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Author
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Topic: can some aspect of Darwinism be falsified?
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John A. Davison
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Member # 1425
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posted 14. May 2006 14:57
Selection, artificial or natural, never had anything whatsoever to do with creative evolution. As a matter of fact the primary role of natural selection is clearly demonstrated today to be what it most probably always was. It PREVENTS organic evolution by maintaining the status quo. It ultimately failed even at that and resulted in extinction for the vast majority of all forms that ever lived. That is why the fossil record is crawling with organisms that suddenly appeared, prevailed for variable periods of time and disappeared unchanged from their original morphology.
Don't take my word for the role of natural selection. Consider the firm conclusion of one of the greatest evolutionists of all time.
"The struggle for existence and natural selection are not progressive agencies, but being, on the contrary, conservative, maintain the standard."
Leo Berg, Nomogenesis, page 406
How wrong can an hypothesis possibly be?
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peter borger
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posted 15. May 2006 06:30
quote:
I am willing to grant that there can be genes without selection. But if a mutation occurs to that gene, that mutation will have no fitness or selective value, either positive or negative.
You. otoh, are arguing that a neutral gene can receive a mutation and that the mutation will have a fitness or selective value (a negative one, is what you have been arguing).
Apparently I wasn't clear, as you keep saying that I say that inactivation of a neutral genes affects the fitness or selective value of the carrier of that gene. But that is not what I say.
I am arguing that selectively neutral genes can accumulate mutations that inactivate the gene without any effect on fitness. These genes are redundant genes. That we do not find all genetic redundacies inactivated during the alleged eons of evolutionary time can mean only one thing: these systems are not as old as claimed.
It is very simple:
Imagine the 8 histon H1 genes present in all mammals, which allegedly evolved over hundreds of millions of time. Remarkably, scientists have succeeded in generating a mouse double-knockout in which 2 of 8 were erased from the genome. The surpise was that there were absolutely no measurable effects on the fitness of the offspring. This shows that two of the genes are redundant and do not contribute to the fitness of the offspring.
What I am saying is that two genes can receive a debilitating mutations (which destroy the function of the gene) without affecting fitness. These genes are redundant genes: they do not affect the fitness (reproduction rate).
These genes proof genetic backup, design of biological systems and speak out against long-aged evolutionary theories.
They falsify Darwinism beyond any reasonable doubt. That is my point.
peebee
[ 15. May 2006, 08:56: Message edited by: peter borger ]
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peter borger
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posted 15. May 2006 06:57
Guys, is the new biology really so hard to understand?
quote:
Peter Borger, I, like Scott, do not understand how on the one hand my "spare tire" metaphore can be in error, yet you can claim that the genes you are referring to are "neutral" and not being preserved by natural selection.
Your spare tire is incorrect for the reason I gave above. Your spare tire is useless as it is the metaphore for an inactivate gene.
Let me reiterate:
I AM the designer of a driving system. I know that if I give the system only four wheels it will last for only ten years. I WANT it to last for twenty years, however, so I design it with 8 tires (and a spare tire in the trunk or two or three, whatever, they are useless anyway as the systems doesn't know how to use them).
quote:
Scott, if my metaphore is correct, then you must surely see that a mutation in the "spare gene" would not be directly deleterious to the organism, not having a direct negitive impact, but costing the organism in the long run -- therefore the mutation is ultimately deleterious. Further, if there are genes sitting around as "redundants", if these genes are not protected by natural selection because they are neutral -- non-coding, then the fact that they have not been mushed by random mutation is puzzling.
You are free to discuss your spare tire in the trunk as long as you wish. It is not the redundancy I am talking about. To me it is clear that the redundancy I am talking about are the deathblow to all long-aged evolutionary theories and that is probably why you don't like it.
