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Author Topic:   molecular genetic proof against random mutation (1)
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 91 of 274 (15103)
08-09-2002 2:29 PM
Reply to: Message 1 by peter borger
07-11-2002 10:27 PM


[QUOTE]Originally posted by peter borger:
[B]Dear Readers
After reading Spetner's book I realised that all it would take to overthrow NDT is molecular genetic evidence against the mechanisms of random mutation, and examples proving the irrelevance of natural selection in the maintenance of the genome. Scientifically speaking, we need only one example that is not in accord with [/QUOTE]
[/B]
Can you say then in Verne Grant's ideas from plants generalized with or without Stebbins, what is the measure of a difference of genetic variation and genetic difference per any genome that can be tested in actual populations? without prejudicing such things as the potential vegatative contribution to polypoloidy factors that even in terms of multiplication of species are often down played ?? The mutation rate is largely irrelevant to this way of framing the question I have remarked as you note yet a simple notion of the environment and future environmental chnages is not adequete in the answer where the internal and external "variable" needs denotation. I do not have the actual assement of this connotation which is the reason I ask a second time. Sincerely, Brad.

This message is a reply to:
 Message 1 by peter borger, posted 07-11-2002 10:27 PM peter borger has replied

Replies to this message:
 Message 93 by peter borger, posted 08-13-2002 2:21 AM Brad McFall has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 92 of 274 (15333)
08-13-2002 1:27 AM
Reply to: Message 90 by mark24
08-09-2002 12:31 PM


dear Mark,
You say:
"Futuyma has clearly set out what random means in the context of RM&NS. Using THAT DEFINITION OF RANDOM, mutations at hotspots ARE random in the sense that the locus for any particular mutation cannot be deterministically predicted, OK? It’s not a difficult concept. So, no, the NDT isn’t expecting you to buy something that is random but not really. IF YOU APPLY THE GIVEN DEFINITION, AND THAT DEFINITION ONLY!!!!!!!!"
For the last time:
Since the mechanism is unknown --and the mechanism is currently not known-- but there are more and more genes that do not change at random, but rather subject to the environment (directed evolution). This falsifies NDT, since the first tenet is randomness independent from the environment. As soon as the mechanism is elucidated we will be able to predict where mutations are introduced. For clarity's sake, imagine the time before the discovery of the genetic code. How was DNA related to protein? Nobody knew, since the mechanism was unknown. Now we know the relationship between DNA and protein since we know the mechanisms involved (including the code, transcription and translation)
For the rest you keep repeating yourself that mutations are random since they cannot be predicted. I simply state that as soon as we know the underlying mechanism, i.e. if we know how the specific proteins integrate/replace nucleotides in the 1G5 gene (and other genes) we will be able to know where they occur and maybe we will also know when these proteins are induced. Maybe in respons to DNA damage, particular environmental factors for which they have receptors, or whatever. I don't know. All I say is that the gene does not change at random with respect to nucleotide substitions.
You seem to be to stuck to Futuyma's definitions. In addition, he does not give me a plausible explanation for mutational hotspots. And he cannot introduce that they are protein/RNA mediated for obvious reasons.
Apparently, you are the only one who is still fighting the non-random mutations in the 1G5 gene. Why?
Peter

This message is a reply to:
 Message 90 by mark24, posted 08-09-2002 12:31 PM mark24 has replied

Replies to this message:
 Message 94 by mark24, posted 08-13-2002 2:43 PM peter borger has replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 93 of 274 (15338)
08-13-2002 2:21 AM
Reply to: Message 91 by Brad McFall
08-09-2002 2:29 PM


dear Brad,
You write:
"Can you say then in Verne Grant's ideas from plants generalized with or without Stebbins, what is the measure of a difference of genetic variation and genetic difference per any genome that can be tested in actual populations? without prejudicing such things as the potential vegatative contribution to polypoloidy factors that even in terms of multiplication of species are often down played ?? The mutation rate is largely irrelevant to this way of framing the question I have remarked as you note yet a simple notion of the environment and future environmental chnages is not adequete in the answer where the internal and external "variable" needs denotation. I do not have the actual assement of this connotation which is the reason I ask a second time. Sincerely, Brad."
Could you please be more clear. (What is Verne Grant's idea and Stebbins?) And, what exactly do you want to know? Thanks,
Peter

