molecular genetic proof against random mutation (1)

Dear Joe,I am still writing/thinking about my opus magnum. Every now and than, I mail to proevolutionary boards/evolutionary biologists to test some examples/ideas. As you can see from this board the resistance is overwhelming. Of course, I consider all comments carefully since I like to know what to expect, and how to improve it. Prior to launching, better prepare carefully.
Whether or not it will be a scientific publisher depends on guys like Mammuthus and SLPx, since usually such guys comprise the proevolutionary editorial board. Did you know that before Behe published his book it was reviewed by several scientific editors. One of them was against publishing since it would question the current paradigms. Apparently, in his land of evolution there is no freedom of thoughts.best wishes,
Peter

Dear mammuthus,If an utterly hypothetical gene duplication --that has been proposed to explain the incongruence of gene trees and species trees-- is not to be found in the genome than something is wrong with the method. It is proof against common descent beyond any doubt, the rooting of gene trees cannot overcome it. The theory falls. That's it. Better get used to it.best wishes,
Peter

Dear Mammuthus,You say:
"Ever going to present your hypothesis with the supporting data, how the theory is falsafiable, yada yada yada?"I say:
Good to have you back. How was the holiday? Convention?In your absence I presented some sort of hypothesis. It says that all organsims have a multipurpose genome and that adaptations to environment can be induced either randomly, or by non-random protein/RNA mediated mechanism. It holds that there should be a lot of redundant genes in the genome of any organism. That is exacly what we observe. In contrast, the hype of evolutinism doesn't have an explanation for redundant genes. So, that in support of my hypothesis. Furthermore, by now I presented 4 examples that cannot be explained by random mutation, but rather involves non-random mechanisms. These examples are the 1G5 gene, the primate ZFY region, the redundant alpha actinin genes, and today I mailed to SLPx that the DNA shuffling in ticks and lizards is exacly identical. These examples all point in the direction of non-random evolution. The overturn of an established paradigm takes time, I know.best wishes,
Peter

Dear SLPx,You wrote in a previous mail I didn't see yet:"--------------------------------------------------------------------------------quote:
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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 wishes
Peter--------------------------------------------------------------------------------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."I say:
It is known that the redundancy in the genetic code leads to neutral positions on the third positions of codons. For instance, the aminoacid leucine can be coded by 6 different codons including CUU, CUC, CUA, CUG. A look at these 4 codons reveals that the third letter of the code is unimportant for determining the aminoacid. This is known as "wobble in the anticodon". The same accounts for the aminoacids valine, serine, proline, threonine, alanine, arginine, and glycine. So, these positions are not under selective constraint (neutral positions) and are expected to behave accordingly. I don't know whether Kimura also had these positions in mind, but I do.best wishes,
Peter

Dear SLPx,Yes, Mister SLPx, these postions are NOT under selective constraint and are per definition neutral. I guess, mister Futuyma forgot about this, I don't. Why don't you just simply address my comments in a scientific way and try to convince me, instaed of repeating that I am a creationist. I am always open for good scientific arguments.best wishes[This message has been edited by peter borger, 10-02-2002]

Dear SLPx,I referred to Roderick Page, the author of "Molecular Evolution, A Phylogenetic Approach".
Sorry for confusing you. I mentioned that I --before registration to this board-- I had a lot of private conversations with evolutionary biologists. As soon as I mentioned the current problems in evolution theory and demonstrated this with examples from literature, there was silence. So I know what I'm talking about.Best wishes,
peter

Dear Mammuthus,If you feel offended: Sorry for that. It happens to me a lot. Try to be a stoic, that helps. And thanks for clearing things and for your comments on the hypothesis. I will take them in consideration. The more scientific comments the better.Best wishes
Peter

