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Author | Topic: How do we know its irreducible? | |||||||||||||||||||
Ahmad Inactive Member |
quote: Right.
quote: Agreed.
quote: Now keep in mind that the system is irreducibly complex (IC) and I don't think I need to remind you its definition. Therefore, say Y is IC and you want to show that it evolved from X. You, not only have to outline the evolutionary pathway (i.e Z), but also outline the function of the system when it was X and provide evidence that via Z it became Y. Your explanation must be consistent with the ToE. On my part, I will then use your explanation to outline the fallacies (if there are any) and demonstrate how the proposed evolutionary pathway is invalid for X to become Y and why evolution of Y is impossible.
quote: I see you misunderstand the very definition of IC. In such a system each component separately has no value unless all the components work together. Coordination is the keyword here. All parts of the system must maintain coordination and work as a whole to keep the system functional. Looking it other way, if, even, one of the components cease to function, the entire system breaks down. In this case, each component is highly valuable. No, I am not contradicting myself... but this is what an IC system really is.
quote: Ok then, you give me the possible, potentional pathways and the redundant features, and I'll tell you why its impossible. Ofcourse, this does not dismiss the possibility of the existence of evolutionary pathways,i.e, if you can show one. Lets take my aforementioned example of the cilia here. Give me the possible potential evolutionary pathway by which the cilia evolved and I'll respond. Fair enough?
quote: Yes he does. Why do you ask? I can use that as an example of a non-biological irreducibly complex system... if you want me to.
quote: Alright, you tell me how evolution explains the emergence of IC systems. As far as I know, the difficulty for Darwinian theory is that an irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. Behe even demonstrated this by many biological and non-biological examples. A mouse-trap for instance. It has five parts that are absolutely necessary for the mousetrap to function. Take any one of these parts away and the mousetrap can no longer catch mice. You can't build a mousetrap by Darwinian natural selection. Let's say you have a factory that produces all five parts of a mousetrap but uses them for different purposes. Over the years as the production lines change, leftover parts of no-longer-made contraptions are put aside on shelves in a storage room. One summer, the factory is overrun with mice. If someone were to put his mind to it, he might run by the storage room and begin to play around with these leftover parts and just might construct a mousetrap. But those pieces, left to themselves, are never going to spontaneously self-assemble into a mousetrap. A hammer-like part may accidentally fall from its box into a box of springs, but it's useless until all five parts are assembled so they can function together. Nature would select against the continued production of the miscellaneous parts if they are not producing an immediate benefit to the organism. Michael Behe simply claims that we have learned that several of the molecular machines in the cell are just as irreducibly complex as a mousetrap and, therefore, just as unable to be constructed by natural selection.
quote: Ok... you tell me the naturalistic explanation of the cilia. Enlighten me.
quote: By function I mean, coordination of various components simultaneously for the effective functionality of a system. How do you determine "selective advantage"? Natural or Conscious?
quote: I did discuss this with mark. Nonetheless, I will use Mike Gene's response for this paper.
quote: To begin with, this pathway according to the authors, can generate complicated structures, but not irreducibly complex structures. So we can see that IC helps to rule out certain evolutionary pathways. This is also very significant in that the most persuasive examples of random mutation and natural selection (RM&NS) entail serial direct Darwinian evolution. The traditional examples of Darwin's finches (and their beaks), giraffe necks, elephant trunks, darkening wings in moths are all examples of serial direct Darwinian evolution. Thus, this means that evidence for this type of evolution is not evidence that IC can/did evolve via the blind watchmaker mechanism (BWM).
quote: "This means approximately synchronous changes in more than one component, so that modification to other components always occurs before the total modification to any one component has become significant." But they also say, [b][i]"Parallel direct Darwinian evolution can generate irreducibly complex structures, but not irreducibly complex structures of functionally indivisible components, and this is the valid conclusion to draw from Behe's thesis.[/b][/i] Thus, once again, we can see that when we are dealing with IC molecular machines (which are composed of functionally indivisible parts), the various examples of Darwinian evolution cited by Dawkins et al.(and used by the authors) are irrelevant. None of it amounts to evidence that Behe's IC examples evolved by the BWM.
