHIZOID EMBOLISM.
PLEASE CALL THE WHITE-SUITED GUYS WITH BUG BUTTERFLY NETS.
This is just a regular comedy!
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Less obvious are the non-random mutational spots on position 49 and position 58 (from left hand side).
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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.
What - you know that poly-putine/poly-pyrimidines are NOT areas in which mutations occur?
How is it that you know this? Where are your publications on this find?
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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.
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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...
All right-on replies!
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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
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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)
Projecting are we? How many times can the creationist claim to have falsified evolution?
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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
Why would I do something so stupid?
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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.
You really should.
Of course, such overconfidence is a sign of neurosis.
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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.
Right. You prefer to make stuff up and call it a better exlanation.
Like I said, best to keep this to yourself.
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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.
Like I said... Classic...
Well, that was a real waste of time.
Unless I am in the mood for some comic relief, I see little reason to engage Borger anymore.
But his posts really are keepers.
(or am I laughing too soon?)
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