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» ISCID Forums   » General   » Brainstorms   » Peter Borger: Shared mutations: Common descent or common mechanism? (Page 2)

 
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Author Topic: Peter Borger: Shared mutations: Common descent or common mechanism?
peter borger
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Icon 1 posted 26. June 2006 09:39      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
Anyway, Peter, we've been over this before back at ARN, and I won't spend too much of my time refuting the same arguments over and over again. My main interest here is not to convince you (since that is clearly impossible), but prevent you from dazzling any readers with a non-scientific background into thinking that your ideas have any substantial merit. So let me open this up to anyone other than Peter - are there any readers out there who are not clear about how Peter's arguments here are mistaken? I'd be happy to clarify my response for you.

You need quite some retoric to address the readers. What do you know about the readers background, anyway?

MESK, whether you like it or not, I have an alternative explanation for all biological phenomena without Darwin's pressuppositions of natural selection and common descent. Is that a crime, or what? O I see, it is not allowed to doubt the evolutionary dogmas. If I were you I'd better get used to it, since Darwin was seriously mistaken. Darwinism has been around too long without explaining anything.

peebee

PS: It was not ARN it was here in 2003.

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peter borger
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Icon 1 posted 26. June 2006 09:42      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
The GULO gene is interesting in that it contains five sites (out of 165) that have been subject to multiple mutations within a comparatively brief period of evolutionary time
This shows you did not read the Inai, Ohta paper. In my paper I only show exon X and here we see 11/21 NRM positions.

peebee

[ 26. June 2006, 11:09: Message edited by: peter borger ]

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peter borger
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Icon 1 posted 26. June 2006 09:49      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
Almost forgot, MESK, but this also still stands:

quote:
due to my analysis, the GULO gene CANNOT be taken as evidence for common descent of the primates. All pro-evolutionary books, journals and internet sites must now retract the GULO sequences as proof of common descent (let's see whether they will do that). That's the scientific method.
peebee
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peter borger
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Icon 1 posted 26. June 2006 10:14      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
Show me a single piece of evidence indicating that Ohta and Nikishimi would disagree with the statement that "sites 1, 22, 31, 58, 79, 81, 109 and 157 indicate mutations in the rat lineage."
See my paper on page 10, line 1-5. Here I quote the Inai, Ohta & Nikishimi paper of 2003:

quote:
Under the assumption of an equal chance of substitution throughout the sequence, the probability of the same substitutions in both humans and guinea pigs occurring at the observed number of positions and more was calculated to be 1.84x10-12. This extreme small probability indicates the presence of many mutational hot spots in the sequences (from Inai et al, 2003)
peebee

[ 26. June 2006, 11:10: Message edited by: peter borger ]

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Scott
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Icon 1 posted 26. June 2006 15:20      Profile for Scott   Email Scott   Send New Private Message       Edit/Delete Post 
quote:
What is more, three years ago I predicted on the EvC site that the GULO gene is subject to NRM, even before the publication of Ohta's paper. I predicted so, because GUToB says there is NO common descent.
Is there a difference between finding evidence which leads to the formulation of a hypothesis of no common descent, and starting out with a theory which says there is no common descent and then going out to look for evidence to support the theory?

PB, what is the difference between your method and the method of the Darwinians?

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Mesk
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Icon 1 posted 26. June 2006 20:56      Profile for Mesk     Send New Private Message       Edit/Delete Post 
quote:
peter:
Listen, MESK, I will do another prediction. When the entire GULO genes are compared in these organisms (and not only exon X as I did) we will still find that around 50% of the point mutations line up as the result of NRM. That would proof that I am right. What is your prediction from standard theory?

Define exactly what you mean by "line up as the result of NRM" - i.e. provide an operational definition of this term explicit enough that someone unfamiliar with your ideas could perform this analysis themselves. When I look at a sequence alignment, precisely what should I be looking for as the signature of NRM? Without a tight operational definition, your prediction is worthless.

As for the predictions from standard theory: 95-99% of sites should be able to map unambiguously onto the standard phylogeny, with no incongruencies. This is a high-risk prediction; if common descent is false, the odds of this proportion of the sites being congruent is minuscule. Yet this prediction is made every time a molecular phylogeny is constructed, and the overwhelming majority of phylogenies bear the prediction out.

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David L. Hagen
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Icon 1 posted 26. June 2006 21:56      Profile for David L. Hagen   Email David L. Hagen   Send New Private Message       Edit/Delete Post 
Comments on: Shared mutations: Common descent or common mechanism? by Peter Borger

Causes
Page 5. A possible alternative/extension to “physiochemical properties of the DNA sequence” might be “or the DNA replication process.”

