molecular genetic proof against random mutation (1)

Dear Taz,You wrote:quote:
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Originally posted by peter borger:
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--------------------------------------------------------------------------------Peter, I just reviewed the structures and I think that you are in error. The only other step that I can see which is likely to have any significant rate of occurance at all in the absence of enzyme would be the formation of the lactone ring from the corresponding acid. This is a common reaction with sugars. THe GLO reaction with the resulting oxidation of the alchohol to the ketone is not likely ro occur without the help of the enzyme. The only reason that the final reaction occurs spontaneously is the assistance of the resonance structure accross the C-C bond and the two oxygens. Please site the source that tells you otherwise so I can look at it.My response:
A careful look at the structures in your reference demonstrates an OH group that can be oxydize spontaneously yielding a double bonded O group. This is sufficient to yield the endproduct in low concentration. I found this information in a communication between Dr. S. Harris and Dr. M. Banschbach on the internet.Best wishes,
Peter[This message has been edited by peter borger, 09-06-2002]

Dear Taz,Thanks for your work. And I look forward to your search on monday.Still you did not provide evidence against Dr. banschbach claim that I refered to. So, let's wait and see.You wonder:
"Now, all of this aside, what does this have to do with the wonderful molecular correlation of the GLO pseudogene (actually non-functional gene product would be a better term) with the predictions of descent with modification? Sorry, while I do want to complete this aspect of ascorbate biosynthesis it is getting a little off track."I say:
"I didn't use the redundancy of the GLO gene to support non-random mutation, since I have better examples of that. What I did was block of the pseudogene argument of evolutionists by demonstrating that the sequence of the inactivated GLO gene does not change at random. I already pointed it out to Mark24. So, if an unknown molecular mechanism generates the mutations one can never use this gene to demonstrate common descent. In fact, one cannot use any shared sequence anymore. I expect the same for shared retroviruses, but it would need a careful scruteny of 'all' known sequences (as demonstrated for the 1G5 gene in Drosophila). It would invalidate the evolutionists' strongest argument for common descent. That's what the fuss is about."Best wishes,
peter

Dear Taz,
Thanks for your scrutiny. I will send a mail to Dr. Banchbach were he got his information.Furthermore, let's have a careful look at the presented sequences in Otha's paper. At first sight one doesn't see anything out of the ordinary and one would assume randomness of mutation. However, have a look at the sequences. From orangutan to chimp 2 aa changed, and 2 aa changed afterwards (from chimp to human). Surprisingly, the aa at position 11 (from righthand side) was two times involved in this change. That is something that I wouldn't expect by chance alone. It certainly is a hotspot and that implicates a mechanism. So, if one position does not change at random why would the others have changed at random? Maybe here a mechanism was involved too. Therefore, you cannot use this gene as proof for common descent. What I like to see now is more sequences of primates including subspecies. That would clear thing up.Furthermore, as mentioned before, it doesn't matter for the mutation rate whether or not the gene has been inactivated. If it is allowed to compare these organisms and assuming paleontological timescales to be correct, the mutation rate observed in primates is (15/163):25 = 3.6(exp)-3 = 0.36% per million years. Similarly, the muation rate if rats are included (and they have a functional GLO gene) is (26/164):50 = 0.31% per million years. So, it doesn't matter whether the gene has been inactivated or not. Another reason to be a little suspicious.Best wishes,
Peter

Dear taz,
I will keep you informed.
Peter

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

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

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

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 wishes
Peter

Dear SLPx,You write:--------------------------------------------------------------------------------quote:
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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:
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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 wishes
Peter

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

Dear Peter,Could yo please elaborate a bit on the road. What kind of road? Where does it wind, become unsealed, is a bar nearby, etcetera. That would shed some light on the cause (mechanism) of the accidents.best wishes,
Peter

