More non-random evolution

So as to let Quetzal continue this without distraction from me, I want to address only one point here. Your theory of repair based "non-randomness" is falisfied for mtDNA which do not have an established DNA repair machanism.It also occurs to me that if you use your definition of non-randomness (though it has changed from time to time) , I should be able to pinpoint exactly the mutation in every somatic cell I have (germ cells as well of course) for any mutation just before it happens. Can you do this...where will the next mutation in my genome occur Peter if it is non-random? Easier question, where will the next mutation in my mtDNA HVI region occur?Cheers,
M

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Since my discovery of non-random mutations I checked some sequences and indeed there is non-random mutation with respect to nucleotide and position. So, let's redefine what a mean by non-randomness of mutations.

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Your discovery? Too funny — you really put your finger on the problem right there. You’re the only one to find this miracle anywhere. No wonder you want to redefine the terminology - it's the only way your assertions have any merit, even in your own mind.

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By non-random mutations I mean non-random with respect to i) type of nucleotide and ii) position where it is introduced. Whether or not there is a mechanism involved is at this point not relevant. This non-randomness can also be demonstrated for mtDNA (PNAS 2001, 98:537-542). A careful look shows non-random mutations on several position of the analyzed mtDNA fragment of 309 base pairs. To be exact, nucleotide positions 107, 184, 201, 223, 263, 264, 301, 307, 362, and 387 involve all this principle of non-random mutation: same nucleotide introduced on same spot, even in bonobo, neanderthaler and human subspecies. Now you have to give me a very good reason to insist on random mutation. MtDNA does not have histons, and I already checked for 5-methyl-cysteine hotspots. Some of them are, the majority isn't.

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I must have missed something. Please indicate specifically where in this paper on human phylogeny you cite, Mitochondrial DNA sequences in ancient Australians: Implications for modern human origins there is any indication of non-random mutations. All the paper is talking about are divergent mtDNA genomes as a basis for re-assessing the validity of mtDNA phylogenies. It basically calls into question the timing of the out of Africa hypothesis. I included a link to the full paper in the hopes that Dr. T or Mammuthus might take a glance at it and address your specific contention concerning the nucleotide positions. To me, it certainly appears you are jumping WAY out on a limb using this paper as support for the existence of non-random mutations.

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(Reference mechanisms)
I already gave a possible explanation in a previous letter. It was something like this: In response to DNA damage an SOS repair mechanism is activated that mends the DNA thereby introducing the same mutations on the same spot. Since the same families have the same repair mechanism and related DNA sequences the nucleotides are non-randomly replaced, and that may give the illusion of common descent. And, you have misunderstood my assumption of morphogenetic fields. By this I mean ‘creaton (virtual particles) interaction with matter in a morphogenetic field (earth) that give rise to genes’. It merely explains the sudden appearance of new gene families in organism during ‘evolution’. You may abbreviate it to ‘creaton interaction’ or ‘creat-ion’ (pronounce: creation), if you like. I don’t need this mechanism to explain shared mutations between related species.

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You seem to be saying that repair mechanisms cause mutation? This is a very odd assertion. As to the creaton particles: what the heck are these? And what is morphogenetic field (earth) supposed to mean? Is it something like N-rays? Congratulations, you’ve actually gone beyond even creationism to something straight out of New Age pseudoscience. Of COURSE you can provide evidence that these magical particles and fields exist? I mean, they’ve been detected, right? There is some journal somewhere that’s got published articles we can read?

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Q: Somehow I doubt that you read the article

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PB: I didn’t read them yet, but I though ‘why not respond for the sake of discussion’. Today, I looked them up and will read them over the weekend.

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Article, singular. Glad you admit you made the whole statement/question up out of whole cloth.

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Q: And here's another one (on line for all you cheapskates): Hatahet, Z., M Zhou, LJ Reha-Krantz, SW Morrical and SS Wallace. 1998. In search of a mutational hotspot PNAS 95: 8556-8561.
Hotspots are caused by structural susceptibility at specific points on the DNA to specific mutagens. All evidence suggests that that it is simply a structural defect, and that location and surrounding codons have a major impact on whether a particular DNA site is a "hotspot" or "coldspot".

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IOW, Peter, there's no god/designer diddling with DNA - just a statistically higher likelihood of mutation caused chemical/structural idiosyncracies and crappy repair.

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PB: Whether or not these hotspots where designed cannot be concluded from the manucripts. However, the article shows that location and surrounding codons may have a decisive role in the outcome of the mutation. If so, than these mutations are non-random (hotspots), and since it may involve specific codons it clearly suggests a mechanism. Therefore, the alignment of mutations observed in related species may be due to such common mechanisms, instead of common descent.

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However, the specific sequences, which ARE inherited, are what cause the hotspots in the first place. If they weren’t inherited, the next generation wouldn’t have them. A particular hotspot shared between two different species means the two species share a common sequence. Since the ONLY way they can share a common sequence is by inheritance, the two species share a common ancestor. You can twist and turn on this as much as you want, it doesn’t change the fact.

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Q: The mechanism that you keep harping on is a chemical/structural failure at that spot. It is no different than a rope with a flaw preferentially breaking at that flaw under strain.

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PB: The mutations I talk about are NON-random with respect to nucleotide and position.

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Nope, wrong again. This assertion only stands if the particular environmental factor ONLY effects a particular spot on the genome 100% of the time. This isn’t the case. A mutagen, for example, CAN effect basically anywhere on a genome. However, there is often a chemical affinity for a particular point. At that particular point, it may be slightly MORE likely to cause a mutation. However, there’s no 100% guarantee. Hence, mutations remain random with respect to location, time, effect, or even IF.