Near neutral mutations not selected
Page 6. Recommend noting that “numerous ‘neutral’ or ‘near neutral’ mutations do not experience individual selective pressure. [Haldane 1957, Kimura 1979, Sanford 2005.]”
Recommend adding several references showing the basis that numerous “near neutral” mutations cannot be selected out. E.g.,
Haldane, J.B.S. 1957. The cost of natural selection. J. Genetics 55:511-524.
Muller, H.J., 1964. The relation of recombination to mutational advance. Mutation Research 1:2-9.
Kimura, M. 1979. Model of effective neutral mutations in which selective constraint is incorporated. PNAS 76:3440-3444.
Sanford, John C. 2005. Genetic Entropy & The Mystery of the Genome. Ivan Press
ISBN 1-59919-002-8.

Different Folds?
Suggest reviewing:
Jakob Skou Pedersen, Gill Bejerano, Adam Siepel, Kate Rosenbloom1, Kerstin Lindblad-Toh, Eric S. Lander, Jim Kent, Webb Miller, David Haussler, [http://compbiol.plosjournals.org/archive/1553-7358/2/4/pdf/10.1371_journal.pcbi.0020033-L.pdf
Identification and Classification of Conserved RNA Secondary Structures in the Human Genome], PLOS Computational Biology April 2006 Vol 2 Issue 4 e33.
Do any of their EvoFold predictions relate to your findings? E.g., as regards to different folds etc.?

Edits
Following are some editorial suggestions on the paper:
Page 3. In citing Darwin, identifying the citation pages may help readers find them.
Suggest adding the term “stochastic” to read:
“as ‘random’ ‘blind chance’ or a ‘stochastic process’.”
Page 4: Suggest make two sentences. “. . .from the start. Otherwise none”
Page 4: “occur only once” Any citation for this?
Suggest saying “and are assumed to occur only once.”
Page 5. Break into two sentences: “... indicated. However, there could be. . .”
Page 5. “. . .but is not a pseudogene.”
Change “1'081" to “1,081" for international thousands convention.
Page 5 “The major parts of the indivdual genes are identical . . . ”
Page 6. Correct reference “[7]”
Page 6 Place ‘neutral’ in quotes to indicate it as an assumption. “. . . from the assumption of a ‘neutral evolution’”
Suggest changing Page 9 Footnote 1 to read: “Neo-Darwinists must demonstrate how inactivation of this GULO gene provided a selective advantage to become fixed.”
Page 9: Correct typo “proofs common decent” to “proves common decent”
Page 11 “the elucidation” to “its elucidation”

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peter borger
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Icon 1 posted 27. June 2006 03:00      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
Define exactly what you mean by "line up as the result of NRM" - i.e. provide an operational definition of this term explicit enough that someone unfamiliar with your ideas could perform this analysis themselves. When I look at a sequence alignment, precisely what should I be looking for as the signature of NRM?
Back in 2002, while looking at the GULO sequences of primates (Ohta & Nishikimi, 1999) I observed that position 55 and 131 are unstable positions. This made me propose NRM in this region. Most genes have such positions and therefore I believe that phylogeneticists simply study this phenomenon. That they are able to construct reasonable congruent trees from distinct regions is because similar MPG have similar sequence and NRM depend on the DNA sequence (this has actually been shown in several organisms). I also believe that it is difficult to distinguish between common descent and a common mechanims (As argued). We may not be able to deduce it from sequence analyses alone, but we may obtain a good indication of NRM when we do intraspecies comparisons. For instance, the ancient human mtDNA sequences I discussed a few years ago are also a good indication that mutations are introduced non-randomly (although we cannot exclude non-random decay of ancient sequences).

The alignment of mutations we observe in for instance primate comparisons may be due to the most unstable positions in the original MPG sequences. This is confirmed by the CpGs which we know to be easily mutable. I can think of several experiments to test the hypothesis in vivo.

peebee

[ 27. June 2006, 03:11: Message edited by: peter borger ]

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peter borger
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Icon 1 posted 27. June 2006 03:17      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
Is there a difference between finding evidence which leads to the formulation of a hypothesis of no common descent, and starting out with a theory which says there is no common descent and then going out to look for evidence to support the theory?
Yes, there is a difference. The molecular data that give the illusion of common descent requires explanation: NRM. Next you have to provide evidence for that supposition. I did that.

