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The Darwinism contradiction of repair systems

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When a thing is false, is false from all points of view. In fact it cannot exist a point of view from which the thing becomes true, given it is false, rather each view point manifests a particular aspect of the falsity of the thing. As a consequence, when a thing is false, whether we suppose it is true we get contradictions, one for every point of view we consider the thing from. All that is simple logic.

When the above principles are applied to Darwinism (which according to ID theory is false) they make us conclude that Darwinism is false from all viewpoints and has internal contradictions. Of course the falsity of Darwinism is its fundamental axiom of unguided macroevolution: all biological complexity arose from a unique simple common ancestor only thank to random mutations and natural selection. RM and NS, individually taken, per se are not false, insofar they really happen. No one denies that and all appreciate Darwin who studied natural selection. The problem is in the infinitely stronger claim about the creative power of RM + NS contained in the fundamental axiom.

Here I will consider, among the Darwinism contradictions, that concerning the control-repair systems, which is particularly clear and easy to understand.

Molecular biology shows that many complex control-repair mechanisms work inside the cell to recover genetic errors. For example there are at least three major DNA repair mechanisms. Without such mechanisms life would be impossible because the internal entropy of the cell would be too high and destructive. Each of them involves the complex and coordinated action of several enzymes/proteins. See here.

In general, in its simplest form, a control-repair system B on a controlled system A is composed of two main parts: a control unit and a repair unit. See the following diagram:

rm

The control unit is able somehow to get an input scenario X from a specific point of the structure or the events-space of A. X is compared to a predefined correct scenario Y and the result is a Boolean value yes/no. This Y scenario is not a trivial thing because it implies that the control/repair system must know what should be the correct scenario in that particular point of A. If the result of the question “X match Y?” is “no” it is inputted into the repair unit. In turn the repair unit takes an action Z on A to recover partially or entirely the X situation. And here again the repair unit must have a (rich enough) correspondence table between the possible couples X,Y and the Z actions to be taken to fix the failure X. In a sense a feedback or loop must be created between the controlled system and the repair system. In another sense we could even say that in some cases between the controlled system and the control system must exist cCSI (see my previous post about “coupled complex specified information”). Repair systems of all sorts have to be designed frequently in engineering, but, despite the simplicity of the above diagram, they are often hard to implement.

At this point, before the presence of repair systems in the cells, one might asks why Darwinian processes create such systems, as evolutionary biology claims. After all what are random mutations but errors? If Darwinian processes are not based on errors are not Darwinian at all. Darwinism says us that random mutations and natural selection are a process that needs errors and in the same time this process creates mechanisms to eliminate them? Non sense, it should create mechanisms to produce errors instead, to accelerate macroevolution. Either Darwinian processes are based on DNA errors and then don’t create DNA-repair mechanisms deleting errors or Darwinian processes do create DNA and its repair systems and then Darwinian processes cannot be based on errors. You cannot have it both ways.

The bottom line is that repair mechanisms are incompatible with Darwinism in principle. Since sophisticated repair mechanisms do exist in the cell after all, then the thing to discard in the dilemma to avoid the contradiction necessarily is the Darwinist dogma.

