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Author
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Topic: Peter Borger: Shared mutations: Common descent or common mechanism?
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John A. Davison
Member
Member # 1425
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posted 31. August 2006 12:38
This time it is for keeps, including being denied viewing. DaveScot, actually David Springer, the man who introduced me to Uncommon Descent as "my good friend Professor John Davison," is taking full credit for it. Isn't that precious?
I love it so!
"A past evolution is undeniable, a present evolution undemonstrable."
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Melvin H. Fox
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Member # 1684
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posted 02. September 2006 20:49
Peter
Excuse my ignorance. You wrote [29 Aug. 2006]
quote:
The second mode (sexual reproduction) is thus completely redundant unless it was predesigned and for a purpose. The purpose is, as we know, to prohibit evolution.
I have not seen this put so bluntly. Could you make reference where this is shown or perhaps take a few minutes to elaborate here how sexual reproduction prohibits evolution?
-Mel
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John A. Davison
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Member # 1425
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posted 03. September 2006 00:44
Melvin
I agree with Peter that obligatory sexual reproduction is incompetent to support evolution beyond the generation of varieties and subspecies and have presented my reasons for believing so in the Manifesto, hopefully under discussion here, and in my paper "Is evolution finished?," Rivista di Biologia, 97: 111-116, 2004, and in my paper "The case for instant evolution," Rivista di Biologia 96: 203-205, 2003, and in my paper "Evolution as a self-limiting process," Rivista di Biologia 91: 199-220, 1998, and in my paper "The 'blind alley': its significance for evolutionary theory," Rivista di Biologia 86: 101-111, 1993. It is also explicitly stated in my first evolution paper "Semi-meiosis as an evolutionary mechanism," Journal of Theoretical Biology 111: 725-735, 1984.
I am convinced that the SOLE purpose of obligatory sexual reproduction IS NOW AND ALWAYS WAS to stabilize the species, thus bringing progressive evolution to a halt, thereby ensuring ultimate extinction without which creative progressive evolution could never have occurred. In other words Mendelian (sexually mediated) genetics never had anything to so with creative evolution, a conclusion which had been reached by William Bateson before I was even born and with which I am in complete agreement.
That is what led me to the Semi-meiotic hypothesis (SMH) as the only conceivable alternative to the Darwinian gradualist model, a position to which I still adhere. Further reasons are contained in the Manifesto and I will be happy to present them if given that opportunity.
"By 1924, Bateson had come to realize and told his son in confidence, 'that it was a mistake to have committed his life to Mendelism, that it was a blind alley which would not throw any light on the differentiaton of species, nor on evolution in general'." (Arthur Koestler, The Case of the Midwife Toad, 1971) as cited in my 1993 paper "The 'blind alley': its significance for evolutionary theory." Rivista di Biologia 86: 101-111.
"A past evolution is undeniable, a present evolution undemonstrable."
John A. Davison
[ 16. March 2007, 05:11: Message edited by: John A. Davison ]
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Melvin H. Fox
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posted 03. September 2006 16:52
John
Thank you. I will probably start with your 1984 paper. I would also like Peter to respond if he is still reading this thread and cares to inform.
-Mel
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peter borger
Member
Member # 722
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posted 18. September 2006 09:47
Mesk,
quote:
I haven't had time to examine your 1G5 data, but your evidence for "non-random mutation" in the GULO gene is actually due to a very basic misunderstanding of phylogenetics. The sites at which humans, chimps, orangs and guinea pigs have one base but rats have another do NOT represent convergent evolution in the first four taxa - they simply represent mutations in the rat lineage. (Seriously, Peter, draw a tree, sit down and think about the data for five minutes - this is glaringly obvious.) So sites 01, 22, 31, 58, 79, 81, 109 and 157 are perfectly congruent with even the simplest model of common descent.
I had a bit of time and looked into some details.None of the mutations in rat cause the GULO protein sequence to change. You cannot propose selection on these sites. How then? Besides, a GULO protein is a GULO protein, isn't it? I mean what would the selective advantage be of the active rat GULO protein relative to that found in, say, cow? They both catalyse the final step in vit C synthesis. Please let me know. Thanks.
Peebee
[ 27. November 2006, 06:43: Message edited by: peter borger ]
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adhitthana
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Member # 2020
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posted 05. November 2006 02:06
So....what has happened with the paper?
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adhitthana
Member
Member # 2020
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posted 10. February 2007 20:35
Does anyone know? How can i access the full 2003 paper by the Japanese scientists?
Can I buy it online?
Did their paper explicitly state that the mutations shared with guinea pigs were independent? That is not the result of guinea pigs and humans sharing a common anscestor?
Did that paper explicitly state that quote:
they reported a large number of shared mutations (substitutions) present in both organisms under the assumption of equal chance of substitution throughout the sequence the probablity of the same sustitutions in both humans and guinea pigs at the observed number of positions and more was calculated to be 1.8 X 10 to the minus 12.
Thank you.