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Q: Environmental factors such as chemical mutagens are the strain that effects the DNA strand. Whereas the strain will be applied across the strand, only the weak point will be effected (or at least, will be effected first). It remains random (although statistically more probable) because it is impossible to predict a) when the mutation will occur; b) whether or not the particular mutagen WILL in fact effect the hotspot — it’s not guaranteed that simply the presence of the mutagen will have any effect at all; and c) whether or not the mutation will have any effect on the organism once it occurs — often it simply kills the cell. Hotspots DO NOT provide any support for your ridiculous assertion concerning non-randomness falsifying evolutionary theory, for the simple reason that a mutation at a specific hotspot remains random under the definition of the term as used in biology and genetics. Your continual attempts to redefine what random means are specious, at best.

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PB: Apparently, hotspots introduced by these mutagens have a different repair mechanisms. Questions: do you think that these mutagens induce only hotspot-mutations in the p53 gene or also in other genes? Randomly? Or dependent on DNA sequence?

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Also in others, especially such things as ionizing radiation. Randomly, but with a non-exclusive affinity for certain sequences. Maybe (still under investigation).

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Q: As far as common descent goes, mutational hotspots — weaknesses in the DNA rope — CAN be used if and only if the specific sequence that creates the hotspot is present in some organisms and not others. On the other hand, they DON’T provide support for common design for the same reason — the exact sequences aren’t present in every organism.

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PB: But the could be present in the same kind of organisms. Family level or even higher levels.

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Hunh?

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Apparently the hotspots are induced by a specific external chemical and induced a particular repair response. I will elaborate on this matter next week, first spell out the article on this topic.

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Oh goody. I can hardly wait.

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Q: What’s YOUR point about repair mechanisms and primates? Your statement is a complete non-sequitur.

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PB: If the hotspots are associated with repair mechanism and these repair mechanism are similar/same in all primates, than I also expect the mutagen to induce the same kind of mutations in --let’s say-- human, chimps, bonobo’s.

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I’d say the latter part about mutagens is quite likely — in fact, is observed. That’s why experiments on primates are usually so indicative. The cruelty to animals folks does tend to put a crimp in experimentation, though. As to the first — mutations are not caused by repair mechanisms. When you first mentioned this above, I thought I was misunderstanding you. You really don’t have a clue about basic biology, do you?

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Originally posted by peter borger:
Dear Dr Page,

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If you like to educate me, go ahead and provide me with the refernces and I will have a look at the methodology.
Convince me that you are right and try to overcome your condescending attitude.

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"My" condesacending attitude? That is rich ... Hmmm... Let's see - an asthma researcher comes here proclaiming that he has falsified NDT, and "I" am being condescending?Well, anyway, again, I should have thought that someone that argues about phylogenetics methods would at least be familkiar with them, but I guess not. I should have remembered - creationists always argue well outside of their actual fields of knowledge, and do so with an unwarranted air of authority.Here is one of many:Science 1991 Oct 25;254(5031):554-8Gene trees and the origins of inbred strains of mice.Atchley WR, Fitch WM.From the abstract:"Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains... "