Comments
Mr Niwrad, My apologies for dyslexicizing your name. I assure you it was unintentional.Nakashima
September 17, 2009
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Hey somebody should make a shirt: "Four billion years of evolution and all I got was this beer belly." lmaotragic mishap
September 17, 2009
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Nakashima #61
Mr Nirwad, In the case of photolyase, I’m not sure what you would say the control function is. It seems to me that the molecule is just taking advantage of a situation opportunistically.
You continue to write my name incorrectly, despite a warning of a reader. I am an IDer and as such I attribute importance to signs. My name represents symbolically the negation of Darwin. Your will to write it incorrectly might have a Freudian explanation: it represents a sign of your unavowed fear that Darwinism finishes. But you must resign, the end of Darwinism is unavoidable (and likely forthcoming) for only the Truth is eternal and Darwinism has nothing to do with truth. About photolyase, it seems clear to me that it fixes damages in DNA. Its action is directed only to the damaged sites and not to other sites. You can, if you like, call it opportunism. I call it control because for me a choice (though Boolean as that between damaged and undamaged sites) necessarily entails detection and detection is synonym of control after all.niwrad
September 17, 2009
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Mr Nirwad, In the case of photolyase, I'm not sure what you would say the control function is. It seems to me that the molecule is just taking advantage of a situation opportunistically.Nakashima
September 17, 2009
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Nakashima #56
But Mr Nirwad, I wouldn’t want you to start moving the goalposts towards a “complete error recovery system” when you’ve just finished telling me that photolyase itself _is_ an example of unevolvable DNA repair. Also, I do think it is close to the second of your three repair mechanisms that you reference in your OP.
I think that it doesn’t matter if the thing that repairs is a single enzyme or a group of enzymes. What matters is the function. If the repairing function is carried out by a single enzyme this means that it contains inside itself the potentiality to carry out the two basic roles of a repairing system: control and fixing. Another thing that matters is that the papers you referenced don’t seem to succeed in showing any unguided evolutionary pathway from basic chemical components to a recovery mechanism, be it a single enzyme or a set of them (and you agree on this).niwrad
September 17, 2009
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Nakashima @86
But Mr Nirwad
Mr Nakashima, please, it's not Mr. Nirwad. That would be Dawrin spelled backwards, and it just doesn't make sense.SpitfireIXA
September 16, 2009
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In billions of years of evolution, some enzymes can change their active sites to catalyze different reactions. Sounds about right to me.tragic mishap
September 16, 2009
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Mr Drawingtheline, Hello, and welcome to the discussion. To your question, I admit to only having access to the abstract. I don't know if this article maps out the photolyase/cryptchrome families and aligns them with other trees.Nakashima
September 16, 2009
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I'm glad several people found those articles helpful. I agree that neither one makes the direct case for the origin of photolyase kinds of DNA repair in exaptation or the recruitment of other functional elements, though I have the impresion that O'Brien's article does come closer to that. But Mr Nirwad, I wouldn't want you to start moving the goalposts towards a "complete error recovery system" when you've just finished telling me that photolyase itself _is_ an example of unevolvable DNA repair. Also, I do think it is close to the second of your three repair mechanisms that you reference in your OP. It sounds as if the concept of "broad specificity" and "enzyme promiscuity" are quite oxymoronic and surprising. How wonderful that the world still can surprise us! Mr Mishap, indeed these terms crop up regularly. Scientists don't have the luxury of waiting a billion years for all of these things to happen at the same rate they do in nature. It is publish or perish after all. Depending on the claim being made, the use of these terms should alert us to greater scrutiny.Nakashima
September 16, 2009
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Interesting paper Mr. Nakashima. I noticed a lot of words like "targeted", "directed evolution" and "site-directed mutagenesis".tragic mishap
September 16, 2009
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Nakashima #49 #50 thank you for the references to the articles and for your polite way of debating. As you suggested, I read the article "Functional evolution of the photolyase/cryptochrome protein family: importance of the C terminus of mammalian CRY1 for circadian core oscillator performance". The article is not fantasy but I must frankly admit that I was unable to find in it a detailed explanation about the arise of the photolyase, as DNA repair system, from a process of random errors. I read also the interesting article "Enzyme promiscuity: evolutionary and mechanistic aspects". Although the article well describes the aspects of plasticity and catalytic promiscuity of enzymes and their microevolution derived by mutations, one cannot properly say that it explains as groups of different enzymes coordinate their actions to obtain a complete error-recovery system, which seems to me at a higher systemic level (beyond what microevolutionary processes can achieve). I am always more convinced that the ID/evo debate will reach more clearness and insight when the fundamental difference between microevolution (plasticity of components) and macroevolution (new functional hierarchical architectures using such components) will be more clarified.niwrad