This message is a reply to:
 Message 91 by Brad McFall, posted 08-09-2002 2:29 PM Brad McFall has not replied

mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 94 of 274 (15379)
08-13-2002 2:43 PM
Reply to: Message 92 by peter borger
08-13-2002 1:27 AM


quote:
Originally posted by peter borger:
dear Mark,
You say:
"Futuyma has clearly set out what random means in the context of RM&NS. Using THAT DEFINITION OF RANDOM, mutations at hotspots ARE random in the sense that the locus for any particular mutation cannot be deterministically predicted, OK? It’s not a difficult concept. So, no, the NDT isn’t expecting you to buy something that is random but not really. IF YOU APPLY THE GIVEN DEFINITION, AND THAT DEFINITION ONLY!!!!!!!!"
For the last time:
Since the mechanism is unknown --and the mechanism is currently not known-- but there are more and more genes that do not change at random, but rather subject to the environment (directed evolution). This falsifies NDT, since the first tenet is randomness independent from the environment.

Cites please for directed evolution.
Now the first tenet is randomness independent from the environment, I do wish you’d make up your mind!
Directed evolution hasn’t been accepted by the scientific community.
Regardless, under Futuymas meaning of random, even alleged directed evolution is random, because individual mutations cannot be deterministically predicted. You still haven’t falsified random mutation, but attempted a goalpost move to directed evolution.
[QUOTE]Originally posted by peter borger:
[B]
As soon as the mechanism is elucidated we will be able to predict where mutations are introduced. For clarity's sake, imagine the time before the discovery of the genetic code. How was DNA related to protein? Nobody knew, since the mechanism was unknown. Now we know the relationship between DNA and protein since we know the mechanisms involved (including the code, transcription and translation) [/quote]
[/b]
We know the mechanism that causes evaporation & rainfall, yet we still cannot predict when & where it will rain. We know that chiasmata prefer high GC concentrations, yet still cannot deterministically predict where the next chiasmata will occur.
I’m very sorry, Peter, but you will NEVER be able to deterministically predict where a given mutation will occur. Take any sequence you like, there are both (statistically) random & non-random loci. Assume you understand everything that is possible to know about mutations.
Q/ At what loci will the next substitution occur?
You have no idea, mate. The best you can do is make a prediction based on stochastically derived probability, this is not the same as a deterministic prediction.
It is random.
Think about it, every loci in a sequence has a probability of mutation. Therefore, regardless of your degree of knowledge on the subject, you cannot make a deterministic prediction about the next mutation.
[QUOTE]Originally posted by peter borger:
[B]
For the rest you keep repeating yourself that mutations are random since they cannot be predicted. I simply state that as soon as we know the underlying mechanism, i.e. if we know how the specific proteins integrate/replace nucleotides in the 1G5 gene (and other genes) we will be able to know where they occur and maybe we will also know when these proteins are induced. [/quote]
[/b]
See above, re. Random mutation & your hope that you will be able to predict mutations.
quote:
Originally posted by peter borger:

Maybe in respons to DNA damage, particular environmental factors for which they have receptors, or whatever. I don't know. All I say is that the gene does not change at random with respect to nucleotide substitions.

Yes they do!!!!!!!!!! Good grief, man. What have I been labouring this past week?
Nucleotide substitutions are random in the intended evolutionary meaning of random. See Futuyma’s meaning in my previous post.
That you don’t like Futuymas definition is tough.
It’s like having a conversation about transport, where I define transport as anything that moves people about. You then say that you have falsified my contention that slaves were transported across the Atlantic, because YOUR definition of transport is the motor car. And they don’t float.
quote:
Originally posted by peter borger:

You seem to be to stuck to Futuyma's definitions.

Because Futuyma is taking the time to describe the meaning of random as it pertains to evolution. That is the intended meaning, & I will stick to it.
I’m sure you will stick to the statistical defintion of random, despite it NOT being the intended meaning.
quote:
Originally posted by peter borger:

In addition, he does not give me a plausible explanation for mutational hotspots.