dear Quetzal,YOU SAY:quote:
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Since my discovery of non-random mutations I checked some sequences and indeed there is non-random mutation with respect to nucleotide and position. So, let's redefine what a mean by non-randomness of mutations.
--------------------------------------------------------------------------------Your discovery? Too funny — you really put your finger on the problem right there. You’re the only one to find this miracle anywhere. No wonder you want to redefine the terminology - it's the only way your assertions have any merit, even in your own mind.I SAY:That remains to be seen.YOU SAY:quote:
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By non-random mutations I mean non-random with respect to i) type of nucleotide and ii) position where it is introduced. Whether or not there is a mechanism involved is at this point not relevant. This non-randomness can also be demonstrated for mtDNA (PNAS 2001, 98:537-542). A careful look shows non-random mutations on several position of the analyzed mtDNA fragment of 309 base pairs. To be exact, nucleotide positions 93,184, 201, 223, 263, 264, 301, 307, 362, and 387 involve all this principle of non-random mutation: same nucleotide introduced on same spot, even in bonobo, neanderthaler and human subspecies. Now you have to give me a very good reason to insist on random mutation. MtDNA does not have histons, and I already checked for 5-methyl-cysteine hotspots. Some of them are, the majority isn't.
--------------------------------------------------------------------------------I must have missed something. Please indicate specifically where in this paper on human phylogeny you cite, Mitochondrial DNA sequences in ancient Australians: Implications for modern human origins there is any indication of non-random mutations. All the paper is talking about are divergent mtDNA genomes as a basis for re-assessing the validity of mtDNA phylogenies. It basically calls into question the timing of the out of Africa hypothesis. I included a link to the full paper in the hopes that Dr. T or Mammuthus might take a glance at it and address your specific contention concerning the nucleotide positions. To me, it certainly appears you are jumping WAY out on a limb using this paper as support for the existence of non-random mutations.I SAY:
Thanks for the link to the paper. If you have a close look at table 1, and read it from top to bottom and concentrate on the positioned I mentioned before you will find out that the mutations on these spots are the same with respect to nucleotide. For instance, compared to CRS position 93 all mutations observed are T-->C transitions, independent of the organism. Similar, position 184, all C-->T; position 223, all C-->T; position 230, all A-->G; position 278, all C-->T; position 311, all C-->T; and position 387, all A-->G. They cannot all be explained by 5-methylcytosine hotspots (= a mechanism). So, my claim of non-randomness with respect to position and nucleotide is valid. Whether or not a mechanism is involved remains to be established. It should be noted that in a previous letter (to Mark24) I already mentioned that two types of mutations may exist, random and non-random. Here I present further evidence for this vision.YOU WRITE:quote:
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(Reference mechanisms)
I already gave a possible explanation in a previous letter. It was something like this: In response to DNA damage an SOS repair mechanism is activated that mends the DNA thereby introducing the same mutations on the same spot. Since the same families have the same repair mechanism and related DNA sequences the nucleotides are non-randomly replaced, and that may give the illusion of common descent. And, you have misunderstood my assumption of morphogenetic fields. By this I mean ‘creaton (virtual particles) interaction with matter in a morphogenetic field (earth) that give rise to genes’. It merely explains the sudden appearance of new gene families in organism during ‘evolution’. You may abbreviate it to ‘creaton interaction’ or ‘creat-ion’ (pronounce: creation), if you like. I don’t need this mechanism to explain shared mutations between related species.
--------------------------------------------------------------------------------You seem to be saying that repair mechanisms cause mutation? This is a very odd assertion.I SAY:
Actually, what I say is that aspecific damage to DNA (by radiation, oxidation, etc) will be repaired, and that the repair mechanism may introduce the same nucleotide on the same spot over and over. This induces the illusion of common descent. Moreover, if comparable mechanisms exist as observed with 5-methylcytosine induced C-->T transitions than this may also contribute to the illusion of common descent.YOU SAY:As to the creaton particles: what the heck are these? And what is morphogenetic field (earth) supposed to mean? Is it something like N-rays?I SAY:I only introduced the idea of a creatons interacting with matter in a morphogenetic field to explain new genes. Evolutionism cannot explain them, this view can. What the heck is a creaton? What the heck is a graviton? I guess nobody knows. Except that gravitons transmit gravitation. Similarly, creatons convey creation. Did you really expect the Creator to be a bearded man on a cloud?You say:
Congratulations, you’ve actually gone beyond even creationism to something straight out of New Age pseudoscience. Of COURSE you can provide evidence that these magical particles and fields exist? I mean, they’ve been detected, right? There is some journal somewhere that’s got published articles we can read?I SAY:
Like gravitons, they have not been detected. But they can be inferred from what we see. We see sudden appearance of new genes, new organisms in the genetic and fossil record: creaton interactions in a morphogenetic field (earth) elegantly explain this. For clarity, I do not need this hypothesis to explain common mutations, since the can be explained by non-random mechanisms.YOU WRITE:quote:
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Q: Somehow I doubt that you read the article
PB: I didn’t read them yet, but I though ‘why not respond for the sake of discussion’. Today, I looked them up and will read them over the weekend.--------------------------------------------------------------------------------Article, singular. Glad you admit you made the whole statement/question up out of whole cloth.quote:
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Q: And here's another one (on line for all you cheapskates): Hatahet, Z., M Zhou, LJ Reha-Krantz, SW Morrical and SS Wallace. 1998. In search of a mutational hotspot PNAS 95: 8556-8561.
Hotspots are caused by structural susceptibility at specific points on the DNA to specific mutagens. All evidence suggests that that it is simply a structural defect, and that location and surrounding codons have a major impact on whether a particular DNA site is a "hotspot" or "coldspot".
IOW, Peter, there's no god/designer diddling with DNA - just a statistically higher likelihood of mutation caused chemical/structural idiosyncracies and crappy repair.PB: Whether or not these hotspots where designed cannot be concluded from the manuscripts. However, the article shows that location and surrounding codons may have a decisive role in the outcome of the mutation. If so, than these mutations are non-random (hotspots), and since it may involve specific codons it clearly suggests a mechanism. Therefore, the alignment of mutations observed in related species may be due to such common mechanisms, instead of common descent.--------------------------------------------------------------------------------However, the specific sequences, which ARE inherited, are what cause the hotspots in the first place. If they weren’t inherited, the next generation wouldn’t have them. A particular hotspot shared between two different species means the two species share a common sequence. Since the ONLY way they can share a common sequence is by inheritance, the two species share a common ancestor. You can twist and turn on this as much as you want, it doesn’t change the fact.I SAY:
Not the ONLY way. Another way involves common design through creation.YOU SAY:quote:
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Q: The mechanism that you keep harping on is a chemical/structural failure at that spot. It is no different than a rope with a flaw preferentially breaking at that flaw under strain.
PB: The mutations I talk about are NON-random with respect to nucleotide and position.--------------------------------------------------------------------------------Nope, wrong again. This assertion only stands if the particular environmental factor ONLY effects a particular spot on the genome 100% of the time. This isn’t the case. A mutagen, for example, CAN effect basically anywhere on a genome. However, there is often a chemical affinity for a particular point. At that particular point, it may be slightly MORE likely to cause a mutation. However, there’s no 100% guarantee. Hence, mutations remain random with respect to location, time, effect, or even IF.I SAY:
Apparently, this is not entirely true judging the 1G5 gene and the mtDNA sequences in subpopulations of humans and primates (see above).YOU SAY:quote:
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Q: Environmental factors such as chemical mutagens are the strain that effects the DNA strand. Whereas the strain will be applied across the strand, only the weak point will be effected (or at least, will be effected first). It remains random (although statistically more probable) because it is impossible to predict a) when the mutation will occur; b) whether or not the particular mutagen WILL in fact effect the hotspot — it’s not guaranteed that simply the presence of the mutagen will have any effect at all; and c) whether or not the mutation will have any effect on the organism once it occurs — often it simply kills the cell. Hotspots DO NOT provide any support for your ridiculous assertion concerning non-randomness falsifying evolutionary theory, for the simple reason that a mutation at a specific hotspot remains random under the definition of the term as used in biology and genetics. Your continual attempts to redefine what random means are specious, at best.
PB: Apparently, hotspots introduced by these mutagens have a different repair mechanisms. Questions: do you think that these mutagens induce only hotspot-mutations in the p53 gene or also in other genes? Randomly? Or dependent on DNA sequence?--------------------------------------------------------------------------------Also in others, especially such things as ionizing radiation. Randomly, but with a non-exclusive affinity for certain sequences. Maybe (still under investigation).I SAY:
And that would make them NON-random mutations with respect to position and (possibly) nucleotide, isn’t it?YOU WRITE:quote:
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Q: As far as common descent goes, mutational hotspots — weaknesses in the DNA rope — CAN be used if and only if the specific sequence that creates the hotspot is present in some organisms and not others. On the other hand, they DON’T provide support for common design for the same reason — the exact sequences aren’t present in every organism.
PB: But the could be present in the same kind of organisms. Family level or even higher levels.--------------------------------------------------------------------------------Hunh?I SAY:
If the genomes have been created similarly (for instance the primates and human), than I expect that shared DNA sequences are equally prone to NON-random mutations. Thus, line up of mutations and an illusion of common descent.quote:
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Apparently the hotspots are induced by a specific external chemical and induced a particular repair response. I will elaborate on this matter next week, first spell out the article on this topic.
--------------------------------------------------------------------------------Oh goody. I can hardly wait.quote:
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Q: What’s YOUR point about repair mechanisms and primates? Your statement is a complete non-sequitur.
PB: If the hotspots are associated with repair mechanism and these repair mechanism are similar/same in all primates, than I also expect the mutagen to induce the same kind of mutations in --let’s say-- human, chimps, bonobo’s.--------------------------------------------------------------------------------I’d say the latter part about mutagens is quite likely — in fact, is observed. That’s why experiments on primates are usually so indicative. The cruelty to animals folks does tend to put a crimp in experimentation, though.I SAY:
I agree, it should be banned.YOU SAY:
As to the first — mutations are not caused by repair mechanisms. When you first mentioned this above, I thought I was misunderstanding you.I SAY:Read my explanation above.YOY SAY:You really don’t have a clue about basic biology, do you?I SAY...
...No comments.Best wishes,
Peter[This message has been edited by peter borger, 10-13-2002]