Furthermore, I am afraid you have a problem with the biology jargon: A NEUTRAL gene is not equivalent to a NON-CODING gene (whatever it is). Probably you mean a neutral mutation due to the redundacy in the genetic code, where up to six triplets can code for one amino acid. A neutral gene is a gene that is not subject to selection: in other words a redundant gene.
quote:
On top of that, Peter is arguing that evolution over great periods of time cannot be true, because random mutation would destroy redundant genes. At the same time he argues that mutations are not random. What's wrong with this picture?
GUToB says there are two types:
1) the mutations that are due to entropy. They are introduced randomly.
2) the mutations that are due to the bio-physicochemical properties of the DNA molecule. They follow a pattern that can be even predicted for some genes.
It should be noted that up to 50% of mutations is due to NRM, which is the part that links humans genetically to chimps. GUToB says: we may not be able to discriminate between common mechanism and common descent.
quote:
As Peter has not spoken, let me suggest that you are viewing his perspective with over-simplification. If both random and non-random mutations happen, if the "good stuff" is non-random, then when an improvement in one organism over the other is analyzed, the analysis is of non-random mutations. However, that does not preclude that random mutations may still be floating around killing non-coding DNA, or creating diseases for that matter.
This is not entirely correct, as the bio-physicochemical properties of the DNA molecule can also induce "bad stuff" mutations, for instance the NRM in the p53 gene.
best wishes,
peebee
[ 17. May 2006, 06:51: Message edited by: peter borger ]
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peter borger
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posted 15. May 2006 07:16
quote:
My only point in this regard has been to try to point out that if it is undergoing selection, it is not neutral. And if it is neutral, then any mutation is by definition neither beneficial nor deleterious.
So one cannot say that neutral genes would accumulate deleterious mutations. It's a non-sense statement.
Imagine two identical genes, say gene 1 and gene 2. (BTW, There are dozens, even hundreds of identical genes in the genome of all living creature, for instance the tRNA gene, the histon genes or the ribosome genes: this is elementary biology and they are known as high abundnace genes). Now, gene 2 undergoes a debilitating mutation (say a deletion that chops of 30 percent of the gene). Gene 2 has become inactivated, isn't it? However, there is still gene 1 that has the same function.
You can find "the paradox of high abundance genes" in most biology text books. For genetic redundancy this paradox also holds, be it that the genes are not identical but have the same function (usually they operate in the same reticulum).
quote:
2. Redundant genes.
I need to know more about these. How do we know they are redundant? How do we know they are not under selection?
I assume the answer to the first is knockout experiments.
Now, is the fact that we can knock out a gene and see no visible effect sufficient to establish that there is redundacy?
Is the fact that we can knock out a gene and see no visible effect sufficient to establish that there is no selection taking place wrt either the knocked out gene or it's counterpart?
I just don't know enough about this yet, but we can examine possibilities.
1. Only one of the genes is expressed.
2. Both genes are expressed all the time.
3. Both genes are expressed, but they alternate.
4. Neither gene is expressed.
1. Only one is expressed, if we knock it out the other then is expressed.
2/3. Both are expressed, if we knock out one the other continues to be expressed.
I think we would have to look and see what is going on. My intuition is that if there are redundant genes, it could be so that the rate of expression or the amount of product can be modified, and thus there would be potential for selection.
You are a Darwinian, aren't you?
See: Pearson, H Nature 2002).
peebee
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Christopher D. Beling
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Member # 723
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posted 15. May 2006 09:57
Hi Pee bee, I am not sure I agree with your conclusion in italics below:
quote:
Imagine the 8 histon H1 genes present in all mammals, which allegedly evolved over hundreds of millions of time. Remarkably, scientists have succeeded in generating a mouse double-knockout in which 2 of 8 were erased from the genome. The surpise was that there were absolutely no measurable effects on the fitness of the offspring. . . What I am saying is that two genes can receive a debilitating mutations (which destroy the function of the gene) without affecting fitness. These genes are redundant genes: they do not affect the fitness (reproduction rate).
