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Author | Topic: molecular genetic proof against random mutation (1) | |||||||||||||||||||||||
Dr_Tazimus_maximus Member (Idle past 3245 days) Posts: 402 From: Gaithersburg, MD, USA Joined: |
quote: I would be interested in seeing any references concerning scurvy and its causes that implicate a gene product other than GLO. As to your other statements, I need to look at the paper again. There is one strain of rats which also has a GLO mutation (a group of Wistar rats if I remember correctly) which makes the homozygotes susceptable to scurvy. I will try to find that paper as well. ------------------"Chance favors the prepared mind." L. Pasteur Taz
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
Dear taz,
I will keep you informed. Peter
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
Dear SLPx,
I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations. One of the guys in field of hypermutations says in the article that you refer to says: "Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal."" If I understand his last sentence properly, he says: "All regions are not equal" In my opinion not equal means that a mechanism (=non-random) is involved, isn't it? If you have an different opinion, please explain how I have to understand this according to your insights. best wishes,Peter
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Philip Member (Idle past 4751 days) Posts: 656 From: Albertville, AL, USA Joined: |
Peter and Dr. Taz,
Thank you for your thoughtful replies. Time constrains adequate counter refutations on the deterministic, vs. random vs deterministic/random nature of mutations. Dr. Taz, you did bring up "simplicity" vs. my "black and white" (Aristotle?) summations. And the fact that my broadness could be expounded upon ad-nauseum. I won't get lost in the similes but still maintain, even by your Webster's use of the word deterministic (pre-destined, etc.), that we both know that the term implies genetic constraints on randomness. I answer that genetic constraints (at mutation spots) themselves imply (empirically, in a black and white manner so to speak) that such constrained randomness, controlled accidents (if you will), non-random intervention via genes and their protein and other DNA factors (as Peter cited) ... suggest APRIORI deterministic phenomena. (Forgive my non-elequent bluntness as I'm very spent) Philip
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
dear Taz,
You say:"One aside concerning the possibility (completely unshown to date) of humans who make their own ascorbic acid. There is a paper that points out, rightly, that there could be undiscovered pathways dealing with the secondary metabolic fluxes L-ascorbic acid biosynthesis - PubMed While the data does not support your earlier assertions..." My comments:Actually, it would support my assumptions, since it would also favour my opinion of redundancy of the GLO gene. "...that does not mean that they are impossible, it just means that there is no data in support of them yet. However, for this one instance, the existence of a shared secondary pathway would not indicate that descent with modification was not supported. Unless a completely different metabolic system appeared in some humans that had no analog or possible original use in either other populations of humans or primates. The appearence of such a pathway in a geologically young species (important point here Tranquility) with no indication of a precursor or analogous pathway could be interpreted as a creation event. The shared GLO pseudogene with one mutation stopping the production of the gene product along with the RANDOM mutation demonstrated by the available evidence indicates common descent." My comments:"That remains to be seen. Time will tell" best wishes,Peter
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
Dear SLPx,
I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations. First of all, the article states that "Cairn's ORIGINAL proposal was untenable". This is of course something different than that he had to reject his proposal. It means that he has to adapt the original proposal. Secondly, one of the guys in field of hypermutations says: "Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal."" If I understand his last sentence properly, he says: "All regions are not equal" In my opinion not equal means that a mechanism (=non-random) is involved, isn't it? If you have an different opinion, please explain how I have to understand this according to your insights. Furthermore, Rosenberg says that "[adaptive mutations] provides the molecular basis for a potential path for the rapid evolution of new traits". This clearly indicates that all necessities for 'evolution' (=variation induction) are present in the genome and may be activated in response to the environment. If so, NDT RIP. In conclusion, I do not see how this article supports your vision. Could you please explain? best wishes,Peter
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Underling Inactive Member |
quote: The main problem I have with your conclusion is that it's demonstrably false. A friend of mine who happens to be a genetic engineer worked for a time with a team that subjected Drosophila to extreme artificial selection (artificial only in that it was regulated in a lab, but still following the basic principles of natural selection). After many dozens of generations, the genetic variance in the resultant population was significant enough to not only taxonomically classify the new population as a different species, but a different genus as well. Both reproductive behavior and morphology were markedly different from the parent population. Thus Drosophila can indeed evolve. As to why a particular gene has remained stable in two species of Drosophila, the obvious answer would be that the gene is selected for in both species, and mutations to that gene are maladaptive. Derek [This message has been edited by Underling, 09-16-2002]
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derwood Member (Idle past 1904 days) Posts: 1457 Joined: |
quote: You mean the ones that you had already claimed in fact support your version of non-random mutations? You hadn't even read them yet, but were claiming them as support for your position? I'm shocked!quote: If by mnechanism you mean some guiding force, I say LOL! If by mechanism (ahh - I love the sound of a semantics game coming!) you mean a tendency to do one thing over another, than of course., However, as has explained to you repeatedly on this board, there are simple physicochemical reasons for mutations occurring in some areas over others. Water tends to collect in low areas rather than high ones. Are you going to suggest that some Ubermensch plays a role in that, too?