Neither have you provided me with one.
Nor would you expect him to in a passage where he describes the word random. It is enough that he points out that a mutation is random if it cannot be deterministically predicted, only probabilistically predicted.
In summary (again), you have tried to falsify the NDT by claiming a definition of random that was never intended to pertain to evolution. In doing so you have created a strawman.
Even if you could show that Futuymas definition is wrong, it would merely force a redefinition. If all loci are subject to the probability of mutation, & such changes are heritable, & therefore subject to genetic drift & natural selection, what really changes?
Adaptive evolution is caused by random mutation culled by natural selection.
Becomes..
Adaptive evolution is caused by all loci being subject to the probability of mutation, that mutation being culled by natural selection.
So what? It’s hardly falsified, is it?
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 92 by peter borger, posted 08-13-2002 1:27 AM peter borger has replied

Replies to this message:
 Message 95 by peter borger, posted 08-14-2002 1:02 AM mark24 has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 95 of 274 (15407)
08-14-2002 1:02 AM
Reply to: Message 94 by mark24
08-13-2002 2:43 PM


dear mark,
You state:
"Think about it, every loci in a sequence has a probability of mutation. Therefore, regardless of your degree of knowledge on the subject, you cannot make a deterministic prediction about the next mutation."
First of all, I did not DENY that there are random mutations (see previous mails, this is inevitable since all DNA is subject to oxydative stress and it will lead to degenaration of the genome). Bit, in addition, there are also NON-RANDOM protein and/or RNA directed mutations. Since they are mediated by some molecule encoded in the DNA, the information is present already. If this all evolved naturalisticly, then I expect an explanation from you how you see this. (one that goes beyond: "organism evolving this mechanism have a better chance to survive in a changing environment", since I am able to invent such non-contributing stories myself).
Presently there is no reason to NOT assume that eventually we will be able to predict where they will be introduced. Similarly, it is thought that antibody improvement is also random. But, since a protein-mediated mechanism is involved I really doubt that. What we observe as random may as well be non-random. (why do I have to repeat myself again and again?)
And you state:
"See above, re. Random mutation & your hope that you will be able to predict mutations.
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
Maybe in respons to DNA damage, particular environmental factors for which they have receptors, or whatever. I don't know. All I say is that the gene does not change at random with respect to nucleotide substitions.
--------------------------------------------------------------------------------
Yes they do!!!!!!!!!! Good grief, man. What have I been labouring this past week?
I say:
You've been trying to tell me that mutations are random. I do not (entirely) agree to your opinion, since I demonstrated that some genes change non-randomly and that falsifies NDT. I recommended you to carefully study the 1G5 gene but --I have the feeling-- that you simply don't do that (it is the first figure in the first mailing in the thread: "molecular genetic proof against random mutations". Read what Percy has to say on it, and see all my responses).
If you had, you wouldn't bring forward the same questions/arguments over and over and over. Luckily, I am very patient.
Furthermore:
"That you don’t like Futuymas definition is tough.
It’s like having a conversation about transport, where I define transport as anything that moves people about. You then say that you have falsified my contention that slaves were transported across the Atlantic, because YOUR definition of transport is the motor car. And they don’t float.
I say:
Where do you find all these inappropriate analogies? I really like them. I am not going to discuss definitions (it's a debating trick). All I did was falsify NDT in its current state.
Furthermore:
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
You seem to be to stuck to Futuyma's definitions.
--------------------------------------------------------------------------------
Because Futuyma is taking the time to describe the meaning of random as it pertains to evolution. That is the intended meaning, & I will stick to it.
I’m sure you will stick to the statistical defintion of random, despite it NOT being the intended meaning."
I say:
"Listen, Mark, maybe NDT's definitions need to be updated. Maybe Futuyma has to explain how he thinks about the mechanism behind hotspots and non-random mutations. That would clear things up. (It is not my fault that NDT is in trouble)".
In response to my qoute:
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
In addition, he does not give me a plausible explanation for mutational hotspots.
--------------------------------------------------------------------------------
You say:
"Neither have you provided me with one."
I say:
Here you demonstrate that you don't listen beyond your own paradigm.
And you state:
"Adaptive evolution is caused by random mutation culled by natural selection.
Becomes..
Adaptive evolution is caused by all loci being subject to the probability of mutation, that mutation being culled by natural selection.
So what? It’s hardly falsified, is it?"
I say:
HARDLY isn't synonymous to NOT.
(Thanks for admitting NDT has been falsified).
Best wishes,
peter

This message is a reply to:
 Message 94 by mark24, posted 08-13-2002 2:43 PM mark24 has not replied

Replies to this message:
 Message 96 by derwood, posted 08-16-2002 1:17 PM peter borger has replied

derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 96 of 274 (15534)
08-16-2002 1:17 PM
Reply to: Message 95 by peter borger
08-14-2002 1:02 AM