These genes proof genetic backup, design of biological systems and speak out against long-aged evolutionary theories.
Are these two genes not most likely the remnants of hitherto functional genes that have been hit by stochastic deleterious mutation. The 4th law of thermodynamics states that either bio-information remains constant (i.e. genes are conserved from their original form) or that bio-information degrades (i.e. a single deleterious point mutation can knock-out a gene from being functional). The fact that the mice in which these two genes had been knocked out were no less fit than the rest of the population - could be easily explained if the whole mouse population has suffered an overal absolute decrease in fitness from its original form?? i.e. these two genes are no longer functional genes in all members of the population.
Having said that I also admit that these two genes could be redundant genes "in waiting". I.E. they are just waiting in case the mouse population has need of them by way of adaptation at a future time.
My second point is - why is it that redundant genes cannot be maintained in their pristine condition by the same repair mechanisms that keep the rest of the genes in good operating condition. It is not just natural selection that keeps genes "locked into" functioning condition is it? genetic repair mechanism are very much more important don't you agree? Actually, I see this as one of the main arguments against your hypothesis of short times-scales for evolution. Surely the "redundant" genes would have been maintained by repair mechanisms - allowing them to survive for very long times in a form that would be useful one day when they were needed?
To put this another way - why is it that you single out functional genes as only those ones that deserve the attention of the DNA repair mechanisms?
Chris
[ 15. May 2006, 10:20: Message edited by: Christopher D. Beling ]
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Bruce Fast
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posted 15. May 2006 12:06
PB, please let me take a whack at this. I want to know that I understand.
Christopher B. Beling: quote:
The 4th law of thermodynamics states that either bio-information remains constant (i.e. genes are conserved from their original form) or that bio-information degrades (i.e. a single deleterious point mutation can knock-out a gene from being functional).
Would the 4th law not require degradation until such point as true randomness is achieved?
Christopher B. Beling:
quote:
My second point is - why is it that redundant genes cannot be maintained in their pristine condition by the same repair mechanisms that keep the rest of the genes in good operating condition.
I believe that a primary mechanism for keeping genes in good condition is natural selection. If these genes can be knocked out, and the organism still works, then the organism should continue to work under the influence of any mutation. Ie, natural selection is not operative.
My understanding from molecular clock theory is that if natural selection is not operative, in mammals, one should see a 1% of nucleotide degeneration per million years. For NDE to be accurate, if these genes still seriously resemble H1 genes, they must have lost their protection by natural selection within the last 2 to 3 million years.
PB, I wholeheartedly agree with you, if there are 8 H1 genes floating around every mammal, they cannot have been floating around in a redundant (if you take it out the organism experiences no degradation) state for more than a couple of million years.
I see three possibilities, the first is that in mice, true redundancy only occured a few million years ago. As all mammals have 8 H1s, however, this seems highly unlikely.
A second possibility is the one you point to, that these genes are young -- that the timeframes for biology are totally bogus!
However, let me propose a third possibility. Could it be that there is a specific mechanism in the DNA that maintains all 8 of these genes with a repair algorithm. In my game, software development, and particularly OCR (optical character recognition) we use a method called voting. When doing OCR, we ask a handfull of OCR engines to express their opinion of what a particular word is. If a majority of engines agree on what the word is, we conclude that they are right.
I could see a similar mechanism in DNA, where all 8 H1 genes are compared. If 7 of the 8 all had the same value, then the 8th would be in error, it could therefore be set back to rights by making it the same as the other 7.
One question that should be asked about the 8 H1s, are they identical? If they are identical, then the above algorithm makes much more sense, is much more likely, than if they are not identical.
(Possibility -- could it be that there are a few H1 variants, but that some of the H1s are identical, because these few are working as a redundant set. Notice that this method of redundant protection requires a minimum of 3 genes to operate.)
I would think that this could be tested for as follows: invoke a specific mutation into one of the H1 genes, both in the male and the female that you will breed. Breed the animals. If this mechanism is at work, your invoked mutation should dissappear.