peebee

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Mesk
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Icon 1 posted 27. June 2006 11:32      Profile for Mesk     Send New Private Message       Edit/Delete Post 
quote:
peter:
Back in 2002, while looking at the GULO sequences of primates (Ohta & Nishikimi, 1999) I observed that position 55 and 131 are unstable positions. This made me propose NRM in this region. Most genes have such positions and therefore I believe that phylogeneticists simply study this phenomenon. That they are able to construct reasonable congruent trees from distinct regions is because similar MPG have similar sequence and NRM depend on the DNA sequence (this has actually been shown in several organisms). I also believe that it is difficult to distinguish between common descent and a common mechanims (As argued). We may not be able to deduce it from sequence analyses alone, but we may obtain a good indication of NRM when we do intraspecies comparisons. For instance, the ancient human mtDNA sequences I discussed a few years ago are also a good indication that mutations are introduced non-randomly (although we cannot exclude non-random decay of ancient sequences).

Peter, you didn't address my question at all. Here it is again:

quote:
Define exactly what you mean by "line up as the result of NRM" - i.e. provide an operational definition of this term explicit enough that someone unfamiliar with your ideas could perform this analysis themselves. When I look at a sequence alignment, precisely what should I be looking for as the signature of NRM?
It's not sufficient to merely state that, "We may not be able to deduce it from sequence analyses alone, but we may obtain a good indication of NRM when we do intraspecies comparisons" - this doesn't say anything specifically about the criteria used to differentiate objectively between a non-random mutation and a standard random mutation. So what is this objective test?
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peter borger
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Icon 1 posted 28. June 2006 03:55      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
It's not sufficient to merely state that, "We may not be able to deduce it from sequence analyses alone, but we may obtain a good indication of NRM when we do intraspecies comparisons" - this doesn't say anything specifically about the criteria used to differentiate objectively between a non-random mutation and a standard random mutation. So what is this objective test?
As mentioned several times and also one of the theses of GUToB:

"For organisms that do not reproduce together, we may not be able to discriminate between mutations introduced by a common mechanism and those resulting from common descent".

This is GUToB's uncertainty principle.

When reproduction between species has been observed an alignment of mutations may indicate common descent, but still NRM must then be excluded. I know of many mutations that are shared between human (sub)populations, but have an independent origin.

peebee

[ 28. June 2006, 04:17: Message edited by: peter borger ]

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John A. Davison
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Icon 1 posted 28. June 2006 07:16      Profile for John A. Davison   Email John A. Davison   Send New Private Message       Edit/Delete Post 
It is insane to deny common decsent as long as one is willing to consider that there may have been multiple creations and/or front-loadings. There is every reason to believe that all primates share a common ancestor and no reason to think otherwise. Furthermore there is no compelling reason to believe that required any input from environmentally generated factors. Beyond the order level, things become problematical and as yet unresolved.
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John A. Davison
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Icon 1 posted 28. June 2006 07:45      Profile for John A. Davison   Email John A. Davison   Send New Private Message       Edit/Delete Post 
Speaking of independent origins of identical mutations, I hAve a Dachshund named Otto in honor of Otto Schindewolf the great paleontologist and evolutionary saltationist. The short legs of the Dachshund are due to exactly the same gene that produces the human achondroplastic dwarf. In both instances the hind limbs are straight and the forelimbs somewhat twisted. The body is of normal size. The condition results from a pituitary defect which causes a premature cessation of growth of the long bones of the appendages. The same allelic mutation has occurred in sheep and elsewhere. It is a Mendelian dominant. Such genes neither have now nor ever had anything to do with creative evolution.
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peter borger
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Icon 1 posted 28. June 2006 10:06      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
The short legs of the Dachshund are due to exactly the same gene that produces the human achondroplastic dwarf.
John, in humans achondrioplasia is due to mutations in the FGFR2 gene. A remarkable observation on the FGFR2 gene is that the major part of the mutations are introduced at the same two spots (755C->G and 755-757CGC->TCT) independent of common descent. This is probably also a NRM in other MPGs such as dogs and sheep.

peebee

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Scott
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Icon 1 posted 28. June 2006 12:07      Profile for Scott   Email Scott   Send New Private Message       Edit/Delete Post 
quote:
As for the predictions from standard theory: 95-99% of sites should be able to map unambiguously onto the standard phylogeny, with no incongruencies. This is a high-risk prediction; if common descent is false, the odds of this proportion of the sites being congruent is minuscule.
Is this really a prediction though? What if they don't map with that high a level of congruence? Wouldn't that just be taken as evidence of a separate evolutionary history rather than as a denial of common descent?

Btw, where do these numbers come from?

[ 28. June 2006, 12:08: Message edited by: Scott ]

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