I notice peter B. has yet to provide any citations for 'directed evolution' or 'directed mutations.'
I, on the other, can provide evidence to the contrary:
"The flurry of studies ultimately revealed that Cairns's original proposal was untenable, and the community, including Cairns, now at the Radcliffe Infirmary in Oxford, United Kingdom, discarded it." 2002. Science.
: **********************************
: EMBO J 1997 Jun 2;16(11):3303-11
: Genome-wide hypermutation in a subpopulation of stationary-phase cells underlies recombination-dependent adaptive mutation.
: Torkelson J, Harris RS, Lombardo MJ, Nagendran J, Thulin C, Rosenberg SM
: Stationary-phase mutation in microbes can produce selected ('adaptive') mutants preferentially. In one system, this occurs via a distinct, recombination-dependent mechanism. Two points of controversy have surrounded these adaptive reversions of an Escherichia coli lac mutation. First, are the mutations directed preferentially to the selected gene in a Lamarckian manner?
: Second, is the adaptive mutation mechanism specific to the F plasmid replicon carrying lac? We report that lac adaptive mutations are associated with hypermutation in unselected genes, in all replicons in the cell. The associated mutations have a similar sequence spectrum to the adaptive reversions. Thus, the adaptive mutagenesis mechanism is not directed to the lac genes, in a Lamarckian manner,nor to the F' replicon carrying lac. Hypermutation was not found in non-revertants exposed to selection. Therefore, the genome-wide hypermutation underlying adaptive mutation occurs in a differentiated subpopulation. The existence of mutable subpopulations in non-growing cells is important in bacterial evolution and could be relevant to the somatic mutations that give rise to cancers in multicellular organisms.
: ******************************
: "Researchers first noticed this happening in 1988 when John Cairns, then at Harvard University, showed that mutation rates in the bacterium Escherichia coli increased when the microbes needed to evolve new capabilities in order to survive changes in their environment.
: At the time, it seemed that only those genes directly involved with the adaptation changed,and this idea of adapative or directed evolution caused quite a stir.
: But then last year, molecular geneticist Susan Rosenberg at Baylor College of Medicine in Houston and her colleagues showed that mutation rates increase throughout the genome, although only in a subset of the population. Another group also found that more than just the relevant genes changed." (How the Genome Readies Itself for Evolution, Elizabeth Pennisi, Science, vol 281,
: Number 5380, Issue of 21 Aug 1998, p1131-1134)
: *******************************
: Imagine that.
:
: *******************************
: Mutat Res 1999 Jul;437(1):51-60
: Mismatch repair is diminished during stationary-phase mutation.
: Harris RS, Feng G, Ross KJ, Sidhu R, Thulin C, Longerich S, Szigety SK, Hastings PJ, Winkler ME,Rosenberg SM.
: Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.
: This paper is an invited Response to a recent Commentary [P.L. Foster, Rev. Mut. Res. 436 (1999) 179-184] entitled "Are adaptive mutations due to a decline in mismatch repair? The evidence is lacking". The Commentary argues that no evidence exists supporting the idea that mismatch repair is limiting specifically during stationary-phase mutation. A primary concern of the author is to question the method that we used previously to measure growth-dependent mutation. In this method, mutation rates are calculated using counts of mutant colonies taken at times when those colonies arise, rather than at a predetermined, fixed time. Here we show further data that illustrate why this must be done to ensure accurate mutation measurements. Such accuracy was necessary for our published determination that mismatch repair proteins are not limiting during growth-dependent mutation, but become so during stationary-phase mutation. We review the evidence supporting the idea that stationary-phase reversion of a lac frameshift mutation occurs in an environment of decreased mismatch repair capacity. Those data are substantial. The data presented in the Commentary, in apparent contradiction to this idea, do not justify the conclusion presented there. Copyright 1999 Elsevier Science B.V.