I would think that if such a mechanism existed, it would obliterate your "these things are young" hypothesis. An 8 times redundant gene, and an active comparative mechanism, should be able to maintain the purity of the genes incredibly well. If natural selection works on the package of 8, then NS + error correction by redundancy should easily last 100 mil.
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John A. Davison
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posted 15. May 2006 17:53
I ask for a single example where it can be ascertained that natural selection played any role in either speciation or the production of any of the higher categories. If no one can produce that example and I predict they cannot, there is only one conclusion. Natural selection has not been an evolutionary factor. All it has ever done was to prevent evolution and ensure ultimate extinction. It is really good at that. Of course that is very important. Think about it. Without mass extinction there could never have been an evolution at all. The flora and fauna would have simply gradually changed as the planet did. How ridiculous can Darwinian gradualism through natural selection be? Why does anyone buy that fairy tale any more? That is the question that should be answered. But will it ever be by the Darwinians? I say not a chance. What say others?
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Bruce Fast
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posted 15. May 2006 19:13
John A. Davison, "What say others?"
What I like most about the PEH is that it makes sense of the pattern of the development of life that life progressed from domain, through kingdom, philum, class, order, family, genus, species in that order. Every bone in my "let's think like a Darwin" body says that this pattern is in conflict with NDE.
Further, as a software developer, I look at DNA and see program code. I see a lot of program code. By the time I look at the 550,000,000 years from multi-cellularity until now, I say hogwash to the view that NDE can account for it all. If NDE does account for it all, we need to seriously rethink how computers are programmed.
However, let me say two things, first I have much less information than you have, second, I like to play scenerios, to "put my Darwinian hat on" so to speak. Though your knowledge on this topic is much greater than mine, your knowledge is not much greater than that of many who disagree with you and hold to NDE. I, therefore, cannot simply say, "Dr. Davison knows more than I, so he must be right." because to do so would obligate me to do the same with all of the other Dr. so-and-so's who have a different opinion than you have. Where would I be then.
Bottom line, I feel a need to work this process carefully, to play Darwinist, to see if this or that makes sense in lite of NDE, to see if I can find bits that definitely cannot make sense in light of NDE.
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John A. Davison
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posted 15. May 2006 20:25
Bruce
I appreciate your candor. What I find most interesteing about my role in internet forums both here and elsewhere is the fact that I am the only professional biologist who presents his convictions. Is there another Ph.D. in biological science who is presently active in participating in this forum or at Uncommon Descent or at Panda's Thumb for that matter who is not already a declared Darwinian? I know of none. Even the professional Darwinians say nothing here, hoping their paradigm will survive by ignoring their critics. That is what they have always done and it won't wash any more. I take great pleasure in disclosing their insecurity by exposing their cowardice for all to see.
Instead, the leadership in both camps, too cowardly to engage with me themselves, send forth their spear chuckers to discredit me for one reason only. I have rejected both of these entrenched camps and identified them as victims of their "precribed" fates. They cannot tolerate the notion that they are wrong and will go to any length to preserve that stance. If I am wrong, and I may very will be, it will never be resolved on internet forums. It will be resolved at the laboratory bench just as every other scientific question has always been.
I have presnted the conclusions, here and elsewhere in my published papers, of many of my predecessors who are agreed that natural selection had nothing to do with organic evolution. If you choose to think otherwise I say good luck.
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Christopher D. Beling
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posted 15. May 2006 21:30
Bruce - I think we are agreeing with each other - that it is not either "repair mechanisms" or "natural selection" that keeps genes in good operating condition but BOTH. But having said this I strongly believe that repair mechanisms are very very much more important - and that natural selection is there as a "last resort" - the final conservative force
quote:
Would the 4th law not require degradation until such point as true randomness is achieved?