quote: Now this pathway is quite interesting. ToE states systems evolved from simple >> complex. Yet this pathway assumes the opposite. Thus, if simple beginnings are needed to "come into existence by chance," the complicated beginning, assumed by this pathway, may be too complicated to "come into existence by chance." In other words, this pathway does not eliminate the design inference behind IC, but instead, suggests that IC is an indirect indicator of an originally designed state. Nevertheless, what we need is evidence that the initial state was more complicated than the IC state. For example, are we talking about flagellum that were originally composed of 60 parts? Where is the evidence for such a claim? It is an interesting thought, but without evidence, we can't take it beyond the realm of philosophy.
quote: They begin with an example: "For example, scale-feather intermediates would offer no aerodynamic advantage, but one can hypothesise a sequence from scales to primitive but airworthy feathers in which each step offers an increased advantage as insulation. Their use for proto-flight motility would therefore only begin after this sequence. Recently discovered fossil evidence suggests that feather evolution did indeed follow such a sequence, with proto-feathers, composed of the same proteins as feathers, in Sinosauropteryx (Chen et al., 1998; Padian, 1999), probably marginally airworthy feathers in the non-flying Caudipteryx and Protarchaeopteryx (Ji et al., 1998), and feathers in the flying Archaeopteryx (Padian, 1998). The proto-feathers and feathers probably also possessed functions in display, camouflage, recognition, etc., and it is possible that the actual sequence was more complicated than the above hypothetical one, with evolution at some stages being driven primarily by selection for such functions (Padian & Chiappe, 1998). However, the proto-feathers in Sinosauropteryx were so thickly distributed that they almost certainly did function as insulation (Padian, 1999)." Now this example is faulty for a number of reasons: 1. The so-called feathers in Sinosauropteryx were nothing but "frayed collagenous fibers beneath the skin." (Anne Gibbons. 1997. Plucking the feathered dinosaur) 2. There is absolutely no evidence that Caudipteryx and Protarchaeopteryx are "scale-feather" intermediates. 3. Protofeathers are nothing but "theoretical construct". (Olson 1999) 4. This is not a clear example of generating IC and this whole topic ignores Behe's points on pp. 40-41. The fact that various proteins can share domains doesn't really support adoption from a different function, as there is no reason to think a designer would ensure that each and every part of a system is truly unique. For example, that both a lawnmower and automobile have spark plugs is not evidence that one motor was co-opted to form another by random changes and selection. The only clear examples, in in my opinion (according to Gene), of adoption from a different function are as follows: 1. Antifreeze glycoprotein in the blood of Antarctic notothenioid fishes, which enables them to survive in icy seas, is considered to have evolved from a functionally unrelated pancreatic trypsinogen-like protease, and the recent discovery of chimeric genes which encode both the protease and an antifreeze glycoprotein polyprotein strongly supports this theory (Cheng & Chen, 1999). 2. Crystallins (proteins with refractive functions in the eye lens) are closely related or identical to stress-protective proteins in non-ocular tissues (eg. Drosophila a-crystallins and small heat-shock proteins are homologous). But note that in both cases, these proteins don't function as well-matched components in an IC system. Thus, while sometimes a protein might adopt a different function since it is not constrained to interact with multiple partners, an IC component is unlikely to arise in this fashion because it is constrained to interact with multiple partners. Since the adoption from a different function explanation relies heavily on pure chance, it is unlikely to be a general solution to IC. In fact, as Behe notes, the more complex the system, the less likely that this pathway is what generated IC (since it relies more heavily on converging independent, random events). Gene provides other counter-examples where adoption from a different function is not possible. For example, imagine a mutation occurred in a bacterium that disabled dnaJ. IC predicts this would be lethal and selection would prevent this organism from altering the gene pool. But if adoption from a different function is common, the mutation need not be lethal and a new chaperone machine would evolve around the protein substituting for the lost component. Why, then, do we not see this occuring? When we look to eubacteria, the three chaperone components are universal. They are found in gm+ and gm- bacteria, thermophiles (Thermotoga and Aquifex), spirochetes, Deinococcus, Campylobacter, cyanobacteria, Neisseria, and even Mycoplasma. Again, this is most likely due to the fact that this chaperone machine is IC (IC predicts functional constraint) and other proteins cannot substitute through adoption from a different function. This is where this pathway collapses. If adoption from a different function was a common IC generator, why do we not see permutations in Archaea, where a laterally transferred dnaK gene would find helpers in the archaeal cytoplasm and evolve a new chaperone machine? And all of this is significant because the chaperone machine is a very simple example of IC having only three parts. In summary, the adoption from a different function explanation is unlikely to be a general solution to IC as it relies too heavily on pure chance as an explanation for apparent design. We thus need independent evidence that this explanation validly applies in any system in question, especially in light of the fact that examples of this pathway do not lend themselves easily to explaining the origin of IC. Furthermore, if we don't see evidence of permutations that run through out the entire IC system, there is good reason to dismiss this explanation.