: **********************
: Ann N Y Acad Sci 1999 May 18;870:275-89
: Mechanisms of genome-wide hypermutation in stationary phase.
: Lombardo MJ, Torkelson J, Bull HJ, McKenzie GJ, Rosenberg SM.
: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
: Stationary-phase mutation (a subset of which was previously called adaptive mutation) occurs in apparently nondividing, stationary-phase cells exposed to a nonlethal genetic selection. In one experimental system, stationary-phase reversion of an Escherichia coli F'-borne lac frameshift mutation occurs by a novel molecular mechanism that requires homologous recombination functions of the RecBCD system. Chromosomal mutations at multiple loci are detected more frequently in Lac+ stationary-phase revertants than in cells that were also exposed to selection but did not become Lac+. Thus, mutating cells represent a subpopulation that experiences hypermutation throughout the genome. This paper summarizes current knowledge regarding stationary-phase mutation in the lac system. Hypotheses for the mechanism of chromosomal hypermutation are discussed, and data are presented that exclude one hypothetical mechanism in which chromosomal mutations result from Hfr formation.
: ***************************
: Science 1998 Nov 6;282(5391):1133-5
: Evidence that gene amplification underlies adaptive mutability of the bacterial lac operon.
: Andersson DI, Slechta ES, Roth JR.
: Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.
: Adaptive mutability is the apparent alteration in specificity or rate of mutability seen in bacteria during stress. A model is proposed by which gene amplification during selective growth can give the appearance of adaptive mutability without requiring any change in mutability. The model is based on two assumptions, that a mutant lac locus with residual function allows growth if its copy number is increased, and that true reversion events are made more likely by replication of chromosomes with many copies of the locus. Apparent directed mutability, its recombination requirement, and its apparent independence of cell growth are all accounted for by the model. Evidence is provided for the required residual function and gene amplification.
: ***********************************
: Mutat Res 2001 Jan 25;473(1):109-19
: Effect of endogenous carotenoids on "adaptive" mutation in Escherichia coli FC40.
: Bridges BA, Foster PL, Timms AR.
: MRC Cell Mutation Unit, University of Sussex, Falmer, BN1 9RR, Brighton, UK. b.a.bridges@sussex.ac.uk
: The appearance over many days of Lac(+) frameshift mutations in Escherichia coli strain FC40 incubated on lactose selection plates is a classic example of apparent "adaptive" mutation in an episomal gene. We show that endogenously overproduced carotenoids reduce adaptive mutation under selective conditions by a factor of around two. Carotenoids are known to scavenge singlet oxygen suggesting that the accumulation of oxidative base damage may be an integral part of the adaptive mutation phenomenon. If so, the lesion cannot be 7,8-dihydro-8-oxoguanine since adaptive mutation in FC40 is unaffected by mutM and mutY mutations. If active oxygen species such as singlet oxygen are involved in adaptive mutation then they should also induce frameshift mutations in FC40 under non-selective conditions. We show that such mutations can be induced under non-selective conditions by protoporphyrin photosensitisation and that this photodynamic induction is reduced by a factor of just over two when endogenous carotenoids are present. We argue that the involvement of oxidative damage would in no way be inconsistent with current understanding of the mechanism of adaptive mutation and the role of DNA polymerases. ****************************************
I think I just falsified Peter's falsification....