September 16, 2009
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If you want a detailed explanation for how the particular cellular mechanism arose then you might want to ask a cell biologist.
I think you provided about the most detailed explanation I'd ever get from anybody. Thanks for trying.tragic mishap
September 16, 2009
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Mr Nakashima, The whole subject of promiscuous proteins is a fascinating one. They may explain how novel protein functions can arise via mutations to that portion of the sequence concerned with promiscuous function, and yet not adversely affect the fitness of the organism, since the core function of the protein is not impacted. Dan Tawfik's lab has been doing quite a bit of work in that area.Dave Wisker
September 16, 2009
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I've been following this site for a while now but have only just now registered. The discussions certainly are interesting to follow! Hi Nakashima, I'm interested whether this part of your referred article was observed or implied. If this reference site below is wrong (I googled it), please let me know: http://www.ncbi.nlm.nih.gov/pubmed/16478995 "the acquirement of different (species-specific) C termini during evolution"drawingtheline
September 16, 2009
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Mr Nirwad, An article on enzyme promiscuity may be of interest to you for insight into how DNA repair mechanisms may have evolved. The source "Catalytic promiscuity and the divergent evolution of DNA repair enzymes" seems to be behind a paywall. Thank you for helping me to learn more, by posing your challenge.Nakashima
September 16, 2009
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Mr Nirwad, So any article titled "Functional evolution of the photolyase/cryptochrome protein family" is a fantasy, correct?Nakashima
September 16, 2009
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BillB: As a matter of clarification, could you provide a list of those features of the cell that we know empirically were caused by evolutionary processes?SpitfireIXA
September 16, 2009
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If we knew empirically that some features of the cell were the product of design then it might be reasonable to ask if other features might also be the result of design. We do know that some features of the cell can be explained by the process of evolution so it is not unreasonable to ask if other mechanisms might also be the result of evolution.
But if we applied it without bias we would have to honestly admit that we don’t know the cause.
Not knowing the cause is very different than assuming a cause based on lack of knowledge. We have a known cause that does account for some features, and may be able to account for others.BillB
September 16, 2009
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BillB: there are plenty of scientists, cell biologists included, who will entertain the idea of an intelligent creator, what they don’t do is conclude that a creator intervened to produce a mechanism before science has come to a thorough understanding of the mechanism in question, and how it relates to other, known natural processes. And yet, given that same absence of information, many seem to have no problem concluding that an as-of-yet unexplained series of accidents produced the same mechanisms. I don't fault your reasoning. But if we applied it without bias we would have to honestly admit that we don't know the cause. Instead "science" seems to assume a vague cause and rule out any line of inquiry that doesn't seek to specify and validate it.ScottAndrews
September 16, 2009
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Scott: Its the old debate about what constitutes evidence FOR design, as opposed to just a gap in existing knowledge which can be filled by invoking an unknown designer with unquestionable motives. Evolution is a known mechanism, how and if it can account for some cellular mechanisms is an on-going research project. niwrad presented, or seemed to present, a lack of knowledge as evidence for design. I suspect that cell biologists who are studying these systems perceive less of a gap than onlookers but, like niwrad, I am not an expert, I just don't see these gaps as ones that can ONLY be filled by design. Contrary to what some on this forum might believe there are plenty of scientists, cell biologists included, who will entertain the idea of an intelligent creator, what they don't do is conclude that a creator intervened to produce a mechanism before science has come to a thorough understanding of the mechanism in question, and how it relates to other, known natural processes.BillB
September 16, 2009