dear SLPx,In response to your comments on my previous mail:You say:
Thanks, Pete. I do find your posts most confusing.I say:
That is because it involves thinking beyond the current paradigm.You say:
You know, it is the strangest thing. Looking at my post #52, I did indeed post a reply to Williams with a link to a Science article containing information on Cairns. But if one looks at the links to replies in the bottom of that post, one sees that you did not respond to it until post #123. This of course is well after I had already reposted a quote from that source and supplied several abstracts to papers that provide direct evidence against 'directed' mutations - the ones you claimed were in fact evidence for them.I say:
Thanks for admitting you were wrong. I agree on the other mail.You say:
While I see that I was in error in so far as interpreting your post #123 and #126, I maintain that you did not read, or perhaps understand, the implications of the abstracts I posted in #96. One has to be a dogmatist extraordinaire to believe that papers explaining how mutations occurred genome-wide really indicate a non-random mechanism.I say:
I know the implications, and I just wait and see for more experiments on the 'hot' regions.You say:
Yes, I see that now. My sincere apologies.I say:
AcceptedYou say:
I am wrong? Well, then, Peter B., please supply us with the documentation for non-random mutations occurring in multicellular eukaryotes that result in phenotypic change. The best he could do was some pap about sea gull wings... Which of course had no genetic analysis in its support...
Spetner the creationist could not do this then, and he has not done it yet.
Help him out.I say:
I already helped him out by showing some interesing examples of non-random mutation (although they are not accepted by some evolutionists, including yourself). So, more research in this particular area will be revealing. I predict: Within 10 years non-random mutations will have their place in NDT.my quote:
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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.
--------------------------------------------------------------------------------So he was wrong then. Good to hear you say that.I say:
The original proposal was false. I just wait and see what the hot regions imply. Maybe it implies an indirect mechanism.my quote:
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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.
--------------------------------------------------------------------------------you say:
I didn't. Indeed, the Cairn's bit was mentioned in regards to "non-random mutation" in general, not to anyone's vanity press book targeting a lay audience.I say:
At least somebody who tries to educate the lay audience in an anti-nihilistic way. My objections to the hype are all the extrapolations from it. That is, the BullS..T I hear on the television and read in the papers. You --as a respectable scientist-- should also object to that.quote:
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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?
--------------------------------------------------------------------------------In reality, so many experiments were carried out to see if he was right (he wasn't), not to try to disprove him.I say:
Maybe they didn't perform the right experiments yet. I think a lot more is going on in this operon than we think there is. And what about the cryptic genes? The distinct stopcodons alternated by sense DNA are nor merely for show. I persist, there is a mechanism that can drain this well, and it will be found. Maybe it cannot be found in the laboratory. Maybe one has to look in subpopulations of extant organisms.my quote:
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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.
--------------------------------------------------------------------------------You say:
What progress would be made by accepting a fringe idea on non-random mutation? I object/deny it because as I have repeatedly explained and supplied references for, the idea of non-randomness is not what it is made out to be by folks like you.I say:
I said this with the 1G5 gene in mind. Denial of observations does not bring science any further.You say (about reconsiliation of gene and species trees):
They do? Examples please.I gave you the IL1-beta incongruence. One should be sufficient.my quote:
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ACCORDING TO EVOLUTIONARY BIOLOGISTS, GENE TREES HAVE TO BE IN AGREEMENT WITH SPECIES TREES.
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you say:
This is a major misrepresentation on your part, Peter B. It is outright false.I say:
Please elaborate a bit on it. References etc.You say:
Your credibility - what little you may have once had here - is now completely gone.I say:
My credibility within the evolutionary community is about zero, I guess. But, so what, I go for truth, not for 'evolutionisms just-so stories'.my quote:
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WHY? OTHERWISE ALL GENES LYING OUT PROVIDE FALSIFICATIONS OF COMMON DESCENT.
--------------------------------------------------------------------------------you say:
This is just asinine, and indicative of your dogmatic ignorance. Any text on molecular evolution not only explains why discrepencies exist, they actually predict that more will be found.I say:
Listen Mr SLPx, I don't adhere any dogma's. I just stand up against nihilism. And as I see it, molecular genetics points in the direction of 'creatons interacting with matter in a morphogenetic field'. And you have to present pretty strong arguments to convince me of the opposite.
And now I am curious what the hype has invented now to predict discrepancies. So, explain plus references please. (BTW, "to predict discrepancies". Hear what you are implying: 'our hype predicts that phenomenon X may be found and otherwise the opposite of X may also be found.' I call that HUMBUG)my quote:
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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.
--------------------------------------------------------------------------------I object to your idiocy, but it won't get me anywhere. Is it a 'trick'? That sounds awfully inflammatory, Peter B. Perhaps you don't understand statistics?I say:
No, your are not going to hide behind statistics. That's another trick to not answer. Besides, statistics has nothing to do with putative duplications that are not present.you say:
Or maybe the workings of genomes? Well, either way, your claims are getting more and more bizarre and more and more desparate.I say:
That the claims seem bizarre is due to the shortcomings of evolutionism on the level of the genome.my quote:
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FOR EXAMPLES: (http://taxonomy.zoology.gla.ac.uk/rod/papers/page97mpe.pdf).
--------------------------------------------------------------------------------The abstract:"The processes of gene duplication, loss, and lineage
sorting can result in incongruence between the phylogenies
of genes and those of species. This incongruence
complicates the task of inferring the latter from the
former. We describe the use of reconciled trees to
reconstruct the history of a gene tree with respect to a
species tree. Reconciled trees allow the history of the
gene tree to be visualized and also quantify the relationship
between the two trees. The cost of a reconciled
tree is the total number of duplications and gene losses
required to reconcile a gene tree with its species tree.
We describe the use of heuristic searches to find the
species tree which yields the reconciled tree with the
lowest cost. This method can be used to infer species
trees from one or more gene trees."you say:
Whats your point?I say:
My point was the incongruence of the IL-1beta family and the absence of the duplication. The only putative duplication to be found in this region is the one that gave rise to human IL-1alpha. Maybe reread my point. And I am not the desperate one.You say:
I am constantly amazed at how the creationist interprets 'explanations' as 'excuses' and the like. Pitiful, really.I say:
Better try to convince me with a scientific explanation instead of these evo-blahblah.quote:I say:
Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude.--------------------------------------------------------------------------------You say:
No, it is a valid conclusion.I say:
Based on what? Could you please lead me through your thoughts and how you draw such conclusions.quote:
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peter borger writes:
THE MOLECULAR GENAEOLGY OF INTERLEUKIN-1-beta demonstrates an aberration from the species tree.you say:
So?I say:
Why did you cut of this falsification of common decent. It was the quintessence. Maybe you could respond to it in a scientific way.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.
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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.--------------------------------------------------------------------------------What genes might be present in humans but not in man, I wonder...I say:
Obviously, you have a very selective memory. The gene in the LCR16a segment: present in human not in apes.You say:
How do you propose this comparison be done?MY RESPONSE:
AS DEMONSTRATED FOR THE 1G5 GENES IN A LARGE AMOUNT OF SUBPOPULATIONS.--------------------------------------------------------------------------------
You say:
What do you mean sub-population?I say:
Remember the Ig5 gene and the peculiar results that gave when the authors compared subpopulations. That's where my discussion started 3 months ago.quote:
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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?
--------------------------------------------------------------------------------You say:
I don't know about that particular gene, but Paabo's group has done an extensive study on the mitochondrial genome and, why, it must be a mere coincidence, the findings fit wquite nicely with evolutionary hypotheses.I say:
Is this really your response? Could you give me the references of Paabo studies. Was it caried out in subpopulations.And you write:
"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 say:
Nice try to stop me from doing. My colleagues like new ideas.
Ye, why not publish somewhere that i'm an ass. That would be fun, isn't ist. You could join Schrafinator's club.You say:
I guess you didn't realize that all those duplicated genes actually fit quite well within an evolutionary framework?I say:
And this shows your lack of knowledge on the topic. Once more for you:
There is NO association between genetic redundancies and gene duplications. So how exactly does it fit in? Please explain, and send a letter to Nature, since you are the first one.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.--------------------------------------------------------------------------------You say:
I am still waiting for your hypothesis...I say:
You could have found it if you actually were reading my posts.You also say:
A response to what?I say:
It once more demonstrates your lack of knowledge on contemporary biology. Notably it was published in Science 2001. Everybody reads Science! Except ostriches, I guess.Best wishes,
Peter