This message is a reply to:
 Message 95 by peter borger, posted 08-14-2002 1:02 AM peter borger has replied

Replies to this message:
 Message 97 by peter borger, posted 08-22-2002 4:15 AM derwood has replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 97 of 274 (15896)
08-22-2002 4:15 AM
Reply to: Message 96 by derwood
08-16-2002 1:17 PM


Dear SLPx,
Thanks for the references.
They clearly demonstrate that the mutations are protein mediated. It remains to be established in what degree the environment directs the induction of these genes. But, as demonstrated by some of your references rec-enzymes are induced, so it does not falsify my assertions but rather provides further evidence for NON-RANDOM, protein directed mutations (in response to environmental change). Thanks, for the examples.
Maybe you could point out where ecactly these abtracts falsify NONRANDOM mechanisms. For instance, "genome wide" does not mean that it is random, rather that mutations can be found in several genes throughout the genome.
You really have to come up with better examples to claim falsification over mine (show me the sequences of a mutated gene in several subspecies of the organism after stationary phase).
Cheers,
Peter

This message is a reply to:
 Message 96 by derwood, posted 08-16-2002 1:17 PM derwood has replied

Replies to this message:
 Message 98 by derwood, posted 08-22-2002 12:59 PM peter borger has replied

derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 98 of 274 (15930)
08-22-2002 12:59 PM
Reply to: Message 97 by peter borger
08-22-2002 4:15 AM


quote:
Originally posted by peter borger:
Dear SLPx,
Thanks for the references.
They clearly demonstrate that the mutations are protein mediated. It remains to be established in what degree the environment directs the induction of these genes. But, as demonstrated by some of your references rec-enzymes are induced, so it does not falsify my assertions but rather provides further evidence for NON-RANDOM, protein directed mutations (in response to environmental change). Thanks, for the examples.
Maybe you could point out where ecactly these abtracts falsify NONRANDOM mechanisms. For instance, "genome wide" does not mean that it is random, rather that mutations can be found in several genes throughout the genome.
I don't know whethyer I admire or am disgusted by this common quality in creatinists - taking something that is clearly evidence against their position and claiming that, in reality, it supports it. Strange...
quote:
You really have to come up with better examples to claim falsification over mine (show me the sequences of a mutated gene in several subspecies of the organism after stationary phase).
Cheers,
Peter
Interesting - I have yet to see ANY 'falsifications' of anything form you. Wild extrapolations are not really evidence of anything.
Better yet, since it is your claim that 'non-random mutations' exist and falsify NDT, and that this 'information' is pre-existing in the genome, maybe you can present some genetic analyses that demonstrate that some gene that is needed for survival but is not active exists in multicellular eukaryotes (provide the sequence of the genome), expose this multicellular eukaryote to some stressor, then demonstrate that the gene needed - and only the gene needed (i.e., not genome wide) is activated via a specific mutation.
Syrely you can do this, since you claim to have falsified NDT.
Your simplistic defintion of 'random' seems awfully out of place.

This message is a reply to:
 Message 97 by peter borger, posted 08-22-2002 4:15 AM peter borger has replied

Replies to this message:
 Message 99 by wj, posted 08-22-2002 5:50 PM derwood has replied
 Message 102 by peter borger, posted 08-22-2002 9:46 PM derwood has replied

wj
Inactive Member


Message 99 of 274 (15944)
08-22-2002 5:50 PM
Reply to: Message 98 by derwood
08-22-2002 12:59 PM


[QUOTE]Originally posted by SLPx:
Better yet, since it is your claim that 'non-random mutations' exist and falsify NDT, and that this 'information' is pre-existing in the genome, maybe you can present some genetic analyses that demonstrate that some gene that is needed for survival but is not active exists in multicellular eukaryotes (provide the sequence of the genome), expose this multicellular eukaryote to some stressor, then demonstrate that the gene needed - and only the gene needed (i.e., not genome wide) is activated via a specific mutation.
Syrely you can do this, since you claim to have falsified NDT.
Your simplistic defintion of 'random' seems awfully out of place.
[/B][/QUOTE]
Wouldn't the GLO pseudogene be a prime candidate for such a demonstration? There is strong evidence that it would be a fully functional gene with a few correcting mutations. Individuals can be stressed by removing dietary sources of vitamin C.
Where is the evidence that such protein directed mutations have occurred? Are these only mutations within somatic cells or do they also occur in gamete cells?
BTW, where is the evidence that members of nomadic tribes have functional GLO genes?

This message is a reply to:
 Message 98 by derwood, posted 08-22-2002 12:59 PM derwood has replied

Replies to this message:
 Message 100 by derwood, posted 08-22-2002 8:30 PM wj has not replied

derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 100 of 274 (15950)
08-22-2002 8:30 PM
Reply to: Message 99 by wj
08-22-2002 5:50 PM


[QUOTE]Originally posted by wj:
[B][QUOTE]Originally posted by SLPx:
Better yet, since it is your claim that 'non-random mutations' exist and falsify NDT, and that this 'information' is pre-existing in the genome, maybe you can present some genetic analyses that demonstrate that some gene that is needed for survival but is not active exists in multicellular eukaryotes (provide the sequence of the genome), expose this multicellular eukaryote to some stressor, then demonstrate that the gene needed - and only the gene needed (i.e., not genome wide) is activated via a specific mutation.
Syrely you can do this, since you claim to have falsified NDT.
Your simplistic defintion of 'random' seems awfully out of place.
[/B][/QUOTE]
Wouldn't the GLO pseudogene be a prime candidate for such a demonstration? There is strong evidence that it would be a fully functional gene with a few correcting mutations. Individuals can be stressed by removing dietary sources of vitamin C.
Where is the evidence that such protein directed mutations have occurred? Are these only mutations within somatic cells or do they also occur in gamete cells?
BTW, where is the evidence that members of nomadic tribes have functional GLO genes?[/B][/QUOTE]
Good questions. I didn't follow the GLO opus, but it would seem that since we have the 'original' sequence, it would be easy enough to test the 'directed mutation' hypothesis.