Hi SLPx,Sorry that I didn't get there yet, but I do not get messages in my mail (anymore), so I miss a lot (may send a direct mail to my email address too). But I will have a look at them and respond.best wishes
Peter

dear SLPx,
quote:
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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!Guess I hit that nail on the head, eh "Peter"?I say:
Why reiterate this, while I already explained to you that the article you referred to was in a mail to Fred Williams not a message addressed to me, so I missed it (look it up, if you like, it was a Science paper in a mailing to Fred. But anyway, it is nit-picking)quote:
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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 mechanism 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.--------------------------------------------------------------------------------And how does your 'conclusion' of non-random mutation falsifying NDT follow from that? In your selective readings of the papers I cited, did you not notice that the mutations were not centered - directed - specifically to the genes 'needed'?
Or did that slip by your razor-keen scientific insight?I say:
Probably prokaryotes differ from eukaryotes in this respect (although they have lots of redundant genes too). In comparison, it was long thought that prokaryotes do not have introns, but now we know that some have. So, a mechanism not optimal/fully present in prokaryotes may be fully operative in eukaryotes. Nobody looked at it yet, so it is a perfect valid hypothesis based on the Ig5 gene in Drosophila. Another difference may be that prokaryotes can be considered as one huge "gene exchanging-organism-that-makes-the-world-go-round", and do not need to have an optimal system to generate mutations.you quote:
--------------------------------------------------------------------------------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"--------------------------------------------------------------------------------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...I say:
Loss of genes is a common mechanism in evolutionism to explain observations. There is even a discipline in evolutionism that postulates utter hypothetical gene additions and gene deletions to reconcile gene trees with species tree.quote:
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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."--------------------------------------------------------------------------------You say:
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 say:
Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude. Challenge me and I will falsify common descent beyond doubt. I will open a new thread, if you like.
And concerning the Uebermensch: you were the one that introduced space-aliens to explain genes in humans not present in apes. I can think of several better 'scientific' non-testable explanations.You say:
I am still waiting for your unequivocal evidence that these unused but maybe someday necessary genes are in the genomes of all creatures......(Creatures? When did you become a creationist? )....just waiting for that one lucky mutation - in the right conditions, of course - to be turned on.I say:
Redundant genes are 'non per niente' in the genome. Yes, my hypothesis of "(non-)random mutation in a multipurpose genome" is ALMOST as incredible as evolutionism. Probably we have to wait for another decade and we will know. At least if the appropriate experiments are carried out. That is: the comparison of subspecies with related species. That is not: the comparison of individuals of distinct species.You say:
Your silly (and typically overconfident) position simply supports something I have believed for some time now - evolutionists base their thoughts on what is known, creationists base theirs on what is not.I say:
The real silly thing is that even the major part of the tiny bit that we know from the genome does NOT point in the direction of evolution. (ever heard of the second DNA associated code of transcription? And there may even be a third code involved in coactivation of transcription. Firstly, there is NO evolutionary explanation for the first code. And now we find that the first code gives rise to a second code through possible another code. So you better present a pretty good story to explain this by a random mechanism). BTW, I already gave an alternative explanation for all observations in the genome. Yes, it is a HYPOTHESIS --just like evolutionism is-- and it should be tested.
Furthermore, I have to admit that the hypothesis of evolution was a nice 19th century attempt to explain life without external intervention (although Darwin acknowledged the need for external intervention to give rise to first living cell). However, the hypothesis that a random mechanism underlays life becomes more and more untenable in the light of 21st century knowledge.
And in regard to "overconfident": All I did was demonstrating that evolution is NOT a fact. Present it as a hypothesis and I don't have a problem, and I wouldn't even have registered to this board. Present it "overconfidently" as FACT and I will blow it up! No problem, just show the right examples.best wishes,
Peter

Dear SLPx,I will respond to your letter more extensively soon, but here are two recent reviews about two additional biological codes involved in eukaryotic gene transcriptional regulation:On the histone code:
Junewein, T, and Allis, CD. Translating the Histone Code. Science 2001, 293:1074.On a possible coactivater code:
Gamble MJ, and Freedman LP. A coactivator code for transcription. Trends in Biochemical Sciences 2002, 27:165.Reasons why I don't believe the hype anymore.Best wishes
Peter