I believe the answer is yes it would if (a) there were no repair mechanism built into the DNA code and (b) there were no natural selection (NS). A computer code continually operated on by random changes is eventually going to fail and be discarded from the family of useful programs. But if the computer code can self generate copies of itself regularly then some of these will proceed in useable form for many generations of copying. All the non-operative programs will just get "dumped" by NS. Without that reproductive "copying" capability though there would be certain death for the program.
Alternatively the programmer could have built in a really clever - "lets check the code and repair it when it goes wrong" code - this code would also be part of the CSI.
This statement:
quote:
I could see a similar mechanism in DNA, where all 8 H1 genes are compared. If 7 of the 8 all had the same value, then the 8th would be in error, it could therefore be set back to rights by making it the same as the other 7.
tells me that you do believe that DNA repair mechanisms are (or could be) operative. I certainly believe that genetic repair mechanisms are very much in operation - in fact I thought this was well established by the molecular biology community (indeed that there are repair mechanisms even for the repair mechanism)?
quote:
I believe that a primary mechanism for keeping genes in good condition is natural selection. If these genes can be knocked out, and the organism still works, then the organism should continue to work under the influence of any mutation. Ie, natural selection is not operative.
I would ask you why you believe that natural selection is the primary mechanism - rather than DNA repair mechanism? Have you any support for this? I know you are here referring to "dormant" or "redundant" genes. Clearly NS cannot operate on such genes, but as you point out is very likely if the programming is good that repair mechanisms can be operating continually to keep these genes in good condition - just waiting for the time when they are needed? Here we must remember the case of the "Russian Dogman" Adrian Jeftichjew, who was unfortunate enough to have the gene for "hair all over the body" switched back on (and we all have this gene in our genome). If cold conditions prevailed for long enough - perhaps this dormant gene would switch on and be passed to all members of the human race!
A "dormant" or a "redundant" non-working gene can be the result of a deleterious mutation (most likely) - but this does not mean it cannot just be waiting there for action - if the need arizes. Its a kind of resource that the organism has at its disposal. I think the case of the peppered moth, Biston betulia, may come under the same category - with a single gene controlling the coloration (melanin pigment)- that can switch on or off according to whether it is needed - a kind of built in resourcefulness put there by the Designer?
Chris
[ 15. May 2006, 22:07: Message edited by: Christopher D. Beling ]
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Bruce Fast
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posted 15. May 2006 23:33
Chris: "I would ask you why you believe that natural selection is the primary mechanism - rather than DNA repair mechanism?"
My understanding of DNA repair mechanisms is dismal. However, I understand that DNA copy and repair is amazingly good, but not perfect. Again I refer to my minimal knowledge of molecular clock theory. Again, if I understand correctly, non-coding DNA seems to take on mutations in mammals at a rate of 1% of nucleotides per million years. This number already factors in all "generalist" DNA repair mechanisms. By generalist, I mean those mechanisms that act on all DNA, as opposed to specific mechanisms. However, what I described above would be an example of a error correction mechanism that protects specific DNA.
However, I seem to recall some other issues re the H1 gene. My understanding is that this gene in particular does not mutate. It is different in only 4 aminos between the bovine and the pea if I recall correctly. I was unaware, until now, that there were 8 copies of the thing in each mammal. But I also understood that the recognized reason that the molecular clock has stopped ticking with the H1 is the heavy re-use that is made of it, where the resultant proteins undergo various transformations and do more and more different things. In doing so, the theory suggests, any mutation would produce destruction and be removed by natural selection. However, the fact that there are 8 of 'em, but you can drop two and the dear organism still works remains amazing. Unless there is a specific error correcting mechanism which involves multiple copies of the dear thing, PB would remain correct that the fact that they have been around presumeably since the animal/plant split would suggest that the split was not a billion years ago.
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Bruce Fast
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posted 16. May 2006 00:31
Ops, I did some checking, the above "this thing doesn't mutate" gene is they hystone 4. Surely a different puppy.