This message is a reply to:
 Message 99 by wj, posted 08-22-2002 5:50 PM wj has not replied

Replies to this message:
 Message 101 by peter borger, posted 08-22-2002 9:29 PM derwood has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 101 of 274 (15957)
08-22-2002 9:29 PM
Reply to: Message 100 by derwood
08-22-2002 8:30 PM


dear SLPx,
I did not claim that nomads still have a functional GLO. Read what I had to say on the topic below:
"In the evolutionary community the shared retroviruses are commonly regarded as evidence of common descent. However, this may only be superficial.
First there is the claim that they do not serve any purpose. That should be scientifically proven. Maybe their function cannot be deduced from knocking them out, but that does not say anything about their function, since you can knock out genes with an open reading frame without any effect on the organism (genetic redundancies). Secondly, I would like to see the complete DNA sequences within the species and between the species before jumping to conclusions.
I checked one claim about the GLO gene (the gene that catalyses the final step in vitamin c synthesis) that has been inactivated in the same spot in primates and is taken as proof for common ancestry. And, indeed a superficial look would immediately convince any evolutionist. However, if you have a careful look at the sequence you will discover that the replacement of nucleotides is not at random between the distinct species. Secondly, you will discover that it does not make a difference for the mutation rate of this gene whether it is functional or not, in contrast to what evolution theory would predict. Thirdly, it violated population genetics: why would the inactivated gene become fixed in the entire population, while the active gene conveys longivity. In addition, evolution never compensated for vitamin C uptake in the gut, and, finally, the gene is redundant anyway since the third step in vit c synthesis already yields vitamin C by spontenaous oxidation. Also not unimportant, at least 2 primates are able to synthesise vitamin c in the liver, indicating the presence of an intact GLO gene (I once had a discussion about this gene with Dr D. Theobald (Talk Origin) so I know a bit about pseudogenes. However, at this level it is mostly speculation since we do not know a lot about it, yet).
In analogy to vestiges (appendix, tonsils) that shouldn't have a function according to evolution theory, it is far too early to say that this is proof for common descent. Show me the DNA sequences of these retroviruses in chimp and man, and I will respond in more detail.
Retrotransposons may have a function in epigenic regulation of gene expression (actually there is some proof for that. See: Dr. E. Max's website Talk Origin. Another one regulates the aghouti colour of fur in mice). It is thought that they may also play a role in eye colour (human), and some diseases like schizophrenia, and B.-W.-syndrome.
Evolutionists are free to claim these genes as evidence for common descent (as they did -- and still do -- for genetic redundancies, but which has actually contributed to the fall of natural selection). I foresee that ultimately there will be an unforeseen solution to these "vestiges".
So what I claimed was:
"the third step in vit c synthesis already yields vitamin C by spontenaous oxidation." The amounts are sufficient to prevent scurvy!
Therefore the GLO gene --which does the fourth and final step in vit C synthesis-- is redundant!!!!!
Reference: http//yarchive.net/med/vitamin_c.html
Best Wishes,
Peter
[This message has been edited by peter borger, 08-22-2002]

This message is a reply to:
 Message 100 by derwood, posted 08-22-2002 8:30 PM derwood has not replied

Replies to this message:
 Message 104 by Dr_Tazimus_maximus, posted 08-22-2002 10:37 PM peter borger has replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 102 of 274 (15958)
08-22-2002 9:46 PM
Reply to: Message 98 by derwood
08-22-2002 12:59 PM


Dear SLPx,
In response to pointing out the scientific evidence for me you reply:
"I don't know whethyer I admire or am disgusted by this common quality in creatinists - taking something that is clearly evidence against their position and claiming that, in reality, it supports it. Strange..."
There can only be two reasons for not responding to my question:
1) You do not know the content of your refernces,
2) You do not understand the content of your references.
If this is the case, do not hesitate to ask.
Best wishes,
Peter

This message is a reply to:
 Message 98 by derwood, posted 08-22-2002 12:59 PM derwood has replied

Replies to this message:
 Message 103 by Dr_Tazimus_maximus, posted 08-22-2002 10:31 PM peter borger has not replied
 Message 106 by derwood, posted 08-23-2002 8:45 AM peter borger has not replied