Dear Mammuthus,You say:
So as to let Quetzal continue this without distraction from me, I want to address only one point here. Your theory of repair based "non-randomness" is falisfied for mtDNA which do not have an established DNA repair machanism.I say:
So, the mechanism is nucleus dependent and/or similar to 5-methylcytosine hostpots. Both would result in alignment of non-random mutations.You say:
It also occurs to me that if you use your definition of non-randomness (though it has changed from time to time) , I should be able to pinpoint exactly the mutation in every somatic cell I have (germ cells as well of course) for any mutation just before it happens. Can you do this...where will the next mutation in my genome occur Peter if it is non-random? Easier question, where will the next mutation in my mtDNA HVI region occur?I say:
Most likely it would involve position 223 or position 311.Best wishes,
Peter

Hmm, we seem to be getting the same arguments on two different threads.Again, with reference to Table 1 in the link I posted, I am not a genomics researcher. I hope that one of our experts here will take a look and provide a more substantive response.

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Actually, what I say is that aspecific damage to DNA (by radiation, oxidation, etc) will be repaired, and that the repair mechanism may introduce the same nucleotide on the same spot over and over. This induces the illusion of common descent. Moreover, if comparable mechanisms exist as observed with 5-methylcytosine induced C-->T transitions than this may also contribute to the illusion of common descent.

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You are aware, of course, that one of the most common point mutations is C-->T deamination? It's usually repaired fairly easily by glycosylase. There are at least 8 different kinds of glycosylase for example - each one repairing a particular kind of base damage. Basically, every single mutation requires a distinct, seperate mechanism for repair. Only when these already-present repair mechanisms fail or are overwhelmed is there mutation that carries over. IOW, repair means it puts the DNA strand back together just like it was. OF COURSE it introduces the same nucleotide during repair - or the same sequence of nucleotides. There's no other way it CAN repair. I think you're missunderstanding how DNA repair works.

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I only introduced the idea of a creatons interacting with matter in a morphogenetic field to explain new genes. Evolutionism cannot explain them, this view can. What the heck is a creaton? What the heck is a graviton? I guess nobody knows. Except that gravitons transmit gravitation. Similarly, creatons convey creation. Did you really expect the Creator to be a bearded man on a cloud?

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Yet there is no evidence anywhere in any literature that indicates that genes have been poofed into existence de novo in response to environmental changes. Quoting from my response to this assertion in the other thread in case you missed it:

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There is absolutely no evidence for this assertion. Please show one single study, with references, on any population of any organism, where the introduction of a new pathogen, mutagen, or environmental factor produced fortuitous variation that allowed the population to adapt to the new conditions.

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Unlike, for instance, the possible existence of the hypothetical graviton particle - which is inferred from the obvious fact that two masses exert an attraction on each other - there is NO evidence of any kind that your creatons and morphogenetic fields exist.

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Like gravitons, they have not been detected. But they can be inferred from what we see. We see sudden appearance of new genes, new organisms in the genetic and fossil record: creaton interactions in a morphogenetic field (earth) elegantly explain this. For clarity, I do not need this hypothesis to explain common mutations, since the can be explained by non-random mechanisms.

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Quite simply, Peter, no we don't, and no it doesn't. You multiplied the assumptions beyond any reasonable explanatory power. Demonstrate your assertion...

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Not the ONLY way. Another way involves common design through creation.

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Please, please show us how creation/common design explains inheritance and the observations from population genetics.

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And that would make them NON-random mutations with respect to position and (possibly) nucleotide, isn’t it?

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Nope, it doesn't, unless you plan on completely redefining statistical probability along with your redefinition of random.

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Originally posted by peter borger:
Dear Mammuthus,

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You say:
So as to let Quetzal continue this without distraction from me, I want to address only one point here. Your theory of repair based "non-randomness" is falisfied for mtDNA which do not have an established DNA repair machanism.

​

I say:
So, the mechanism is nucleus dependent and/or similar to 5-methylcytosine hostpots. Both would result in alignment of non-random mutations.

​

You say:
It also occurs to me that if you use your definition of non-randomness (though it has changed from time to time) , I should be able to pinpoint exactly the mutation in every somatic cell I have (germ cells as well of course) for any mutation just before it happens. Can you do this...where will the next mutation in my genome occur Peter if it is non-random? Easier question, where will the next mutation in my mtDNA HVI region occur?

​

I say:
Most likely it would involve position 223 or position 311.