quote: Thats easy. I outlined some of the fallacies of the mechanism of the proposed pathways. Now to explain why an IC system could not have arisen from any of the four evolutionary pathways as outlined above. I'll take the bacterial flagella as my example here. Lets list out the four pathways first: 1. Serial direct Darwinian evolution.2. Parallel direct Darwinian evolution 3. Elimination of functional redundancy 4. Adoption from a different function Since the flagella is irreducibly complex and functionally indivisible molecular machine, we can predict that it couldn't have evolved by pathways (1) and (2), the reasons of which I already outlined with quotes from the authors. Now (3) which predicts that the flagella evolved from something more complex than flagella in the present stage. This pathway is as interesting to Mike as it is to me. Now say the flagella was originally composed of 60 parts just to produce the motion of cilia instead of the 30 parts. Where is the evidence? We are claiming that the flagella is irreducibly complex and functionally indivisible; so if the evolutionists apply (3), they do need to show the evidence. In other words, for (3) the burden of proof lies on the evolutionists... not us. Therefore, number (3) pathway cannot be applied to the evolutionary pathway for the IC of flagella. Now evolutionary pathway (4) which relies heavily on chance. A functioning flagellum requires about 30 gene products (components). So what does (4) pathway predict? That prior to the existence of the flagellum, these 30 gene products (or their duplicates) all existed doing something else. Then, they just happened to all fit together by chance to create a flagellum. And afterwards, the other 30 or so hypothetical functions of these original gene products disappeared. For it is chance that determines whether the 30-or-so gene products just happen to come together to form a functioning flagellum, as selection was pruning these gene products in accord with 30-or-so different functions. Thus, the (4) evolutionary pathway is really a return to using chance as an explanation for apparent design, and just as it was not convincing in pre-Darwinian days, it is not convincing today. Thus, pathway (4) blown off. There is no absolutely no evidence that pathway (4) could have resulted in the emergence of flagella and it is highly very unlikely.
quote: I will reply to this later. Insha Allah (if God willing), day after tomorrow Regards,Ahmad
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Ahmad Inactive Member |
quote: Incorrect. Darwinian evolution merely deals with (1) and (2) pathway, i.e, Serial Direct and Parallel direct evolution both of which, as the authors say, cannot give rise to irreducibly complex and functionally indivisble molecular machines. The PCP degradation pathway is an example of a metabolic pathway. If you have read his works, do you forget the important distinction he gives between an IC machines and the IC nature of metabolic pathways? There is a huge difference between molecular machines like the ribosome or flagellum and the PCP degradation pathway. What you want to prove by calling it Gene's admission is bizarre.
quote: Hmm... now I need some sites for that. Show me where Gene says so. Just curious.. so that at least I can read his whole article. Regards,Ahmad
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Ahmad Inactive Member |
quote: Now where does Behe state the non-evolvability of metabolic pathways that are IC? His main arguments focuses around the examples of IC molecular machines which are very distinct, in function and nature, from metabolic pathways. So where exactly does Behe get it wrong, I wonder.