Dear SLPx,I guess, Kimura had in mind when he invented the neutral theory all neutral positions in the DNA. In my opinion that includes third 'wobbly' codon position. So I expect to find them to change with a higher rate. What do you expect?Best wishes,
Peter

Dear SLPx,You write:PB:quote:
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You say:
While I see that I was in error in so far as interpreting your post #123 and #126, I maintain that you did not read, or perhaps understand, the implications of the abstracts I posted in #96. One has to be a dogmatist extraordinaire to believe that papers explaining how mutations occurred genome-wide really indicate a non-random mechanism.
I say:
I know the implications, and I just wait and see for more experiments on the 'hot' regions.--------------------------------------------------------------------------------And the backtracking continues. You wrote in direct response to my posting of those citations that they were in fact supportive of your fantasy. Now you will 'wait and see.' Common creationist tactic- jumping to totally unwarranted conclusions.quote:
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You say:
I am wrong? Well, then, Peter B., please supply us with the documentation for non-random mutations occurring in multicellular eukaryotes that result in phenotypic change. The best he (Spetner) could do was some pap about sea gull wings... Which of course had no genetic analysis in its support...
Spetner the creationist could not do this then, and he has not done it yet.
Help him out.
I say:
I already helped him out by showing some interesing examples of non-random mutation (although they are not accepted by some evolutionists, including yourself). So, more research in this particular area will be revealing. I predict: Within 10 years non-random mutations will have their place in NDT.--------------------------------------------------------------------------------Nothing you have presented even remotely does what you claim it to. Your GLO schtick has been blown out of the water. Nothing else produces an altered phenotype by 'turning on' pre-existing genes (ala NREH). So, you have done nothing at all.MY RESPONSE:I DO NOT NEED THE GLO SCHTICK (WHATEVER IT MEANS) TO SHOW NON-RANDOM MUTATIONS, AND YOU KNOW THAT. IF YOU HAD READ MY MAILS ON THAT TOPIC YOU WOULD HAVE KNOWN THAT I HAVE MUCH BETTER EXAMPLES OF NON-RANDOMNESS AND YOU KNOW THAT TOO. PURPOSELY REFERRING TO THE WRONG GENE DOESN'T HELP YOU. I USED THE GLO EXAMPLE TO BLOCK THE PSEUDOGENE ARGUMENT aND YOU KNOW THAT TOO. DELIBERATELY MISREPRESENTATION OF MY WORDS: SAD. I THOUGHT YOU COULD DO BETTER AFTER I SHOWED 4 DISTINCT EXAMPLES IN THE GENOME THAT CANNOT BE EXPLAINED BY A RANDOM NDT MECHANISM. YOU KNOW THAT, BUT YOU SIMPLY DON'T WANT TO SEE IT: IGNORANCE. WHY NOT DISCUSS THE ZFY REGION IN HUMAN Y CHROMOSOME? LET'S FIND OUT HOW MANY AD HOC HYPOTHESIS YOU HAVE TO INTRODUCE, WHILE I HAVE TO INTRODUCE ONLY ONE HYPOTHESIS: NON-RANDOM MUTATIONS. MAYBE MARK24 CAN EDUCATE YOU ON OCCAM'S RASOR. AND IF YOU LIKE, YOU ARE ALLOWED TO BRING ALL YOUR EVO-FRIENDS-OF-THE-FIELD TO HELP YOU.quote:
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my quote:
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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.
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So he was wrong then. Good to hear you say that.I say:
The original proposal was false. I just wait and see what the hot regions imply. Maybe it implies an indirect mechanism.--------------------------------------------------------------------------------This is in direct opposition to your earlier proclamations. But it is good to see that you are starting to try to reclaim some integrity.quote:
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my quote:
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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.
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you say:
I didn't. Indeed, the Cairn's bit was mentioned in regards to "non-random mutation" in general, not to anyone's vanity press book targeting a lay audience.I say:
At least somebody who tries to educate the lay audience in an anti-nihilistic way.--------------------------------------------------------------------------------Your metaphysical views of evolution are interesting. Common for creationists to try to 'blame' evolution for this or that, as you are implicitly doing. Irrelevant to science, of course, but interesting. You dislike evolution because of where you think it will lead philosophically or culturally or whatever.Too friggin bad.MY RESPONSE:INDEED TOO BAD FOR ATHEISTS THAT NDT HAS FALLEN.quote:
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My objections to the hype are all the extrapolations from it. That is, the BullS..T I hear on the television and read in the papers. You --as a respectable scientist-- should also object to that.
--------------------------------------------------------------------------------I do object to the terms used by some when talking about evolution. But I wouldn't were it not for the fact that I know how creationists will interpret and twist what they say. When a paleontologist says on TV that "This fossil is one of our ancestors" or something like that, "I" know what he means. But "I" also know how cretins will spin it. That is why I object to scientists saying things like "This fossil is one of our ancestors" .
Of course, I very strongly object to creationists saying thngs like "There is no evidence for evolution" or some such nonsense. And they say it all the time. because they are either totally ignorant or because they are being purposely deceptive.Which are you?MY RESPONSE:IF TRUE, THE HYPOTHESIS OF NON-RANDOM MUTATIONS IN A MULTIPURPOSE GENOME CAN EXPLAIN ALL EVOLUTIONARY PHENOMENA AND MORE. SO, WHAT IS IT EXACLY THAT MAKES YOU SAY THAT THERE IS EVIDENCE FOR EVOLUTION? IF MY HYPOTHESIS IS CORRECT --AND EVOLUTIONISM IS WRONG-- IT IS ALL EVIDENCE FOR CREATION AND DE-EVOLUTION. I REALLY DON'T UNDERSTAND WHAT IS WRONG WITH INTRODUCING A NEW TESTABEL HYPOTHESIS? wE DO THAT ALL THE TIME IN RESEARCH. OYE, NOW I SEE, THE HYPOTHESIS OF EVOLUTION IS A PRIORI TRUE AND ONLY HAS TO BE VERIFIED!!!! WELL, SLPX, DREAM ON.quote:
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quote:
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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?
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In reality, so many experiments were carried out to see if he was right (he wasn't), not to try to disprove him.I say:
Maybe they didn't perform the right experiments yet.--------------------------------------------------------------------------------Yes, that must be it. I guess looking at the whole genome beforew and after exposing these critters to strssful environments to see if changes are 'directed' just isn't the right thing to do.quote:
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I think a lot more is going on in this operon than we think there is. And what about the cryptic genes? The distinct stopcodons alternated by sense DNA are nor merely for show. I persist, there is a mechanism that can drain this well, and it will be found. Maybe it cannot be found in the laboratory. Maybe one has to look in subpopulations of extant organisms.
--------------------------------------------------------------------------------So, proof for creation is just around the corner, right?I COULD GIVE YOU COMPELLING EVIDENCE FOR CREATION. IN FACT GENETIC REDUNDANCIES ARE POINTING IN THAT DIRECTION, AND YOU KNOW THAT SINCE I ALMOST SPELLED IT OUT FOR YOU. BUT YOU SIMPLY DON'T WANT TO SEE IT. GENETIC REDUNDANCIES ALMOST SCREAM FROM THE GENOME: CREATED!!! NOW, YOUR EVO-FRIENDS TRY TO EXPLAIN TO ME THAT THEY ARE IN THE GENOME BECAUSE OF 'VERY WEAK PURIFYING SELECTION'. JUST ANOTHER MEANINGLESS TERM. LIKE THE OTHER YOU INTRODUCED TO 'EXPLAIN' THE EXACTLY THE SAME DNA REARRANGEMENT OF LIZARDS AND TICKS. MEANINGLESS WORDS.
I GUESS THAT IF WE DISCOVER IN THE GENOME A CODE THAT READS 'COPYRIGHT THE CREATOR' OR 'MADE IN HEAVEN' OR SOMETHING LIKE THAT, YOU STILL TRY TO INVENT A RANDOM ATHEISTIC EXPLANATION. YOU ARE SO STUCK IN EVOLUTIONISM YOU CANNOT THINK BEYOND THE PARADIGM ANYMORE.quote:
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my quote:
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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.
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You say:
What progress would be made by accepting a fringe idea on non-random mutation? I object/deny it because as I have repeatedly explained and supplied references for, the idea of non-randomness is not what it is made out to be by folks like you.I say:
I said this with the 1G5 gene in mind. Denial of observations does not bring science any further.MY RESPONSE:
IF THERE IS A NONRANDOM MECHANISM (I POSTULATED IT AS HYPOTHESIS, NOT AS FACT) ELUCIDATING IT MIGHT BENEFIT MANKIND, PROBABLY THROUGH INTERVENTION OF DRUG RESISTANCE IN MUSQUITO'S, LEUKEMIA'S ETCETERA. SO, DENIAL OF AN OBSERVATION BLOCKS SCIENTIFIC PROGRESS.--------------------------------------------------------------------------------Indeed. Nor does claiming support from evidence that is in reality contrary to one's position. That is brainwashing, not science.quote:
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You say (about reconsiliation of gene and species trees):
They do? Examples please.
I gave you the IL1-beta incongruence. One should be sufficient.--------------------------------------------------------------------------------Oh, right. I forgot - one anomoly can disprove evolution, but several examples countering 'directed mutations' just don't have any effect on alternative 'hypotheses', especially those favored by creationists. Haven't done the right experiments yet, that sort of thing.MY RESPONSE:
IT WOULD OVERTURN NDT. AND IS THAT SO BAD? IT NEVER CONTRIBUTED ANYTHING TO KNOWLEDGE OR MANKIND. SO, WHAT'S THE LOSS. ATHEISM? I DON'T MIND IF ATHEISM IS SACRIFICED. AND WHAT IS WRONG WITH CREATONS (VIRTUAL PARTICLES) INTERACTING WITH MATTER IN A MORPHOGENETIC FIELD GIVING RISE TO GENETIC PROGRAMS?quote:
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my quote:
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ACCORDING TO EVOLUTIONARY BIOLOGISTS, GENE TREES HAVE TO BE IN AGREEMENT WITH SPECIES TREES.
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you say:
This is a major misrepresentation on your part, Peter B. It is outright false.
I say:
Please elaborate a bit on it. References etc.--------------------------------------------------------------------------------Was it not YOU that claimed:"ACCORDING TO EVOLUTIONARY BIOLOGISTS, GENE TREES HAVE TO BE IN AGREEMENT WITH SPECIES TREES. "It seems to me that YOU should be the one to provide documentation, since YOU are the one that claims that evolutionary biologists DO believe this. I am an evolutionary biologist (unlike you) and I know this is incorrect. I am the source.
But, you seem to know Futuyma. Maybe you have his text? Well, I do, And it took me all of about 15 seconds to find this:MY RESONSE:
IF IT DOESN'T MATTER THAT GENES ARE NOT IN ACCORD WITH SPECIES TREES, WHY IS THERE A DISCIPLINE THAT RECONSILES THESE GENES IN AN UTTERLY SPECULATIVE MANNER BY INTRODUCING/DELETION OF DUPLICATIONS? I WAS PRETTY SURPRISED TO FIND OUT ABOUT IT AND SINCE YOU ARE THE EVO-BIOLOGIST ( I THOUGHT YOU WERE ANATOMIST BY EDUCATIN IN ANOTHER MAIL? 'HOMO UNIVERSALIS', I GUESS, LIKE ME) MAYBE YOU COULD EXPLAIN IT."Coalescent theory tells us that under some circumstances, this gene tree, even if correct, may not be the same as the species tree, i.e., the phylogeny of the species form which the gene copies were taken."MY RESPONSE:
WHO IS FUTUYMA? YOUR GOD? AND COALSESCENT HYPOTHESIS DOESN'T TELL ANYTHING, IT MERELY HOLDS SOMETHING. ANOTHER ATTEMPT TO BRING AN HYPOTHESIS AS FACT?p. 332, "Evolutionary Biology", 3rd Ed.
Emphases in original. He then goes on for some several paragrapgs explaining why this can be.Quote-mining and selective interpretations - not to mention baseless assertion - are hallmarks of cretinsm.MY RESPONSE:
PRESENTING HYPOTHESES AS FACT, HALLMARK OF EVOLUTIONISM. YOU SHOULD KNOW BY NOW THAT I OBJECT TO THAT. (DO YOU REALLY READ WHAT I WRITE, OR SIMPLY SKIM IT, AND TRY TO CATCH ME ON SOMETHING MINOR=NITPICKING)quote:
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You say:
Your credibility - what little you may have once had here - is now completely gone.
I say:
My credibility within the evolutionary community is about zero, I guess. But, so what, I go for truth, not for 'evolutionisms just-so stories'.--------------------------------------------------------------------------------Now its at about - 10. Your 'truth', it seems, is predicated on misinterpretations, personal beliefs, shallow grasps of science, etc.Common.MY COMMENTS:
MAYBE I HAVE TO GET A PHD IN EVOLUTIONISM. HOWEVER, THAT IS NOT REQUIRED LOOKING AT MR DAWKINS. AS LONG AS YOU TELL THE SAME OLD STORIES IN THE EVO-WAY YOU'RE MEMBER OF THE CLUB. I RECKON THAT AS LONG AS I HAD PRESENTED SOME DATA HERE THAT CAN BE INTERPRETED AS EVIDENCE FOR EVOLUTION I WOULD HAVE BEEN YOUR BIG HERO. IN ADDITION, MAYBE FUTUYMA IS NOT INFALLIBLE. AT LEAST HE DOESN'T MENTION THE 3RD CODON NEUTRAL POSITIONS ANYWHERE, AS FAR AS I KNOW. SO, ONCE MORE, HERE I INTRODUCE SOMETHING NEW.quote:
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my quote:
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WHY? OTHERWISE ALL GENES LYING OUT PROVIDE FALSIFICATIONS OF COMMON DESCENT.
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you say:
This is just asinine, and indicative of your dogmatic ignorance. Any text on molecular evolution not only explains why discrepencies exist, they actually predict that more will be found.I say:
Listen Mr SLPx, I don't adhere any dogma's. I just stand up against nihilism.--------------------------------------------------------------------------------What bullshit.. You 'stand up' for your creationism beliefs, and that is it.MY RESPONSE:
I RESTORE THE BALANCE. AND MAYBE YOU CAN EXPLAIN TO ME WHY THESE DISCREPANCIES EXIST, INSTEAD OF STATING SOMETHING AND NOT ELABORATING ON IT. ANOTHER JUST-SO STORY?quote:
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And as I see it, molecular genetics points in the direction of 'creatons interacting with matter in a morphogenetic field'. And you have to present pretty strong arguments to convince me of the opposite.
--------------------------------------------------------------------------------Frankly, I don't care what an asthma researcher thinks about evolution. I don't have to convince you personally of anything, for, as has been shown on this very forum for at least 2 posters that I can easily recall, no matter what is presented, you will simply reject or twist it. That is what the adherents of supernaturalistic antimaterialsims are all about - sophism to protect their beliefs.MY RESPONSE:
I GUESS THAT YOU CARE ABOUT THE OPINION OF THE ZOOLOGIST DAWKINS, SO WHAT ON EARTH DOES MY PROFESSION HAS TO DO WITH MAKING UP AN OPINION?quote:
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And now I am curious what the hype has invented now to predict discrepancies. So, explain plus references please. (BTW, "to predict discrepancies". Hear what you are implying: 'our hype predicts that phenomenon X may be found and otherwise the opposite of X may also be found.' I call that HUMBUG)
--------------------------------------------------------------------------------See my Futuyma ref.MY RESPONSE:
O I SEE, WELL IF THAT'S IT I AM NOT IMPRESSED. WHAT IS IT? PHILOSOPHY? IF I WANNA READ STORIES I BUY MYSELF A NEW DAWKINS-NOVEL. (THEY ARE PRETTY INTERESTING FROM A PSYCHOLOGICAL STANCE).In addition, one would thnk that a molecular biologist - even a creationist one - would undestand that not all loci mutate with the same regularity. Though I once encountered a PhD creationist - also from Australia - that claimed to be a geneticist yet didn't know the difference between nucleotides and codons. Creationists like to append polysyllabic words to their titles/credentiasl to impress their target audiene - layfolk.
Funny - when I corrected him, he, likemost cretins, actually engaged in condescension towards me - told me that I should get my "science straight" before daring to correct a PhD geneticist like him....MY RESPONSE:
SO YOU MET SOMEBODY WHO DIDN'T UNDERSTAND SOMETHING? HAPPENS TO ME ALL THE TIME. YOU WILL GET USED TO IT. I WONDER THOUGH WHY YOU MENTION THIS IN THIS CONTEXT? SUBTLE LITTLE ATTACK BASED ON GENERALISATION? GET OPEN MINDED!!!quote:
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my quote:
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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.
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I object to your idiocy, but it won't get me anywhere. Is it a 'trick'? That sounds awfully inflammatory, Peter B. Perhaps you don't understand statistics?I say:
No, your are not going to hide behind statistics. That's another trick to not answer. Besides, statistics has nothing to do with putative duplications that are not present.--------------------------------------------------------------------------------Refs please. (who do I sound like?)MY RESPONSE:
AND HERE YOU DEMONSTRATE THAT YOU DO NOT READ MY REFERENCES. I MAILED ALL THE REFERENCES YOU NEED, BUT YOU SIMPLY KEEP ASKING FOR IT. LOOK THEM UP, THAN WE CAN CONTINUE OUR DISCUSSION.quote:
--------------------------------------------------------------------------------
you say:
Or maybe the workings of genomes? Well, either way, your claims are getting more and more bizarre and more and more desparate.
I say:
That the claims seem bizarre is due to the shortcomings of evolutionism on the level of the genome.--------------------------------------------------------------------------------I see. So everyone else is wrong, and the asthma guy creationist is right.MY RESPONSE:
YE, THAT COULD BE IT.quote:
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my quote:
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FOR EXAMPLES: (http://taxonomy.zoology.gla.ac.uk/rod/papers/page97mpe.pdf).
----------------------------------------------------------------------
The abstract:"The processes of gene duplication, loss, and lineage sorting can result in incongruence between the phylogenies of genes and those of species. This incongruence complicates the task of inferring the latter from the former. We describe the use of reconciled trees to
reconstruct the history of a gene tree with respect to a species tree. Reconciled trees allow the history of the gene tree to be visualized and also quantify the relationship between the two trees. The cost of a reconciled tree is the total number of duplications and gene losses required to reconcile a gene tree with its species tree.
We describe the use of heuristic searches to find the species tree which yields the reconciled tree with the lowest cost. This method can be used to infer species trees from one or more gene trees."you say:
Whats your point?I say:
My point was the incongruence of the IL-1beta family and the absence of the duplication. The only putative duplication to be found in this region is the one that gave rise to human IL-1alpha. Maybe reread my point. And I am not the desperate one.--------------------------------------------------------------------------------I think you are - after all, what you see as an evolution disproofing anomoly is actually a fairly well understood phenomenon. Well, understood by those in the field anyway. Like the anti-non-random mutation abstracts I posted, I do have to wonder if you even read the abstact of this paper?MY RESPONSE:
SO, YOU CONCUR THAT IT IS AN ANOMALY THAT CANNOT BE EXPLAINED BY EVOLUTIONISM? SINCE YOU ARE IN THE FIELD OF EVOLUTIONISM, PLEASE EXPLAIN THIS LITTLE ABERATIONS TO ME THAN IN A SCIENTIFIC WAY. LET'S SEE HOW MANY AD HOC HYPOTHESIS YOU HAVE TO INTRODUCE. AFTER THAT THERE ARE THE GLOBIN GENE, THE LDH GENE, ETCETERA. ACCORDING TO MAMMUTHUS THERE ARE THOUSANDS OF THEM, SO WE BETTER START NOW.quote:
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You say:
I am constantly amazed at how the creationist interprets 'explanations' as 'excuses' and the like. Pitiful, really.
I say:
Better try to convince me with a scientific explanation instead of these evo-blahblah.--------------------------------------------------------------------------------Again, I really don't care what megalomaniacs think.YOU DON'T CARE ABOUT MEGALOMANICS, YOU DON'T CARE ABOUT CREATIONISTS, YOU DON'T CARE ABOUT ASTHMA RESEARCHERS. WHAT DO YOU CARE ABOUT? I CARE ABOUT PEOPLE, INDEPENDENT HOW THEY THINK. I ALSO CARE ABOUT HOW YOU THINK, OTHERWISE I WAS NOT INVOLVED IN THIS DISCUSSIONquote:
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quote:
I say:
Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude.
----------------------------------------------------------------------You say:
No, it is a valid conclusion.I say:
Based on what? Could you please lead me through your thoughts and how you draw such conclusions.--------------------------------------------------------------------------------Well, you edited out what I was responding to, and I don't want to open a new window and reread the thread to see. I think it is pretty clear that I was right. Look at the post I am responing to here, for example...MY RESPONSE:
I DID NOT EDIT OUT. I FOUND THE MAIL PRETTY LONG, THAT'S WHY I COPIED ONLY YOUR COMMENTS AND RESPONDED TO THAT. IN CONTRAST, YOU EDITED OUT MY COMPLETE IL-1BETA INCONGRUENCE STORY, WITHOUT DISCUSSING IT (SEE BELOW). WHY?quote:
--------------------------------------------------------------------------------
quote:
---------------------------------peter borger writes:
THE MOLECULAR GENAEOLGY OF INTERLEUKIN-1-beta demonstrates an aberration from the species tree.MY RESPONSE:
HERE YOU LEFT OUT THE COMPLETE IL-1BETA INCONGRUENCE AND HOW IT FALSIFIES COMMON DESCENT BEYOND DOUBT. WHY IS THAT?you say:
So?I say:
Why did you cut of this falsification of common decent. It was the quintessence. Maybe you could respond to it in a scientific way.--------------------------------------------------------------------------------LOL! Yeah, it was a falsification. Read the Futuyma ref, for one. Maybe you can support your claims in a scientific way, instead of digging through the lit to find what you consider anomolies which disproof evolution.MY RESPONSE:
THE FUTUYMA STORY? READ AGAIN? TO WHAT PURPOSE? LULLABY?quote:
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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.
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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.----------------------------------------------------------------------What genes might be present in humans but not in man, I wonder...I say:
Obviously, you have a very selective memory. The gene in the LCR16a segment: present in human not in apes.--------------------------------------------------------------------------------Gee, Petey - never heard of deletions before? Of course, look at what you wrote:"...GENES PRESENT IN HUMAN NOT PRSENT IN MAN. "MY RESPONSE:
SLIP OF THE PEN. IT SHOULD HAVE READ ...PRESENT IN HUMAN NOT PRESENT IN PRIMATES. BUT NOW I SEE, DELETED 'AD RANDOM' IN ALL PRIMATES BUT MAN. YE, I COULD HAVE EXPECTED THAT. WELL, DEAR SLPX, THE STORY OF EVOLUTION GETS BETTER AND BETTER.......CONVINCING.quote:
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You say:
How do you propose this comparison be done?
MY RESPONSE:
AS DEMONSTRATED FOR THE 1G5 GENES IN A LARGE AMOUNT OF SUBPOPULATIONS.----------------------------------------------------------------------
You say:
What do you mean sub-population?I say:
Remember the Ig5 gene and the peculiar results that gave when the authors compared subpopulations. That's where my discussion started 3 months ago.--------------------------------------------------------------------------------So you can't just say what you mean?MY RESPONSE:
YOU KNOW WHAT I MEAN BY SUBPOPULATIONS SINCE YOU READ MY COMMENTS OF THE 1G5 GENE AND YOU REFER TO TE ARTICLE BELOW.Nature 2000 Dec 7;408(6813):708-13Mitochondrial genome variation and the origin of modern humans.Ingman M, Kaessmann H, Paabo S, Gyllensten U.The analysis of mitochondrial DNA (mtDNA) has been a potent tool in our understanding of human evolution, owing to characteristics such as high copy number, apparent lack of recombination, high substitution rate and maternal mode of inheritance. However, almost all studies of human evolution based on mtDNA sequencing have been confined to the control region, which constitutes less than 7% of the mitochondrial genome. These studies are complicated by the extreme
variation in substitution rate between sites, and the consequence of parallel mutations causing difficulties in the estimation of genetic distance and making phylogenetic inferences questionable. Most comprehensive studies of the human mitochondrial molecule have been carried out through restriction-fragment length polymorphism analysis, providing data that are ill suited to estimations of mutation rate and therefore the timing of evolutionary events. Here, to improve the information obtained from the mitochondrial molecule for studies of human evolution, we describe the global mtDNA diversity in humans based on analyses of the complete mtDNA sequence of 53 humans of diverse origins. Our mtDNA data, in comparison with those of a parallel study of the Xq13.3 region in the same
individuals, provide a concurrent view on human evolution with respect to the age of modern humans.Subpopulations like this?MY RESPONSE:
I WILL LOOK IT UP AND I HOPE THAT THEY SHOW THE SEQUENCES, NOT ONLY THE FIGURES/PERCENTAGES SINCE IT DOESN'T SAY ANYTHING.quote:
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quote:
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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?
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You say:
I don't know about that particular gene, but Paabo's group has done an extensive study on the mitochondrial genome and, why, it must be a mere coincidence, the findings fit wquite nicely with evolutionary hypotheses.I say:
Is this really your response? Could you give me the references of Paabo studies. Was it caried out in subpopulations.--------------------------------------------------------------------------------Oh - see above. 53 subpopulations.MY RESPONSE:
THANKS FOR THE REFERENCE.quote:
--------------------------------------------------------------------------------
And you write:
"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 say:
Nice try to stop me from doing. My colleagues like new ideas.
Ye, why not publish somewhere that i'm an ass. That would be fun, isn't ist. You could join Schrafinator's club.--------------------------------------------------------------------------------It is fun, I agree. But there is no need to publish the obviousMY RESPONSE:
ANY SCIENTIST NOT AGREEING ON NDT BASED ON PRETTY GOOD ARGUMENTS IS AN PAIN IN THE ASS, ISN'T IT? MAYBE THE THEORY SHOULD BE A LITLE LESS CONSERVATIVE. IT HASN'T CHANGED FOR ALMOST 70 YEARS. INCREDIBLE, ESPECIALLY NOW WE HAVE KNOWLEDGE ON THE GENOME.quote:
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You say:
I guess you didn't realize that all those duplicated genes actually fit quite well within an evolutionary framework?
I say:
And this shows your lack of knowledge on the topic. Once more for you:
There is NO association between genetic redundancies and gene duplications.--------------------------------------------------------------------------------Yes, my lack of knowledge. Maybe you heard of a paper that came out in Science a bit ago. It contained a working draft of 90% of the human genome? It showed that not only have individual genes been duplicated, but in fact much of the genome consists of huge duplicated blocks.YES, I KNOW ABOUT THIS ONE AND I WILL STUDY IT IN MORE DETAIL WHAT EXACTLY IT IMPLICATES. IT DOES NOT HOWEVER IMPLICATE THAT THE GENOME EVOLVED THROUGH CHROMOSOMAL DUPLICATIONS, SINCE THAT HAS BEEN FALSIFIED OVER AND OVER (BY HUGHES? I GUESS). MAYBE THERE IS SOME NON-RANDOM SEGMENTAL DUPLICATION INVOLVED TOO. WHAT WE DO KNOW IN THE MEDICAL WORLD IS THAT SEGMENTAL DUPLICATIONS ARE BAD FOR CHROMOSOMAL STABILITY, SO I WILL LOOK IT UP.I was talking about duplications, you now add another criterion. Good for you!MY RESPONSE:
BE MORE SPECIFIC IN YOUR TALKINGS, TO AVOID MISCOMMUNICATION.quote:
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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).
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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.----------------------------------------------------------------------You say:
I am still waiting for your hypothesis...I say:
You could have found it if you actually were reading my posts.You also say:
A response to what?I say:
It once more demonstrates your lack of knowledge on contemporary biology. Notably it was published in Science 2001. Everybody reads Science! Except ostriches, I guess.--------------------------------------------------------------------------------Yeah, ostiches and arrogant overconfident creationists, I guess.THANKS FOR THE DISCUSSION, AND HAVE A NICE WEEKEND,
PETER[This message has been edited by peter borger, 10-05-2002]