​

Best wishes,
Peter

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*********************Hi Peter,Quetzal's post above addresses questions that I would also like to see answered so I won't post more than to ask the following.Likely positions 223 or 311? If it is non random than why not with absolute certainty? There are individuals with mutations outside of these positions. How do you explain those?Your definition of non-random just became one of randomness cheers,
M

PB writes:

quote:

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Actually, what I say is that aspecific damage to DNA (by radiation, oxidation, etc) will be repaired, and that the repair mechanism may introduce the same nucleotide on the same spot over and over. This induces the illusion of common descent. Moreover, if comparable mechanisms exist as observed with 5-methylcytosine induced C-->T transitions than this may also contribute to the illusion of common descent.

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Wow...So disparate - non-related, of course - species have DNA repair mechanisms that do the exact same thing to the exact same nucleotides AT the EXACT SAME LOCUS.Truly amazing discovery...Odd then that when one looks at actual data (I assume that PB has yet to actually look at any data) one sees nothing at all like what should be expected if repair mechanisms in unrelated taxa worked as indicated above.

Dear Quetzal,YOU SAY:Hmm, we seem to be getting the same arguments on two different threads.
Again, with reference to Table 1 in the link I posted, I am not a genomics researcher. I hope that one of our experts here will take a look and provide a more substantive response.MY RESPONSE:
You don't have to be a genomic researcher. It is obvious from the sequences of the 1G5 gene and the mtDNA in subpopulations.YOU SAY:quote:
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Actually, what I say is that aspecific damage to DNA (by radiation, oxidation, etc) will be repaired, and that the repair mechanism may introduce the same nucleotide on the same spot over and over. This induces the illusion of common descent. Moreover, if comparable mechanisms exist as observed with 5-methylcytosine induced C-->T transitions than this may also contribute to the illusion of common descent.
--------------------------------------------------------------------------------You are aware, of course, that one of the most common point mutations is C-->T deamination? It's usually repaired fairly easily by glycosylase. There are at least 8 different kinds of glycosylase for example - each one repairing a particular kind of base damage. Basically, every single mutation requires a distinct, seperate mechanism for repair. Only when these already-present repair mechanisms fail or are overwhelmed is there mutation that carries over. IOW, repair means it puts the DNA strand back together just like it was. OF COURSE it introduces the same nucleotide during repair - or the same sequence of nucleotides. There's no other way it CAN repair. I think you're missunderstanding how DNA repair works.MY RESPONSE:
In addition to this mechanism that always introduces C-->T tranversions, there is also the mechanism of C--> tranversions due to 5-methylcytosine conversions. After reading your reference, I realised there is another mecahnism involved in generation of oxidative stress induced mutations. As described by Hatahet et al (PNAS 1998, 95:8556) there is a consensus sequence that modulate the frequency of misincorporation 8-oxoguanine by DNA polymerase. This mechanism is also likely to contribute to the illusion of common descent. In particular in mtDNA sequences. Finally, it is becoming increasingly evident that junk DNA may be used to repair DNA (Nature Genetic JUNE 2002, if I recall properly) and may also lead to the introduction of the same nucleotide on th same spot.YOU WRITE:quote:
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I only introduced the idea of a creatons interacting with matter in a morphogenetic field to explain new genes. Evolutionism cannot explain them, this view can. What the heck is a creaton? What the heck is a graviton? I guess nobody knows. Except that gravitons transmit gravitation. Similarly, creatons convey creation. Did you really expect the Creator to be a bearded man on a cloud?
--------------------------------------------------------------------------------Yet there is no evidence anywhere in any literature that indicates that genes have been poofed into existence de novo in response to environmental changes. Quoting from my response to this assertion in the other thread in case you missed it:quote:
--------------------------------------------------------------------------------
There is absolutely no evidence for this assertion. Please show one single study, with references, on any population of any organism, where the introduction of a new pathogen, mutagen, or environmental factor produced fortuitous variation that allowed the population to adapt to the new conditions.
--------------------------------------------------------------------------------Unlike, for instance, the possible existence of the hypothetical graviton particle - which is inferred from the obvious fact that two masses exert an attraction on each other - there is NO evidence of any kind that your creatons and morphogenetic fields exist.MY RESPONSE:
No evidence? Whole families of new genes show up in the genomic record. If I'm correct, this is Tranquility Base's major point. The sudden appearance of such new gene families in organisms should be sufficient evidence.
If you really want me to completely falsify and overturn evolution theory, let me know, and I will present the example of an organism that are gentically identical without being a clone. So, this organism can be interpreted as being created yesterday, last year, last century, whenever. It hasn't been published in peer reviewed journals (for the obvious reason), but a book on the topic was published in 2000. It is the final blow to evolution theory, and strong support for the hypothesis of 'creation of a multipurpose genome'.YOU WRITE:quote:
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Like gravitons, they have not been detected. But they can be inferred from what we see. We see sudden appearance of new genes, new organisms in the genetic and fossil record: creaton interactions in a morphogenetic field (earth) elegantly explain this. For clarity, I do not need this hypothesis to explain common mutations, since the can be explained by non-random mechanisms.
--------------------------------------------------------------------------------Quite simply, Peter, no we don't, and no it doesn't. You multiplied the assumptions beyond any reasonable explanatory power. Demonstrate your assertion...MY RESPONSE:
I supported my assertions several times. However, evolutionism also seems to have an 'explanation'. So, it will be my explanation against evolutionism's explanation.YOU WRITE:quote:
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Not the ONLY way. Another way involves common design through creation.
--------------------------------------------------------------------------------Please, please show us how creation/common design explains inheritance and the observations from population genetics.MY RESPONSE:
In the multipurpose genome 'all' genes that contribute to variation are already present. Variation is induces by genetic elements that affect gene regulation --and therefore gene expression--, and probably shuffle from one place in the genome to another. All observations of population genetics can be explained since it only involves (regulation of) frequencies of alleles. If populations get isolated they may 'speciate' due to loss and/or shuffling of genes. Furthermore, entropy acting on the genome can account for all degenerative observations in the genome (for instance, the inactivation of genes that are more or less redundant). Finally, mechanisms that introduce mutations non-randomly can explain the illusion of common descent.YOU WRITE:quote:
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And that would make them NON-random mutations with respect to position and (possibly) nucleotide, isn’t it?
--------------------------------------------------------------------------------Nope, it doesn't, unless you plan on completely redefining statistical probability along with your redefinition of random.MY RESPONSE:
Maybe we have to do that.Best wishes,
Peter[This message has been edited by peter borger, 10-14-2002]

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You don't have to be a genomic researcher. It is obvious from the sequences of the 1G5 gene and the mtDNA in subpopulations.