quote: How is it a retreat? Behe merely outlines the several problems with traditional explanations for the origin of metabolic pathways. He makes no such claim of that metabolic pathways can't evolve for him to be wrong. Gene elaborates it further.
quote: Interesting. What I got from Gene's webpage has this to say: "What all of this means is that any evidence for the evolution of metabolic pathways does not translate as evidence for the evolution of IC machines. This is especially true if dealing with a sluggish pathway, composed of three enzymes, all borrowed from other pre-existing pathways, as with the PCP degradation pathway. There is a huge difference between molecular machines like the ribosome or flagellum and the PCP degradation pathway." And I am interested in knowking more about how this PCP is used as an insecticide as you claim. Any links?
quote: How do you know how much he knows? Whatever it is, just because he didn't defend them does not at all favor your claim about him. I'll try to email him and hear it from the horse's mouth. Regards,Ahmad
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Ahmad Inactive Member |
Nic Tamzek,
quote: But there is a difference. Behe never makes any such claim of the unevolvability of metabolic pathways. There is a difference and Gene outlines it beautifully: "I would like to introduce an important distinction concerning the IC nature of molecular machines when compared to the IC nature of metabolic pathways. The IC nature of the two differ in that the former depend on direct, specific contacts between components while the latter do not. A molecular machine functions when energy (usually in the form of ATP binding/hydrolysis) enters the complex through a specific input portal. This energy input then triggers a cascade of unidirectional, conformational changes among the parts. Using our symbolic conventions above, think of A changing shape to induce a shape change in B, which induces a shape change in C, which induces a shape change in D, which then elicits the functional output. The parts require a series of direct contacts to convey the energy/information/mechanical flow that brings about the function. Removing any part interrupts this flow and renders the entire complex functionless, such that all the non-affected gene products are now without function. A metabolic pathway functions differently. In this case, protein A reacts with an original substrate to produce product 1. Product 1 is then converted into product 2 by protein B. Protein C then converts product 2 into product 3. And finally, protein D converts product 3 into product 4. We then define the appearance of product 4 from the original substrate as the function (F). One could reasonably interpret this as IC as proteins A,B,C and D are needed to convert the original substrate into product 4. Yet such a pathway could evolve because various metabolic pathways are typically interlocked through their substrates/products. That is, product 2 may bind to protein C (for conversion into product 3), but product 2 may also react with several other proteins and thus be useful elsewhere. Since metabolic pathways produce products that can exist apart from any particular pathway, it is easier for the proteins in a pathway to exist apart from any particular function. To appreciate just how different this is from an IC machine, consider the following. As mentioned above, you can isolate each individual component on the bacterial flagellum and fill test tubes with those individual parts. Most of the parts will not do anything in that test tube, except for the input portal which binds ATP. In contrast, you can take any protein from a metabolic pathway and fill a test tube with it and it will do something significant - catalyze a specific chemical reaction. In other words, the components of a pathway are not F-dependent; they will perform their subfunction apart from F. In contrast, most parts of a molecular machine are F-dependent and will not perform their subfunction apart from F. This means that a metabolic pathway may be poised to evolve (as we might expect from ID). Using nothing more than simple chemical rules and selection pressures, various components of metabolic pathways may realign themselves to carry out new functions. Since the proteins of any pathway interact through the intermediaries of their substrates and products, and these can exist independently of the proteins, readjustments are plausible, especially when aided by gene duplication. The parts of a molecular machine, however, are not interacting through independent intermediaries, but through direct physical contact. And this places much more stringent constraints on the system."
quote: But there is a difference as outlined by Gene. Beheeven ACKNOWLEDGES such pathways may have evolved (see DBB 151 ff.) quote: Well metabolic pathways are not irreducibly complex as Behe stated on page 150-151 of his book. Thus metabolic pathways simply aren’t in the same category as the blood clotting cascade. There is a difference.