Dear SLPx:THIS IS WHAT YOU WROTE. MY RESPONSE IS IN CAPITAL LETTERS< SO YOU WILL NOT GET CONFUSED.quote:
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Originally posted by peter borger:
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!Guess I hit that nail on the head, eh "Peter"?I say:
Why reiterate this, while I already explained to you that the article you referred to was in a mail to Fred Williams not a message addressed to me, so I missed it (look it up, if you like, it was a Science paper in a mailing to Fred. But anyway, it is nit-picking)--------------------------------------------------------------------------------I have no need to look it up. It is right here:http://EvC Forum: molecular genetic proof against random mutation (1) -->EvC Forum: molecular genetic proof against random mutation (1)Message 96. I DIRECTLY address you in reply to a request from you. You replied in Message 97 that these citations support your position. As is so common with creationists, you then actually went on condescendingly how I must not understand the content of the papers (message 102, Aug.22) and such.Yet it was not until SEPTEMBER 12 that you actually even read the papers! (YOUR message 123 in the linked thread).So, "Peter B", your 'memory' is a bit clouded.MY RESPONSE:
THE ONLY ONE HERE TO MISREPRESENT THINGS IS YOU. iF YOU GO BACK IN THE THREAD THAN YOU WILL FIND OUT THAT I REFFERRED TO THE SCIENCE PAPER IN YOUR MAIL TO FRED. THIS MAIL CAN BE FOUND IN THIS THREAD #52, THE CAIRNS EXCERPT. SO NEXT TIME BEFORE YOU START TO BLAME ME READ BACK AND PREPARE PROPERLY.You have: 1)Tried to misrepresent the situation by claiming that I was writing to Williams, not you. That is demonstably false. 2) You arrogantly and overconfidently implied that it was I that had not read the papers or could not understand them when in reality it took you nearly a month to get around to looking at them DESPITE the fact that you had previously proclaimed them supportinve of your claims, and then still ignored the fact that not of them even comes close to supporting the notion of 'directed mutation' as you describe it.Nitpicking, indeed...quote:
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quote:
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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"MY RESPONSE:
THIS CAN BE FOUND IN MAIL #52 TO FRED, THE CAIRNS EXCERPT. NOT IN A MAIL TO ME.In my opinion not equal means that a mechanism (=non-random) is involved, isn't it?----------------------------------------------------------------------If by mechanism 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.----------------------------------------------------------------------And how does your 'conclusion' of non-random mutation falsifying NDT follow from that? In your selective readings of the papers I cited, did you not notice that the mutations were not centered - directed - specifically to the genes 'needed'?
Or did that slip by your razor-keen scientific insight?I say:
Probably prokaryotes differ from eukaryotes in this respect (although they have lots of redundant genes too). In comparison, it was long thought that prokaryotes do not have introns, but now we know that some have. So, a mechanism not optimal/fully present in prokaryotes may be fully operative in eukaryotes.--------------------------------------------------------------------------------Just so stories form the creationist. You have learned well from creationist Spetner, who also had no actual supportive evidence for his fairy tales occurring in multicellular eukaryotes.MY RESPONSE:
YOU ARE WRONG. WHEN SPETNER WROTE HIS BOOK (BEFORE 1997) THESE EXPERIMENTS HAD RECENTLY BEEN PUBLISHED, SO SPETNER WAS PRETTY UP TO DATE WITH HIS BOOK. THAT THE MECHANISM IS NOT EXACTLY AS HE (AND CAIRNS) THOUGHT IT WAS, IS NOT SURPRISING SINCE NOTHING IN BIOLOGY IS AS WE EXPECT IT TO BE. FURTHERMORE, THE CAIRNS INTERPRETATION IS ONLY A MINOR POINT IN SPETNER'S BOOK SO YOU CANNOT REJECT HIS ENTIRE BOOK ON CAIRN'S PARTIAL RECANTATION. BETTER READ HIS BOOK INSTEAD OF ONLY HIS OPPONENTS. AND WHY DO YOU THINK THERE HAVE BEEN CARRIED OUT SO MANY EXPERIMENTS TO FALSIFY CAIRNS INTERPRETATION? THE NDT WOULD HAVE FALLEN, AND THAT IS EXACTLY WHY YOU OBJECT/DENY THE NON-RANDOMNESS OF MUTATION IN THE 1G5 GENE. AND THAT'S WHY NDT BLOCKS SCIENTIFIC PROGRESS.quote:
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you quote:
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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"---------------------------------------------------------------------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...I say:
Loss of genes is a common mechanism in evolutionism[sic] to explain observations. There is even a discipline in evolutionism that postulates utter hypothetical gene additions and gene deletions to reconcile gene trees with species tree.--------------------------------------------------------------------------------Please expand on this. Please provide citations, as well. Also, please explain why it is that you believe that all gene trees should be exactly the same.MY RESPONSE:
ANY RECENT BOOK ON MOLECULAR EVOLUTION HAS A CHAPTER CONCERNING ‘RECONCILIATION OF GENE TREES WITH SPECIES TREES'. ACCORDING TO EVOLUTIONARY BIOLOGISTS, GENE TREES HAVE TO BE IN AGREEMENT WITH SPECIES TREES. WHY? OTHERWISE ALL GENES LYING OUT PROVIDE FALSIFICATIONS OF COMMON DESCENT. YOU CAN FIND THIS HIGHLY DISPUTABLE MATHEMATHICAL TRICK FOR INSTANCE IN 'MOLECULAR EVOLUTION, A PHYLOGENTIC APPROACH by R. PAGE'. WHAT EVO’S DO IS THE OTHER WAY AROUND REASONING. THEY CLAIM THAT SINCE EVOLUTION IS TRUE, THE EVIDENCE FOR PUTATIVE DUPLICATIONS IS SIMPLY THE INCONGRUENCE BETWEEN THE GENE AND THE SPECIES TREE. I OBJECT TO SUCH SIMPLISICISM.
FOR EXAMPLES: (http://taxonomy.zoology.gla.ac.uk/rod/papers/page97mpe.pdf).quote:
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quote:
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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."----------------------------------------------------------------------You say:
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 Reads too much into posts and tries to make much of their shallow comprehensive skills.I say:
Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude.--------------------------------------------------------------------------------You may recall that I was not the one claiming that articles that I had not read support my position. THAT is overconfidence. Also, I was not the one that 'explained' that perhaps I didn't understand what was in the articles... the ones that you hadn't yet read...
The analogy was clear, and it fulfilled its purpose. That you could not understand it has nothing to do with anyone's overconfidence, real or imagined.quote:
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Challenge me and I will falsify common descent beyond doubt. I will open a new thread, if you like.
--------------------------------------------------------------------------------Consider this a challenge. Similar to the other challenge that you suggested, discussing gene trees and such.
I think I will find your beyond-doubt falsification most informative, and will gingerly forward it to the appropriate authorities such that we can immediately informa those thousands of scientists that utilize evolutionary theory in their research that they are going about their work all wrong.MY RESPONSE:
THE MOLECULAR GENAEOLGY OF INTERLEUKIN-1-beta demonstrates an aberration from the species tree. A careful sequence comparison reveals that the human interleukin-1beta gene is more closely related to the mouse than to the homologue genes in pig and sheep. Evolutionists have to admit that this is not in accord with the species tree and postulate that a fourth gene duplication event is required that caused the aberration. Yet, a thorough scrutiny for IL-1-related genes in the human genome doubts that this event ever took place. Eight members of the IL-1 related genes in man’s chromosome 2, to be precise in location 2q11-2q14 (OMIM). Sequence comparison of the IL-1 related genes does not present evidence that a recent duplication of IL-1 beta took place in this region. On the contrary, the family tree of the IL-1 genes clearly demonstrates that the common ancestor copy of the IL-1 beta gene duplicated 3 times maximally, and gave rise to IL-1 alpha and IL-1 beta (Smith, D.E. et al. Four new members expand the interleukin-1 superfamily Journal Biological Chemistry 2000, vol275, pp1169-1175). Thanks to the human genome project, the evolutionary explanation of the aberration of mouse and human IL-1 beta from the species tree can readily be falsified. It should be realised that once a hypothesis is falsified, it remains falsified forever. It cannot be overruled by new experiments, and it doesn't become old-fashioned.
BTW, I discussed this already with Dr page himself and he couldn't address it beyong 'maybe it isn't properly rooted'. So, evolutionists root it properly, otherwise it is a falsification beyon doubt of common descent!quote:
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And concerning the Uebermensch: you were the one that introduced space-aliens to explain genes in humans not present in apes. I can think of several better 'scientific' non-testable explanations.
--------------------------------------------------------------------------------I did no such thing. Please stop misrepresenting me and trying to erect straw man arguments.MY RESPONSE;
YES, YOU DID. IN RESPONSE TO THE GENES PRESENT IN HUMAN NOT PRSENT IN MAN.quote:
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You say:
I am still waiting for your unequivocal evidence that these unused but maybe someday necessary genes are in the genomes of all creatures......
(Creatures? When did you become a creationist? )--------------------------------------------------------------------------------When did you become such a moron?MY RESPONSE:
JUST KIDDING.quote:
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....just waiting for that one lucky mutation - in the right conditions, of course - to be turned on.I say:
Redundant genes are 'non per niente' in the genome. Yes, my hypothesis of "(non-)random mutation in a multipurpose genome" is ALMOST as incredible as evolutionism. Probably we have to wait for another decade and we will know. At least if the appropriate experiments are carried out. That is: the comparison of subspecies with related species. That is not: the comparison of individuals of distinct species.--------------------------------------------------------------------------------How do you propose this comparison be done?MY RESPONSE:
AS DEMONSTRATED FOR THE 1G5 GENES IN A LARGE AMOUNT OF SUBPOPULATIONS. I AM INTERESTED IN THE SEQUENCES OF ONE PARTICULARE GENE (SAY HEMOGLOBIN OR CYTOCHROME C) THROUGHOUT THE DIFFERENT HUMAN SUBPOPULATIONS. I WONDER WHETHER THESE DATA ARE PRESENT INLITERATURE?quote:
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You say:
Your silly (and typically overconfident) position simply supports something I have believed for some time now - evolutionists base their thoughts on what is known, creationists base theirs on what is not.I say:
The real silly thing is that even the major part of the tiny bit that we know from the genome does NOT point in the direction of evolution.--------------------------------------------------------------------------------And there is the gem - that nugget of creationist stupidity that pops its head out once in a while.I wonder what your more knowledgible and rational colleagues would think if they knew that you were writing - and apparently believe - something so asinine?
I guess you didn't realize that all those duplicated genes actually fit quite well within an evolutionary framework? Nah - you are a creationist, and your personal opinions are the REALLY important things! facts be damned!quote:
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(ever heard of the second DNA associated code of transcription? And there may even be a third code involved in coactivation of transcription. Firstly, there is NO evolutionary explanation for the first code. And now we find that the first code gives rise to a second code through possible another code. So you better present a pretty good story to explain this by a random mechanism).
--------------------------------------------------------------------------------Frankly, no, I have not heard of this. Please provide some verifiable documentation that I can check to see if your depiction of this is accurate.MY RESPONSE:
I ALREADY GAVE THE REFERENCES. I AM WAITING FOR A REPONSE.quote:
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BTW, I already gave an alternative explanation for all observations in the genome. Yes, it is a HYPOTHESIS --just like evolutionism is-- and it should be tested.
--------------------------------------------------------------------------------test away. You're the expert scientist, right?
Oh - where is this hypothessis again?MY RESPONSE:
SOMEWHERE IN A MAIL IN THE THREAD GENERAL THEORY OF EVOLUTIONquote:
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And in regard to "overconfident": All I did was demonstrating that evolution is NOT a fact. Present it as a hypothesis and I don't have a problem, and I wouldn't even have registered to this board. Present it "overconfidently" as FACT and I will blow it up! No problem, just show the right examples.
--------------------------------------------------------------------------------Whatever you say, Petey....Whatever you say....THAT’S IT.BEST WISHES,
PETER[This message has been edited by peter borger, 10-01-2002][This message has been edited by peter borger, 10-01-2002]