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
dear Derek,
you say:"The main problem I have with your conclusion is that it's demonstrably false. I say:Please expand. What, according to you, is my conclusion and what is false? You say:A friend of mine who happens to be a genetic engineer worked for a time with a team that subjected Drosophila to extreme artificial selection (artificial only in that it was regulated in a lab, but still following the basic principles of natural selection). After many dozens of generations, the genetic variance in the resultant population was significant enough to not only taxonomically classify the new population as a different species, but a different genus as well. Both reproductive behavior and morphology were markedly different from the parent population. Thus Drosophila can indeed evolve. I say:"Where do I dispute that Drosophila are able to change (evolve)? What I dispute is that it is due to a random mechanism. How long did it take for the Drosophila in your friends lab to change? And more importantly, was a symbiontic microorganism involved or not? I know these kind of experiments and often it involves a microorganism." You say:"As to why a particular gene has remained stable in two species of Drosophila, the obvious answer would be that the gene is selected for in both species, and mutations to that gene are maladaptive." I say:"Read something on neutral evolution (NT). You will find out that according to NT genetic change is expected on third positions in AA codons (due to redundancy in the genetic code). They are not present for the major part of protein coding genes. I think that's a bit peculiar in the light that it took these organsims millions of years to evolve." best wishesPeter
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
Dear SLPx,
You write: -------------------------------------------------------------------------------- quote:-------------------------------------------------------------------------------- Originally posted by peter borger: Dear SLPx, I had a bit of time to spare so I read a couple of articles you refered to in an attempt to disprove non-random mutations. -------------------------------------------------------------------------------- You mean the ones that you had already claimed in fact support your version of non-random mutations? You hadn't even read them yet, but were claiming them as support for your position? I'm shocked! quote:-------------------------------------------------------------------------------- One of the guys in field of hypermutations says in the article that you refer to says: "Over the past decade, researchers have been dissecting the molecular underpinnings of these so-called adaptive mutations. And within the last 2 years, they have made impressive strides. They have found, for example, that although these mutations are not directed to particular genes, as Cairns originally suggested, they don't uniformly pepper the bacterial genome either. "There are hot and cold regions for hypermutation," says Rosenberg, who is now working on defining these regions. "All regions are not equal."" If I understand his last sentence properly, he says: "All regions are not equal" In my opinion not equal means that a mechanism (=non-random) is involved, isn't it? -------------------------------------------------------------------------------- If by mnechanism you mean some guiding force, I say LOL! I say:The driving force could be the environment that induces certain proteins (e.g. polymerases) that carry out the mutations. You say:If by mechanism (ahh - I love the sound of a semantics game coming!) you mean a tendency to do one thing over another, than of course., However, as has explained to you repeatedly on this board, there are simple physicochemical reasons for mutations occurring in some areas over others. I say:"Molecular mechanism in biology usually involve proteins and/or RNA molecules. If so, all necessities are present in the genome" You say:Water tends to collect in low areas rather than high ones. Are you going to suggest that some Ubermensch plays a role in that, too? I say:You use similar faulty analogies as Mark24. You cannot compare gravity and protein mediated mechanism. I know you have to use such analogies, since you need naturalistic explanations for NDT. However, if all things are in the genome to respond to environmental change, a naturalistic explanations is untenable." best wishesPeter
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peter borger Member (Idle past 7694 days) Posts: 965 From: australia Joined: |
dear Taz,
I am still contemplating your response. I have some additional remarks/comments. You say that vit c is stored in the liver. As a oxygen radical scavenger I wondered whether the reduced form of vit c can be stored that long. In general, if oxygen is present it is expected that vit c is oxydized. So, storage of vit c in the liver should be under anaerobic conditions, or in the presence of strong reducing agents. Isn't it?Furthermore, I got my email back from Dr Banschbach --undeliverable, wrong address-- so I will try to find it out another way. Best wishes,peter