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It is quite easy to make assertions. Anyone — expert or not — can do that. However, to counter the assertions it is often necessary to have in-depth expertise. This is one of those times. I simply don’t have the background necessary to argue this point. I’m sure someone else does.

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Q: You are aware, of course, that one of the most common point mutations is C-->T deamination? It's usually repaired fairly easily by glycosylase. There are at least 8 different kinds of glycosylase for example - each one repairing a particular kind of base damage. Basically, every single mutation requires a distinct, seperate mechanism for repair. Only when these already-present repair mechanisms fail or are overwhelmed is there mutation that carries over. IOW, repair means it puts the DNA strand back together just like it was. OF COURSE it introduces the same nucleotide during repair - or the same sequence of nucleotides. There's no other way it CAN repair. I think you're missunderstanding how DNA repair works.

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PB: In addition to this mechanism that always introduces C-->T tranversions, there is also the mechanism of C--> tranversions due to 5-methylcytosine conversions. After reading your reference, I realised there is another mecahnism involved in generation of oxidative stress induced mutations. As described by Hatahet et al (PNAS 1998, 95:8556) there is a consensus sequence that modulate the frequency of misincorporation 8-oxoguanine by DNA polymerase. This mechanism is also likely to contribute to the illusion of common descent. In particular in mtDNA sequences. Finally, it is becoming increasingly evident that junk DNA may be used to repair DNA (Nature Genetic JUNE 2002, if I recall properly) and may also lead to the introduction of the same nucleotide on th same spot.

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Actually, the mechanism repairs C-->T deamination errors. If you’ll check, I think you’ll find that 5-methylcytosine is implicated in G-->T mispairing. The glycosylases TDG or MBD4 are the specifics for repair of this particular error. You seem to be confusing repair mechanisms such as the glycosylases with the mutagens that cause the problem in the first place. On another note, here’s a good article on the repair of 8-oxo-G errors: Substrate specificity and Reaction Mechanisms of Murine 8-Oxoguanine-DNA glycosylase.Please provide the full reference for the article you cite. If you're going to use something as evidence, we need to be able to check it.

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No evidence? Whole families of new genes show up in the genomic record. If I'm correct, this is Tranquility Base's major point. The sudden appearance of such new gene families in organisms should be sufficient evidence.

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If you really want me to completely falsify and overturn evolution theory, let me know, and I will present the example of an organism that are gentically identical without being a clone. So, this organism can be interpreted as being created yesterday, last year, last century, whenever. It hasn't been published in peer reviewed journals (for the obvious reason), but a book on the topic was published in 2000. It is the final blow to evolution theory, and strong support for the hypothesis of 'creation of a multipurpose genome'.

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You are merely repeating your assertion. I wouldn’t bank too much on TB’s sudden appearance, as he has yet to show any evidence for this. I’d say the obvious reason your amazing discovery hasn’t been published in the literature is because it doesn’t exist. What book? And why a book and not a journal? The great Evilutionist Conspiracy again?You have failed to answer the question, so I’ll repeat it:

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Q: There is absolutely no evidence for this assertion. Please show one single study, with references, on any population of any organism, where the introduction of a new pathogen, mutagen, or environmental factor produced fortuitous variation that allowed the population to adapt to the new conditions.

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I supported my assertions several times. However, evolutionism also seems to have an 'explanation'. So, it will be my explanation against evolutionism's explanation.

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You have consistently failed to support your assertion. You’ve merely repeated it ad nauseum and then dragged in pointless details that have no bearing on your contention. If there’s evidence, present it. Reveal your magical organism. I promise I won’t steal your Nobel Prize.

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In the multipurpose genome 'all' genes that contribute to variation are already present. Variation is induces by genetic elements that affect gene regulation --and therefore gene expression--, and probably shuffle from one place in the genome to another. All observations of population genetics can be explained since it only involves (regulation of) frequencies of alleles. If populations get isolated they may 'speciate' due to loss and/or shuffling of genes. Furthermore, entropy acting on the genome can account for all degenerative observations in the genome (for instance, the inactivation of genes that are more or less redundant). Finally, mechanisms that introduce mutations non-randomly can explain the illusion of common descent.

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Once again, you’re simply repeating your assertion concerning multipurpose genomes without evidence. Your first part is simply a restatement (simplistically, and leaving out a number of different mechanisms btw) of the random mutation part of RM&NS. The last bit about entropy and degenerative observations doesn’t make any sense. Finally, you have NOT shown that non-random mutations exist — only that you have absolutely no idea what random means in statistics.

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Q: Nope, it doesn't, unless you plan on completely redefining statistical probability along with your redefinition of random.

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PB: Maybe we have to do that.

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Wow — you’re really reaching now, Peter. Gonna re-invent mathematics as well as evolution? Okay — please show the probability equations you propose that overturn current understanding of statistics.[edited for clarity, 'cause there were two back-to-back quotes and it wasn't obvious who said what to whom. ][This message has been edited by Quetzal, 10-15-2002]

This is actually a reply to Peter Borger but I am using the reply to Quetzal as I wanted to expand on a few things he brought up. I also want to know Peter if you are thinking about responses to the points I have brought up or just ignoring me.Originally posted by Quetzal:

quote:

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You don't have to be a genomic researcher. It is obvious from the sequences of the 1G5 gene and the mtDNA in subpopulations.