quote: Incorrect. It is actually Ken Miller who claimed that the lactose system was irreducibly complex. Why did he say that? Because he claimed to have shown the evolution of the lactose system, right in the laboratory using Hall's work, to an irreducibly complex system. Behe disproved him here.
quote: Show me where in DBB does Behe explicity claim that IC metabolic pathways can't evolve. You can't, 'cause he does not make any such claim. In response to Miller, Behe says: "I clearly stated in Darwin’s Black Box metabolic pathways are not irreducibly complex (Behe 1996, pp. 141-142; 150-151), because components can be gradually added to a previous pathway."
quote: Irrelevant. Read again. There is a distinct difference IC molecular machines and the IC nature of metabolic pathways. Molecular machine's assembly-dependant nature makes it different from metabolons.
quote: You are wrong on two premises: 1. If you had fully read Gene's explanation, you would have not failed to notice the glaring distinction between the possibility of co-option hypothesis in a molecular machine and in a metabolic pathway. Metabolic pathways produce products that can exist apart from any particular pathway, so it is easier for the proteins in a pathway to exist apart from any particular function. An analogy is also given to understand this very vital point and I pasted it above. he components of the metabolic pathway are not F-dependent; they will perform their subfunction apart from F. In contrast, most parts of a molecular machine are F-dependent and will not perform their subfunction apart from F. F stands for "Function". He makes it very clear that using nothing more than simple chemical rules and selection pressures, various components of metabolic pathways may realign themselves to carry out new functions. Since the proteins of any pathway interact through the intermediaries of their substrates and products, and these can exist independently of the proteins, readjustments are plausible, especially when aided by gene duplication. This does not exist in the case of molecular machines. The parts of a molecular machine, however, are not interacting through independent intermediaries, but through direct physical contact. And this places much more stringent constraints on the system. 2. Co-Option hypothesis, as Gene stated, is entirely dependent on chance and thus highly unlikely. You say that almost all gene origins is done by the co-option hypothesis. Give me some examples. Let me review your websites now: 1. Co-option/change of function, Citations of this in the literature The (presumably yours) first post discusses about the origin of feathers. You say: " I was struck by this passage from Maynard Smith's The Theory of Evolution. It almost sounds like it was written to respond to Behe, except that it was written in 1958 (I think; I have the 1993 Canto edition which is the fourth edition):" Similar assumtions were also made by Thornhill and Ussery in their classification of darwinian pathways. But it is not clear this is an example of generating IC and this whole topic ignores Behe's points on pp. 40-41. The fact that various proteins can share domains doesn't really support adoption from a different function, as there is no reason to think a designer would ensure that each and every part of a system is truly unique. For example, that both a lawnmower and automobile have spark plugs is not evidence that one motor was co-opted to form another by random changes and selection. To quote Smith: "In this case the difficulty disappears once it is realized that during the early stages of the evolution of feathers, the latter were probably of selective advantage because they conserved heat, and only later did they become functional in flight." The so-called ‘feathers’ of reptiles were likely frayed collagen fibres. It’s also most unlikely that flight feathers would evolve for heat insulation first, because natural selection for heat insulation would tend to remove any complexity, because a hairlike structure is much better for insulation. In fact, flightless birds have feathers superficially similar to hair, and in some cases this can be explained by loss of information for the complexity of flight feathers. In your next post, you quote darwin as saying: "We should be extremely cautious in concluding that an organ could not have been formed by transitional gradations of some kind. Numerous cases could be given amongst the lower animals of the same organ performing at the same time wholly distinct functions;" Darwin, himself, was confounded on the lack of transitional species... let alone their organs. Therefore in his book The Origin of Species he wrote the following in the chapter "Difficulties of the Theory": "Why, if species have descended from other species by fine gradations, do we not everywhere see innumerable transitional forms? Why is not all nature in confusion, instead of the species being, as we see them, well defined? But, as by this theory innumerable transitional forms must have existed, why do we not find them embedded in countless numbers in the crust of the earth? But in the intermediate region, having intermediate conditions of life, why do we not now find closely-linking intermediate varieties? This difficulty for a long time quite confounded me." (page 179) Your fourth post deals with an increase in genetic information with a resultant increase in complexity. The article cites two ways of doing so: 1. Exon-Shuffling This mechanism merely produces genetic and phenotypical variety, in an organized way by producing new exon combinations and thus greater genetic diversification. It does not play any role in the "origin of genetic information" as you claim, because it does not add any new genetic information in the first place but recombines existing gene sequences to provide variety. 