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Nakashima #40 I am claiming that any error-correction mechanism cannot evolve by mean of a process of random errors inside a complex system. A process of random variations is non teleological for definition (randomness has no purpose). A repair system is teleological for definition (has the purpose of fixing errors because "know" how things should be). Here "know" has to be intended in metaphorical sense, in that the real knowledge is in the designer, who necessarily knows the controlled system and its repair mechanisms. A teleological thing cannot arise from a non teleological thing. In other words, purpose or goal cannot come from nothingness. About the photolyase enzymes, since after all they repair damages in DNA, they belong to the group of repair systems. Of course there are many different kinds of repair systems, depending on how the control unit detects the wrong X scenario (see my drawing), on how it compares X to the correct Y scenario, on how it interfaces with the repair unit, and what action Z the repair unit takes. The details of how photolyase works are sure very different from those of the three DNA repair systems I referenced in my post. Nonetheless photolyase repairs, doesn’t destroy the DNA information and this is what matters. As a general principle, consider that repairing and correction are things going directly against the thermodynamic trend towards disorder (entropy). The default trend in nature is disorder, not order. The natural evolution of all non intelligent things is towards errors, not towards repairing errors. Also from this viewpoint repair mechanisms cannot be "natural" and have to be designed.niwrad
September 16, 2009
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BillB: If only the scientific community would show the objectivity and open-mindedness you suggest. Do you have any evidence, beyond your own personal disbelief, that these mechanisms can ONLY be the result of design? If not then what is wrong with trying to understand how they might be a result of evolution or other natural processes, rather than assuming design and closing the book? Switch design and natural processes in that statement and get everyone to agree that we should keep an open mind and examine the evidence before jumping to conclusions and closing the book. Half of this debate will disappear.ScottAndrews
September 16, 2009
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Tragic, I'm making no such claim anywhere, I'm just trying to illustrate how niwrad's idea that foresight is required to construct regulatory mechanisms doesn't seem to hold true. If you want a detailed explanation for how the particular cellular mechanism arose then you might want to ask a cell biologist. Do you have any evidence, beyond your own personal disbelief, that these mechanisms can ONLY be the result of design? If not then what is wrong with trying to understand how they might be a result of evolution or other natural processes, rather than assuming design and closing the book?BillB
September 16, 2009
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Bill, you simply don't understand the kind of repair mechanisms we are talking about. Are you really suggesting that membrane-spanning proteins involved in chemical transport evolved into DNA-binding enzymes with active sites that do not reside in membranes but as globular proteins in the nucleus? That is the most ridiculous story I have ever, I repeat, ever heard from an evolutionist. If you have any sort of evidence for this, I would wet my pants and suck them clean.tragic mishap
September 16, 2009
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Mr Nirwad, Just to be specific, you are claiming that photolyase could not evolve, correct?Nakashima
September 16, 2009
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You cannot have in the same time and in the same mechanism variety and stability, variations (read errors) and errors “regulation” (read deletion)
Yes you can. Simple control systems admit errors. Take a simple proportional controller for example, perturbing it will introduce an error but it will also try and oppose the error with more effort as it gets larger. If you have a weak proportional control it will admit a wide variety of errors (variation) but still try and limit these errors to maintain a degree of stability. The example I used works to reduce errors that occur when the entity is functioning, the refinement of that error reduction system occurs via reproduction with modification and selection for individuals with better error correction. It is not as refined as your diagram but it is a step towards a more refined system.BillB
September 16, 2009
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BillB #37
The process of descent with modification coupled with the filtering effect of selection can generate variety, and will select for variations that reproduce better, both by regulating errors in copying, and by improving the stability of the entities during their lives.
You cannot have in the same time and in the same mechanism variety and stability, variations (read errors) and errors "regulation" (read deletion), exactly as you cannot have a single figure that in the same time is a circle and a square.
You have an entity and part of that entity has an aperture that allows molecules to pass through, the aperture is large and admits many types of molecule, some of which will damage or destroy the entities ability to function. The entity can reproduce, and during reproduction the copies have apertures of varying shapes and sizes – structural differences. [...] This structural change in the aperture functions as an error checking mechanism and to an observer we could look at it in terms of niwrads diagram and say that it is checking molecules to see if they are ‘correct’. No foresight is required, just variation in structure.
Your example is not an implementation of a repair system (as illustrated in my block diagram). DNA error-checking mechanisms, which are real repair systems, work on the basis of what is correct and what is not correct in the DNA string. They don’t work on the terms of global fitness or reproductive capacity or other selection functions. They work for the stability of DNA and to decrease its degeneration. We could say that they work specifically and locally to fix errors based on the knowledge of the relative correct values. In your natural selection example there is a fitness function which globally selects individuals, eliminating the unfitted. This selective force can be unintelligent because its job is easy. Natural selection doesn’t work based on knowledge. Natural selection at the very end is simply the survival of the fittest and the death of the unfitted. Selection is the individuals. As a consequence, to compare your selection example with a real repair system is like to compare a horizontal bar placed at 2 m that selects who jumps it and who doesn’t with a math prof while correcting a student on a formula.niwrad