Dr_Tazimus_maximus
Member (Idle past 3216 days)
Posts: 402
From: Gaithersburg, MD, USA
Joined: 03-19-2002


Message 103 of 274 (15967)
08-22-2002 10:31 PM
Reply to: Message 102 by peter borger
08-22-2002 9:46 PM


[QUOTE]Originally posted by peter borger:
There can only be two reasons for not responding to my question:
1) You do not know the content of your refernces,
2) You do not understand the content of your references.
If this is the case, do not hesitate to ask.
[/B][/QUOTE]
Peter, I have to say that after reading a number of your posts and the associated references that I think that you are the person who either does not know the content or meaning of your own references. While I have not had the chance to get the references that SLPx was citing the abstracts appear to support his position far more than yours. And this would not be the first time that your statements were in direct opposition to the references that you cite, ie Ascorbic acid in a debate on the ID section of this board.
EvC Forum: evidence that intelligent design can't explain
------------------
"Chance favors the prepared mind." L. Pasteur
Taz

This message is a reply to:
 Message 102 by peter borger, posted 08-22-2002 9:46 PM peter borger has not replied

Dr_Tazimus_maximus
Member (Idle past 3216 days)
Posts: 402
From: Gaithersburg, MD, USA
Joined: 03-19-2002


Message 104 of 274 (15969)
08-22-2002 10:37 PM
Reply to: Message 101 by peter borger
08-22-2002 9:29 PM


quote:
Originally posted by peter borger:
So what I claimed was:
"the third step in vit c synthesis already yields vitamin C by spontenaous oxidation." The amounts are sufficient to prevent scurvy!
Therefore the GLO gene --which does the fourth and final step in vit C synthesis-- is redundant!!!!!
Reference: http//yarchive.net/med/vitamin_c.html
Best Wishes,
Peter
Peter, I missed this one in a reply to you other post but it is germane to my post. This is WRONG!. Please see my referenced post for the correct sequence for the synthesis for ascorbic acid. While the final step is spontaneous GLO is required for the step prior to the spontaneous one. In other words, the gene is not redundent. If you do not believe me please see the synthetic pathway that I provided for you.
Opps, sorry I just noticed that the original synthetic pathway was missing. Here is a different copy
The Natural History of Ascorbic Acid in the Evolution of the Mammals
I will try to find the other one as it was far more complete from a biochemical point of view. However, please note that step 4 is GLO, while the sponteous step occurs farther down the biosynthetic pathway only AFTER GLO performs it required function. So you are still wrong
------------------
"Chance favors the prepared mind." L. Pasteur
Taz
[This message has been edited by Dr_Tazimus_maximus, 08-22-2002]
[This message has been edited by Dr_Tazimus_maximus, 08-22-2002]

This message is a reply to:
 Message 101 by peter borger, posted 08-22-2002 9:29 PM peter borger has replied

Replies to this message:
 Message 105 by peter borger, posted 08-23-2002 1:16 AM Dr_Tazimus_maximus has replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 105 of 274 (15977)
08-23-2002 1:16 AM
Reply to: Message 104 by Dr_Tazimus_maximus
08-22-2002 10:37 PM


dear Tazimus,
Thanks for your mail. I will check it out.
However, --according to my information-- cessation of biosynthesis in humans can result from two different gene defects. Firstly, through inactivation of the GLO gene that specifies an enzyme that converts the final step that involves an enzyme (step 4 in your reference). Secondly, trough a defect in the lactonase gene, that specifies a gene that converts the 3rd step in your reference.
The lactonase defect prevents any vitamin C synthesis at all, while the defect in the GLO gene still yields measurable amounts of vit C, because the substrate will spontaneously decompose to 2-keto-gulono-gamma-lactone in the presence of oxygen (this step in normally carried out by GLO gene product). The final step is a spontaneaous conversion to vit C (Thus, there are two spontaneous steps in the presence of oxygen). So, the only difference --if you don't express the GLO gene-- is speed of production. If one has an active lactonase gene spontaneous Vit C productions are around 15-20 mg/day. Sufficient levels to prevent scurvy.
Best wishes,
Peter

This message is a reply to:
 Message 104 by Dr_Tazimus_maximus, posted 08-22-2002 10:37 PM Dr_Tazimus_maximus has replied

Replies to this message:
 Message 107 by Dr_Tazimus_maximus, posted 08-23-2002 9:13 AM peter borger has replied

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