​

It is quite easy to make assertions. Anyone — expert or not — can do that. However, to counter the assertions it is often necessary to have in-depth expertise. This is one of those times. I simply don’t have the background necessary to argue this point. I’m sure someone else does.

​

Q: You are aware, of course, that one of the most common point mutations is C-->T deamination? It's usually repaired fairly easily by glycosylase. There are at least 8 different kinds of glycosylase for example - each one repairing a particular kind of base damage. Basically, every single mutation requires a distinct, seperate mechanism for repair. Only when these already-present repair mechanisms fail or are overwhelmed is there mutation that carries over. IOW, repair means it puts the DNA strand back together just like it was. OF COURSE it introduces the same nucleotide during repair - or the same sequence of nucleotides. There's no other way it CAN repair. I think you're missunderstanding how DNA repair works.

​

PB: In addition to this mechanism that always introduces C-->T tranversions, there is also the mechanism of C--> tranversions due to 5-methylcytosine conversions. After reading your reference, I realised there is another mecahnism involved in generation of oxidative stress induced mutations. As described by Hatahet et al (PNAS 1998, 95:8556) there is a consensus sequence that modulate the frequency of misincorporation 8-oxoguanine by DNA polymerase. This mechanism is also likely to contribute to the illusion of common descent. In particular in mtDNA sequences. Finally, it is becoming increasingly evident that junk DNA may be used to repair DNA (Nature Genetic JUNE 2002, if I recall properly) and may also lead to the introduction of the same nucleotide on th same spot.

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Actually, the mechanism repairs C-->T deamination errors. If you’ll check, I think you’ll find that 5-methylcytosine is implicated in G-->T mispairing. The glycosylases TDG or MBD4 are the specifics for repair of this particular error. You seem to be confusing repair mechanisms such as the glycosylases with the mutagens that cause the problem in the first place. On another note, here’s a good article on the repair of 8-oxo-G errors: Substrate specificity and Reaction Mechanisms of Murine 8-Oxoguanine-DNA glycosylase.Please provide the full reference for the article you cite. If you're going to use something as evidence, we need to be able to check it.
******************************************************M: I wanted to add that mitochondrial DNA has a primitive repair system at best (for which the evidence of any repair at all is limited). Similarly, there is no "junk DNA" in mitochondria thus it cannot be postulated as a repair mechanism for mtDNA. Thus, your premise is falsified on this count.Second, that transitions are more common than transversions is basic chemistry and hardly constitutes and novel discovery. However, you still cannot pinpoint where the next mutation will occur in a given portion of any DNA sequence thus, non-randomness is falsified.PB: No evidence? Whole families of new genes show up in the genomic record. If I'm correct, this is Tranquility Base's major point. The sudden appearance of such new gene families in organisms should be sufficient evidence.M: If you read the "kinds" thread where I debated TB on this topic for every example he provided I could find primitive versions of the gene families he claimed appeared spontaneously. He was fixated on hemoglobin and I found data demonstrating its presence in bacteria. This propostion of sudden appearance is not supported.PB continued:
If you really want me to completely falsify and overturn evolution theory, let me know, and I will present the example of an organism that are gentically identical without being a clone. So, this organism can be interpreted as being created yesterday, last year, last century, whenever. It hasn't been published in peer reviewed journals (for the obvious reason), but a book on the topic was published in 2000. It is the final blow to evolution theory, and strong support for the hypothesis of 'creation of a multipurpose genome'M: Two fallacies in this statement, genetically identical organisms are by definition clones. If you are referring to twinning this is also natural cloning and twins are actually not 100% identical.
Second fallacy, even if evolutionary theory were to fall, it would neither provide evidence for creationism or for your multipurpose genome idea.Q:
You are merely repeating your assertion. I wouldn’t bank too much on TB’s sudden appearance, as he has yet to show any evidence for this. I’d say the obvious reason your amazing discovery hasn’t been published in the literature is because it doesn’t exist. What book? And why a book and not a journal? The great Evilutionist Conspiracy again?PB:
You have failed to answer the question, so I’ll repeat it:

quote:

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There is absolutely no evidence for this assertion. Please show one single study, with references, on any population of any organism, where the introduction of a new pathogen, mutagen, or environmental factor produced fortuitous variation that allowed the population to adapt to the new conditions.