September 16, 2009
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Tragic: The issue of self replication and self repair are tied together by niwrad:
Molecular biology shows that many complex control-repair mechanisms work inside the cell to recover genetic errors.
This is referring to internal self repair mechanisms in an organism.
before the presence of repair systems in the cells, one might asks why Darwinian processes create such systems, as evolutionary biology claims. After all what are random mutations but errors? If Darwinian processes are not based on errors are not Darwinian at all.
And this is referring to reproductive errors. Niwrad also states:
RM and NS, individually taken, per se are not false, insofar they really happen.
The two different issues here, that of internal repair mechanisms and of errors in copying, are both related in that they both affect reproductive success, and are therefore regulated by selection. Niwrad makes this claim as well:
For example there are at least three major DNA repair mechanisms. Without such mechanisms life would be impossible because the internal entropy of the cell would be too high and destructive.
This may be true when looking at a modern single celled organism but is it true of a much simpler self replicating system? How can we establish if any of the simplest possible self replicators actually require error correcting mechanisms to function? Bear in mind that 'function' in this context simply means the ability to produce at least one copy that is also capable of producing a copy, so the error rate in reproduction and the likelihood of the entity falling apart can be very high. When you have an entity like this, one that can just about manage to copy its self successfully, and one that introduces some variety into those copies, then you are generating variety in both the internal stability of the organism and in its ability to generate functional copies, so the two issues are tied together via reproduction, variation and selection. I happen to agree that there are plenty of interesting and difficult questions surrounding the ways in which simple self replicators can function, and the way they can vary. This impacts on the possible ways in which self repairing mechanisms can arise, but I think the lines between internal stability and active repair are blurred. Can slight modifications to an organisms molecular structure increase its resilience and stop it falling apart as fast, and if so where do you draw the lines between these structural improvements and what we would observe to be a self repair mechanism? On the issue of foresight, I just don't see why it is needed provided you have variety and selection. These provide a mechanism for rejecting errors already, it just happens at the generational level rather than within an individuals life cycle. The process of descent with modification coupled with the filtering effect of selection can generate variety, and will select for variations that reproduce better, both by regulating errors in copying, and by improving the stability of the entities during their lives. In terms of the idea of structural stability and error correction, try this very simplified example. You have an entity and part of that entity has an aperture that allows molecules to pass through, the aperture is large and admits many types of molecule, some of which will damage or destroy the entities ability to function. The entity can reproduce, and during reproduction the copies have apertures of varying shapes and sizes - structural differences. The entities from the parent generation might have low reproductive success rates because there is a high probability that some will suffer damage, but those that do manage to reproduce may produce copies with an aperture that admits fewer harmful molecules, and increases their reproductive success. This structural change in the aperture functions as an error checking mechanism and to an observer we could look at it in terms of niwrads diagram and say that it is checking molecules to see if they are 'correct'. No foresight is required, just variation in structure.BillB
September 16, 2009
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Mr PaulN, The Mendel Museum is located in the Augustinian Abbey in Brno. Mendel entered as a monk and eventually became Abbot. The museum covers all aspects of his life, and how the Abbey supported basic science in the 19th century. Mendel's experiments are given context in his life and society. Basic genetic principles of heredity are reviewed to explain Mendel's data gathering. The exhibits are very modern. You can view the garden where Mendel's experiments were carried out. The exhibits make clear that Mendel was aware of Darwin's work. He read several of Darwin's books in German translations. Mendel's copy of OoS with his pencilled marks is still in the Abbey Library. He was just finishing his experiments when he read OoS and marked several passages where his results were at odds with Darwin's ideas about heredity. I also visited Olomouc to see the university where Mendel went to school.Nakashima
September 15, 2009
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Dar-win is a misnomer, Dar-lose is more accurate.Clive Hayden
September 15, 2009
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