Dear Dr Page,Why don't you just answer this very simple little question?Are neutral positions in the DNA expected to change faster over time?If yes, please explain.
If no, please explain.Best wishes,
Peter[This message has been edited by peter borger, 10-06-2002]

dear mammuthus,
thanks for the references, and you are right w.r.t the unwarranted conclusion.BW,
Peter

Dear WI,The single mutation you are referring to is the deletion of a nucleotide in exon X that induced a frameshift, I presume. I do not know of any study in which the frameshift was reversed to assess whether vit c synthesis was restored. It can be expected that after the frameshift in exon X more mutations have been introduced in other exons of the gene too.BW
Peter

Dear Taz,you write:
Hi Peter, the largest problem with your statements concerning mutation and randomness appear to me to be a confusion with respect to: 1) randomness with an equal probability of a specific occurance over the range of possibilities, 2) randomness with a non-equal proability of a specific occurance over a range of possibilities, 3) and a non-random occurance of a specific possibility over a range. I am sure that there is a better statistical means of saying this, my stats are self taught although sufficient to compile, analyze and submit clinical and production data through the FDA.NDS deals with the second, not the first as you seem to be indicating.I say:
Let's assume you are right.Next you say:
In fact, every reference that you have pointed out supports this treatment of the results far more than number 3 (your apparent approach).I say:
Could you please expand a bit for the 1G5 gene.
In my opinion, the mutations are introduced in the 1g5 gene independent of histons, since then one would expect them to occur roughly every 200 bp, and they don't. Besides, the mutations are also non-random with respect to NUCLEOTIDE and POSITION. Two non-random phenomena in one gene.You say:
The Science paper on Histones, which I had on hand, is very supportive of this interpretation as well.I say:
What Science paper on histones? Ref?You say:
The higher rate of mutations in actively transcribing genes has been well known for years.I say:
So, mutations are independent from DNA replications? A similar observation has been demonstrated for ZFY in comparison to ZFX regions (Kim et al, J of ? will look it up) So, it is dependent on transcription? Nicely fits in my hypothesis.You say:
The fact that both the primary and secondary structure of genes play a role in the probability of a mutational event at those sites is also well known.I say:
So, actually you say there is a mutation inducing mechanism that involves the structure of genes? That would also nicely fit in my hypothesis. Could you expand a bit on this with references, please?You say:
The mutational frequency that everyone talks about is an average of the much higher probability sites and the much lower probability sites. Your directed mutation seems to me to be nothing more than the increased probability based on structural features and is therefor not in conflict with NDS at all.I say:
God doesn't play dice .best wishes,
Peter

dear taz,You write:
quote:
--------------------------------------------------------------------------------
Originally posted by wj:
I am curious as to whether the GLO pseudogene issue, previously mentioned on this thread, was ever resolved.
Is there any evidence that humans synthesise ascorbic acid, either through spontaneous oxidation (message #101) or some undiscovered pathway? Is there any evidence of a population of vitamin C synthesisers such as nomads or eskimos?--------------------------------------------------------------------------------I have been able to find no evidence to back up PB's claims (Peter, I am using PB to differentiate you from the other pro-evolution Peter, hope that you do not mind).I say:
No, I don't.You say:
Peters "source" for the two fold mutation was a comment by a person claiming to be a researcher posting onto a medical questions board.
He essentially claimed that 1) there was also a mutation in a lactonase based activity gene and 2) that the reaction which glo performed occured at low rates in situ. I have been unable to find ANY data suporting assertion number one in any of the medical, biological or biochemical publications and I have associates with access to the most wide ranging databases in the world.I say:
Thanks for your searches. We need this elusive Dr Banschbach, I guess.You say:
I think that assertion number two is in error as the oxidation/reduction event required for the generation of the same intermediate as the GLO gene synthesises occurs under more stringent conditions than are generally found in vivo, namely strong acids and a metallic catalyst (info from Strietweiser, Organic Chemistry).I say:
Has anybody ever attempted to look at these things in vitro? I mean, have hepatocytes been cultured and assessed for vit c production and/or lactonase expression? And has been discriminated between productions and release? (For instance, does addition of a protein synthesis inhibitor block lactonase production, but not the release of vit c?). I am not aware of such studies, but I would really like to know. Otherwise they have to be performed.You say:
The second oxidation/reduction event which actually produces ascorbic acid is spontaneous but it is helped along by its position next to the first and by a resulting partial resonance structure. Finally, the rate of production cited by PB's source is actually the release rate by the liver in dietery scurvy conditions.I say:
The release rate does not say anything about the production rate (if still produced, I mean). If it is stored in the liver how long would it take for the liver to be depleted? Do you know, Taz?
However, there were considerable amounts of survivers during the long overseas voyages in the 15-16 century that could last up to 6-12 months, indicating that this part of the population still had vit c, since they didn't die from scurvy. Was it due to an excellent storage system or due to low productions? Both would make the GLO gene redundant, though.You say:
As to the eskimoes and nomads, the only data that I found dealt with eskimo's and it was discovered that, beofre their diets changed, they ate a lot of raw fish which was rich in ascorbic acid. So much for a sub-population which made ascorbic acid.quote:
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In Peter Borger's scenario of directed (by environmental factors) mutations, wouldn't deprivation of dietary vitamin C be a significant directing environmental factor? If only a single mutation is required to convert the GLO pseudogene back to a functional GLO gene and prevent scurvy, why hasn't this mutation been witnessed in dietary stressed humans?
--------------------------------------------------------------------------------If the vitamin was not present in the diet (a level of 200 - 400 mg/day is easily achieved) then yes, it would be a stresor. As to the mutations, I believe that there have been subsequent, non-shared, mutations in the glo gene since the first primate mutational event long ago. I have been unable to get to the NIH to get the paper so I do not have sequence data here. The final answer is that I do not think that there is data in eukaryotes to support PB's directed mutagenesis claims, in any genes.I say:
The latter is only a matter of opinion. As mentioned in previous letters to this board, there may be two types of mutations: random and non-random. Therefore, it can be speculated from exon X of the GLO gene that both types of mutations play a role in the accumulation of mutations in this gene.
The evolutionary vision is that the shared mutations have been introduced in the ancestor and are inherited afterwards. So you see a nice alignment of mutations on certain spots. Evidence for common descent! Other mutations are not shared and have therefore recently been mutated and are not shared. At least that is the evolutionary claim. However, if both a non-random and a random mechanism are involved, the shared mutations could be due to a mechanism, while the non-shared mutations are due to randomness (= equivalent to the evolutionary explanation). We would also observe alignment of mutations, albeit not due to common descent.
A close look at the 1G5 gene in Drosophila demonstrates that shared mutations can be introduced irrespective of common descent. To be specific, the mutations introduced in the subpopulations found in Italy, Peru and USA III are non-random with respect to position and nucleotide, i.e. same spot, same nucleotide. If the study was carried out in only these three subpopulations the evolutionary conclusion would be that they are all derived from the same ancestor. However, since there are 10 additional subpopulation for comparison, direct common ancestry is highly doubtful (As explained in mail #1 of this thread).
Similar results are found for mutations in subpopulations in Australia III and USA I, and for Japan and Peru. These are the non-random mutations. In addition, one also finds random mutations. The Ig5 gene in D. simulans demonstrates similar, albeit less pronounced, results. Even indel-mutations may be non-random as observed in these sequences.
In conlusion, mutations in the same spot in genes from distinct but related organisms may be the result of a non-random mechanism, while also random mutations exist. Bottomline is, it may be impossible to discriminate between common descent or a common non-random mechanism.Best wishes,
Peter[This message has been edited by peter borger, 10-07-2002]