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adhitthana
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posted 11. February 2007 03:14
I would like to get a copy of the 2003 paper. can anyone assist me...how can i get one?
thanks
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peter borger
Member
Member # 722
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posted 12. February 2007 05:41
adhitthana,
quote:
under the assumption of equal chance of substitution throughout the sequence the probablity of the same sustitutions in both humans and guinea pigs at the observed number of positions and more was calculated to be 1.8 X 10 to the minus 12.
This is what the authors stated in their original 2003 paper. A few years ago, I asked the auhors to send me a copy of their GULO paper and they did. It cannot be accessed via the internet (only the abstract is available) and what I got was a hardcopy by regular mail. In the meantime, the GULO data have been reanalysed and the paper, coauthored by me and Royal Truman, will be published in "The Journal of Creation". It appeared my initial analyses was not entirely correct, but the evolutonist's analyses is not correct either. Still the bottomline of our paper is: the GULO gene cannot be taken as evidence for common descent. quote:
[ 12. February 2007, 05:45: Message edited by: peter borger ]
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adhitthana
Member
Member # 2020
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posted 06. March 2007 22:28
quote:
This is what the authors stated in their original 2003 paper. A few years ago, I asked the auhors to send me a copy of their GULO paper and they did. It cannot be accessed via the internet (only the abstract is available) and what I got was a hardcopy by regular mail. In the meantime, the GULO data have been reanalysed and the paper, coauthored by me and Royal Truman, will be published in "The Journal of Creation". It appeared my initial analyses was not entirely correct, but the evolutonist's analyses is not correct either. Still the bottomline of our paper is: the GULO gene cannot be taken as evidence for common descent.
Thanks for you time again Peter. I did find the email address of one of the authors and wrote huim asking for a copy of the paper, but did not get a reply (maybe I needed to write in japanese) ![[Wink]](wink.gif)
I have been discussing this elsewhere trying to get a grip on it.
I wonder if you have time, could you comment on this comment on your paper?
quote:
The mutation that led to inactivation is different in guinea pigs then in primates.
This is probably what we observe in figure 2 at position 97.
Meaning that the inactivation of the gene occured independently in both species.
One mutation does not necessarily always inactivate the gene. There are 40 sites that show mutations, 8 of which line up exactly and are the same, those were probably caused in the common ancestor and didn't lead to inactivation of the gene. In total there are only 3 mutations that line up, but in which guinea pig shows a different mutation. 8 mutations are unique to guinea pigs and in total that accounts for all of the 19 mutations in guinea pigs(8 + 3 + 8). Only one mutation in guinea pigs is interesting because it overlaps the deletion at position 97.
8+3=11 those are the 11 mutations out of the 21 Borger talkes about and he claims those 11 were caused after lineages split up. I'm saying he hasn't substantiated that claim in any way shape or form. There are only 3 of those 11 which can logically be after lineages split up, the other 8 require independent proof that they arose after lineages of guinea pig and humans split up before he can justify his claims. He fails to do so.
Thanks... ![[Smile]](smile.gif) I wonder if you may be able to PM me with some details as to how i might get a copy of the paper of the japanese scientists.
If not all the best.
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peter borger
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Member # 722
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posted 12. March 2007 10:30
bottom line is:
The GULO analysis as it has been published is WRONG.
Our new analysis will be published soon. Then I will discuss it here. If you wish.
Kind regards,
Peter
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adhitthana
Member
Member # 2020
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posted 12. March 2007 17:38
quote:
The GULO analysis as it has been published is WRONG.
Our new analysis will be published soon. Then I will discuss it here. If you wish.
Kind regards,
Peter
Sounds good.
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Bruce Fast
Member
Member # 924
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posted 12. March 2007 21:38
Peter, Adhitthana isn't the only one patiently waiting for your publication of GULO. I am dying to get my hands on it.
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adhitthana
Member
Member # 2020
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posted 15. March 2007 17:37
Well this post may be a bit late, but I am wondering if Mesk still posts here. If so i would like to take you up on your offer.
quote:
Mesk:. 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.
Peter quoted the 2003 paper twice saying...
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)
and then
quote:
A comparison of the remaining human exon sequences with the corresponding sequences of the guinea pig nonfunctional GULO gene revealed that the same substitutions from rats to both species occurred at a large number of nucleotide positions .
FROM: Inai Y, Ohta Y, Nishikimi M. Department of Biochemistry, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan.
These quotes seem to indicate that the mutations must be the result of a common mecahnism. I mean one common mutation might be explainable but not many of them, I dont think?
I might be missing something, as I have no training whatsoever in these matters and am probably just the kind of person who could be "dazzled" by something that was incorrect.
Can you help here?
Thanks.
[ 15. March 2007, 17:37: Message edited by: adhitthana ]
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peter borger
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Member # 722
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posted 27. September 2007 07:06
The GULO gene is not the only evidence. I know of many, many examples from the bio-medical and evolutionary literature that proof my argument of non-random mutations. I am currnetly in the process of writing a manucript on the topic, in which I will proof my point without any doubt. Mutations are not only random. The common descnet interpretation of shared mutations in the Darwinian framework requires a second thought.
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