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John A. Davison
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posted 16. May 2006 02:24
Has anybody else noted that the Darwinians are not even talking about much any more about natural selection and mutation as evolutionary devices. They have siezed up, as it were, and seem to be stuck right where they were decades ago. Meanwhile, everything we are learning from molecular biology and chromosome structure and function points to predetermination in phylogeny with "preferred pathways" and "hot spots" of chromosome breakage and recombination. There is absolutely nothing in this literature to support a model based on randomness either at the level of the gene or the chromosome. How can natural selection be involved in a system which offers nothing to select?
Once again the development of the individual provides a model for phylogeny. Is there a role for selection in ontogeny? The PEH presumes that exactly as ontogeny now proceeds solely on the basis of contained original instructions, so then did phylogeny do the same.
We must change our whole perspective in order to study the mechanism of evolutionary change. It is difficult because change is no longer in progress beyond the trivial production of varieties. Darwinism was doomed from the beginning and has been kept alive by an ideology which demands that evolution has an identifiable external cause. That cause has never been identified because it never existed. There has never been a role for chance in either ontogeny or phylogeny. One of the reasons I have so much respect for Leo Berg is because he recognized as early as 1922 that which the Darwinians still cannot accept. Speaking of both ontogeny and phylogeny:
"Neither in the one nor in the other is there room for chance."
Nomogenesis, page 134.
As a Russian he was able to escape the mass hysteria which engulfed the west, especially England and America, with the publication of the Origin of Species, the contents of which had nothing to do with the title of the book - absolutely nothing.
It is hard to believe isn't it?
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peter borger
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posted 16. May 2006 03:24
Bruce,
quote:
However, let me propose a third possibility. Could it be that there is a specific mechanism in the DNA that maintains all 8 of these genes with a repair algorithm. In my game, software development, and particularly OCR (optical character recognition) we use a method called voting. When doing OCR, we ask a handfull of OCR engines to express their opinion of what a particular word is. If a majority of engines agree on what the word is, we conclude that they are right.
I could see a similar mechanism in DNA, where all 8 H1 genes are compared. If 7 of the 8 all had the same value, then the 8th would be in error, it could therefore be set back to rights by making it the same as the other 7.
One question that should be asked about the 8 H1s, are they identical? If they are identical, then the above algorithm makes much more sense, is much more likely, than if they are not identical.
This is the only remaining possibility and I have also argued a similar mechanism for the 8 tRNA(tyr) genes in Saccharomyces. They are identical (except for one that has a single neutral point mutation):
quote:
Even multigene families that are not tandemly repeated are kept homogenous. In yeast there are eight identical genes that all specify a transfer RNA molecule specific for tyrosine. The eight genes are located on eight different chromosomes. The coding part of those genes and the 14 nucleotide intervening sequence are identical except at one position at each locus, although the flanking regions of the genes display no obvious sequence similarities. It is very hard to explain such localised homogeneity, by a Darwinian selection mechanism.
[O]ur biological intuition would anticipate that the eight individual genes in this small multigene family would have diverged slightly from each other through the accumulation of various minor or neutral mutations. The absence of such divergence indicates that these eight genes are coevolving; that is, their sequences all change together [1, p 660].
Co-evolution implies that the genes must know what they look like, and what their identical twin-genes look like. How does a gene know that? And how does a gene know the other gene changed? Genes on different chromosomes that change simultaneously have to communicate with each other trans-chromosomally.
(FROM Borger's GUToB)
From GUToB we can understand why there is NO molecular clock, as some parts of the genome are kept stable, while other parts deliberately introduce mutations, and still other parts are subject to a combination of NRM and RM.
peebee
[ 16. May 2006, 03:26: Message edited by: peter borger ]
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peter borger
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posted 16. May 2006 03:34
John,
quote:
Is there another Ph.D. in biological science who is presently active in participating in this forum
I am,
peebee
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