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derwood Member (Idle past 1904 days) Posts: 1457 Joined: |
quote: Guess I hit that nail on the head, eh "Peter"?quote: And how does your 'conclusion' of non-random mutation falsifying NDT follow from that? In your selective readings of the papers I cited, di dyou not notice that the mutations were not centered - directed - specifically to the genes 'needed'?Or did that slip by your razor-keen scientific insight? quote: LOL! Yeah, I guess those "kinds" must have been jammy-packed with all sorts of genes that they didn't need and that are, dammit, no longer present in their in-kind descendants...quote: My "analogy" was not to NDT, rather it was to demonstrate that there are perfectly natural reasons for apparently 'specified' outcomes. As is so often the case, the creationist eads too much into posts and tries to make much of their shallow comprehensive skills.I am still waiting for your unequivocal evidence that these unused but maybe someday necessary genes are in the genomes of all creatures, just waiting for that one lucky mutation - in the right conditions, of course - to be turned on. Your silly (and typically overconfident) position simply supports something I have believed for some time now - evolutionists base their thoughts on what is known, creaetionists base theirs on what is not.
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derwood Member (Idle past 1904 days) Posts: 1457 Joined: |
[QUOTE]Originally posted by peter borger:
I say:"Read something on neutral evolution (NT). You will find out that according to NT genetic change is expected on third positions in AA codons (due to redundancy in the genetic code). They are not present for the major part of protein coding genes. I think that's a bit peculiar in the light that it took these organsims millions of years to evolve." best wishesPeter[/B][/QUOTE] Hi Peter, I was hoping that you could point out where in Kimura's works he explains that genetic change is expected on third positions in AA codons. I think what the creationist is doing is engaging in a classic cart-before-the-horse misrepresentation here. But, please, Peter, prove me wrong. I possess a collection of Kimura's works, and I am fairly certain that I will have the paper(s) you cite.
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derwood Member (Idle past 1904 days) Posts: 1457 Joined: |
quote: I was wondering - did/do any of these papers deal with multicellular eukaryotes?quote: I already have a couple of times, but again - the mutations are not 'directed' at specific regions of the genome, therefore, they are not non-random in the way that you want them to be. You have focused - as do all creationists that try to use this flawed 'logic' - on the fact that some regions of the genome are more prone to mutation than others I am unaware of any evidence indicating that the regions that are more likely to receive mutations are those that would help the prokaryotic bacteria to adapt to its new environment. Indeed, in the papers I cited, which you have apparently finally read (long after claiming that they supported your position) it is pointed out that only a subset of the bacteria were able to survive. Clearly, if there were some "direction" mechanism, we should be able to see near;y 100% survivability. I mean, if the needed genes and apparatus are already in the genome, and there is this non-random mechanism, it should be a bit more efficient, don't you think? What you appear to be doing in Woodmorrapping - claiming that a set of anomalies indicate that the opposite position is correct. Bad logic, bad science, good zealotry. [This message has been edited by SLPx, 09-17-2002]
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Dr_Tazimus_maximus Member (Idle past 3245 days) Posts: 402 From: Gaithersburg, MD, USA Joined: |
quote: Yes it can.
quote: Most intracellular environments are reducing. THat is one reason why, during protein purification, biochemists often add reducing agenst such as DTT in vitro, it helps to keep reduced thiols in proteins reduced. There are also a number of reducing systems that ensure that ascorbate remains reduced, the main one being reduced glutathione. There are a number of papers by Levine, Mark A. et al. that describe this system and its relationship to ascorbic acid.
quote: That would be good because all of my sources indicate that he is in error. I still have not made it to the library to get the original of the GLO mutation paper, I hope to get there next week. ------------------"Chance favors the prepared mind." L. Pasteur Taz
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