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M: Look up Richard Lenski. He has published extensively on this subject. I listed two of his papers in the Punctuated Equilibrium thread yesterday. In addition there were the E. coli experiemnts demonstrating that those with retrotransposons were better able to adapt to selection than those without. If YOU would look this stuff up for yourself rather than asserting it does not exist you might gain some credibility.PB:
I supported my assertions several times. However, evolutionism also seems to have an 'explanation'. So, it will be my explanation against evolutionism's explanation.M: It will be your falsified assertions against a theory with supporting evidence.Q:
You have consistently failed to support your assertion. You’ve merely repeated it ad nauseum and then dragged in pointless details that have no bearing on your contention. If there’s evidence, present it. Reveal your magical organism. I promise I won’t steal your Nobel Prize.M: Ig nobel prize perhaps You know, the one for non-reproducible science and unsupportable theories like the origin of belly button lint.PB:
In the multipurpose genome 'all' genes that contribute to variation are already present. Variation is induces by genetic elements that affect gene regulation --and therefore gene expression--, and probably shuffle from one place in the genome to another.M: However, you have ignored my questions with regards to extinction and heredity. Also why there should be any variation at all and why any two organisms should be more similar than any others if all mutation is non-random.PB:
All observations of population genetics can be explained since it only involves (regulation of) frequencies of alleles. If populations get isolated they may 'speciate' due to loss and/or shuffling of genes.M: Do you believe that you are related to your parents Peter or do you believe that storks brought you? If you pick up any book on the genetics of disease you can observe specific alleles segregating in families (not just the disease allele)...this is transmission genetics and is what you are denying occurs. You are stating that at each birth, the genome is reformed poof bang de novo and "created" to appear like the genomes of the parents in some sort of "designed" attempt to mimic hereditary similarity. This is completely unsupported. Genetics in general, Lenski's studies of 10,000 generations of bacterial evolution, and 100 years of hereditary study falsify your contentions as well.PB:
Furthermore, entropy acting on the genome can account for all degenerative observations in the genome (for instance, the inactivation of genes that are more or less redundant).M: This sounds like an L.Ron Hubbard statement. Inactivation of genes can occur by methylation, histone acetylation, insertional mutagenesis, point mutation, deletion etc. Where is entropy involved?PB:
Finally, mechanisms that introduce mutations non-randomly can explain the illusion of common descent.M: This has been falsified by myself, others on this board, and thousands of other researchers who actually know what random means.Q:
Once again, you’re simply repeating your assertion concerning multipurpose genomes without evidence. Your first part is simply a restatement (simplistically, and leaving out a number of different mechanisms btw) of the random mutation part of RM&NS. The last bit about entropy and degenerative observations doesn’t make any sense. Finally, you have NOT shown that non-random mutations exist — only that you have absolutely no idea what random means in statistics.
Q: Nope, it doesn't, unless you plan on completely redefining statistical probability along with your redefinition of random.PB: Maybe we have to do that.M: If you have to mis-define random for your hypothesis to be valid then it was falsified from the beginning without us wasting effort to show the other reasons why it is falsified.Q: Wow — you’re really reaching now, Peter. Gonna re-invent mathematics as well as evolution? Okay — please show the probability equations you propose that overturn current understanding of statistics.M: I would like to see the equations to...and I am still waiting for him to tell me exactly where in HV1 will my next mutation occur? I am making it easy Peter...make it a somatic cell mutation.cheers,
M

Yet another problem for your sudden appearance of gene duplications..Hidden gene duplications
10 October 2002 - Proc. Natl. Acad. Sci. U.S.A.
Arabidopsis thaliana offers botanists a model plant genome. As in other advanced forms of life, the genome of Arabidopsis has experienced gene duplications on a large scale. These may even have included the duplication of all of the plant’s genes. Duplicated genes, however, are often lost, making it difficult to document gene duplication. A new report demonstrates that it is possible to recognize blocks of duplicated genes, despite gene loss, if indirect comparisons are made with other gene segments. In this way, researchers are able to get a good idea of how many times genes have been duplicated during the course of the plant's evolution.Reference: Simillion, C., Vandepoele, K., Van Montagu, M.C.E. et al. 2002. The hidden duplication past of Arabidopsis thaliana. Proc. Natl. Acad. Sci. U.S.A. (online), October 8.

sorry that should have read sudden appearance of novel gene families

In fact mtDNA ONLY appears to have BER for DNA repair and is exposed to much higher oxidative stress. Thus nuclear DNA repair and mtDNA are qualitatively and quantitatively different....where is the next mutation going to occur in my HV1 region? If you cannot tell me then it is a random mutation.1: Prog Nucleic Acid Res Mol Biol 2001;68:257-71 Related Articles, LinksEnzymology of mitochondrial base excision repair.Bogenhagen DF, Pinz KG, Perez-Jannotti RM.Department of Pharmacological Sciences, SUNY at Stony Brook, Stony Brook, New York 11794, USA.A number of laboratories have shown that those types of DNA damage that are generally reparable by base excision repair are efficiently repaired in mtDNA. In contrast, most types of damage that require other sorts of repair machinery are not effectively repaired in mtDNA. We have shown that a set of highly purified mitochondrial proteins, including AP endonuclease (APE), DNA polymerase gamma, and mtDNA ligase, is capable of efficiently repairing abasic (AP) sites in mtDNA. These three enzymes appear to conduct all four steps in a conventional BER mechanism: incision, removal of the 5'-deoxyribosephosphate by dRP lyase, polymerization, and ligation. Both DNA polymerase gamma and mtDNA ligase possess some dRP lyase activity. DNA polymerase gamma is a member of the family A of DNA polymerases, with clear homology to DNA pol I of E. coli, while mtDNA ligase is an alternatively expressed form of DNA ligase III. The dRP lyase activities discovered in these mitochondrial enzymes are not unique, but are found in all representatives tested of the family-A DNA polymerases and of the ATP-dependent DNA ligases. These dRP lyase activities have low turnover rates that may have important implications for the overall process of BER. All proteins involved in maintenance of mtDNA are encoded in the nuclear genome and must be directed to mitochondria in order to act on mtDNA. Thus, it is evident that the scope of DNA repair activities undertaken within mitochondria is determined by the set of nucleus-encoded DNA repair enzymes that are capable of being imported into the organelle. A review of DNA repair proteins that may be imported into mitochondria in various organisms will be presented.

OOps,
I miscredited the quote of Quetzal's to Peter as I read the quote to mean that random mutation cannot produce beneficial mutations that by selection can become frequent in a population which would be consistent with other statements of Borger's.I see that the request was actually for an example of spontaneous genome adaptation that Peter is stating is obvious. In any case, the Lenski publications further falsify Peter's claims.My apologise to both Peter and Quetzal for mis-crediting the quote....doh!Cheers,
MPB:
You have failed to answer the question, so I’ll repeat it:quote:
----------------------------------------------------------------------------
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There is absolutely no evidence for this assertion. Please show one single
study, with references, on any population of any organism, where the
introduction of a new pathogen, mutagen, or environmental factor produced
fortuitous variation that allowed the population to adapt to the new
conditions.
----------------------------------------------------------------------------
----M: Look up Richard Lenski. He has published extensively on this subject. I
listed two of his papers in the Punctuated Equilibrium thread yesterday. In
addition there were the E. coli experiemnts demonstrating that those with
retrotransposons were better able to adapt to selection than those without.
If YOU would look this stuff up for yourself rather than asserting it does
not exist you might gain some credibility.