2. Gene Duplication This predicts a number of duplicated genes with specialized functions. One question to ask here is to develop the specialized functions, the duplicated genes still had to evolve structural changes. What drove the changes? In all likelihood, a number of specializations would have had to develop simultaneously to have any value. An additional concern here is the high probability of the evolving genes messing up the original system. This is very likely with an abundance of structurally similar gene products. If one of these gene products becomes nonfunctional, it could get in the way of the function of original gene product. This phenomena is readily observed today. For instance, the chemotherapy drug methotrexate looks like the B-vitamin folacin, but does not work like it. The drug will compete with the real vitamin for binding to functional sites, but will not actually function. This action kills cancer cells. Another problem with gene duplication is that it doesn't account for all, or even most, of the complexity in many systems. For example, the complexities of oxygen transport involve many genes which are not structurally similar. This is obvious when one considers anemia, a breakdown in oxygen transport. Overall, like exon shuffling, gene duplication does not add any new genetic information and for it to provide complexity.. is highly unlikely. At the articles conclusion, the authors say: "However our results provide another indication that biological evolution works like a tinkerer, "who does not know exactly what he is going to produce, but uses whatever he finds around him whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a `bricoleur' who uses everything at his disposal to produce some kind of workable object". Now where does it explain the "origin" of the string, fragments of wood, or old carboards?? And do they consider the high improbability that these three structures will, naturally, combine together to form a well-built string boats?? Seems very unlikely... unless a supernatural force is added to the scenario, i.e, "creation". 2. The Origin of "Information" (new genes especially) via natural causes, Refuting a key ID claim (refs, webpages) Well to begin with, Johnson stood unrefuted. The examples you gave show nothing of the "creation" of genetic information just as Johnson predicts. Let me begin by quoting Musgrave again to prove my point: "My second favorite example is the Sdic gene, where the annexin and dynenin intermediate chain genes were duplicated in tandem, then the intervening sequences deleted to form a single new gene, (the Sperm specific dynenin intermediate chain gene Sdic). The good thing about this example is that a previously non-coding part of the sequence became the protein coding sequence, and the protein coding sequence has a non-coding role." (Emphasis mine) Where is this so-called "creation" of genetic information that you have been talking about? All I see is the deletion of intervening sequences of intermediates to form a gene. This deletion is loss of information... not the other way round. There is no increase in specified complexity either. And note... this is a "selective sweep" which is the directional selection of genes that already existed rather than creation of novel genes. The second example is given by theyeti about the creation of jingwei gene in Drosophilia by exon recombination. Once again.. no new genetic information is added but new genetic recombinations are expressed. Speaking of the efforts to change the fruit fly's genes, Lester and Bohlin make the following statement: "But this sort of reshuffling is not likely to result in major evolutionary change. It simply recognizes what already exists. Even with new mutations, it will not likely lead to new original metabolic functions and new protein molecules." (Lester LP, Bohlin RG. 1984. The natural limits to biological change. Grand Rapids, MI: Zondervan Publishing House, p 69.) "It simply recognizes what already exists." This is an important statement. The new Jingwei gene was produced by shuffling or recombining preexisting genes. Nothing new has been created; only new genetic (exon) combinations have been expressed! The same explanation also goes for the sphinx gene in Drosophilia except that this is an "unusual" retroposition process, as the authors claim. They give three hypothesis for the origin of the sphinx gene.. all of which require the retroposition and thus nothing new is created. AFGB is produced by the "the recruitment and iteration of a small region spanning the boundary between the first intron and second exon of the trypsinogen gene (Fig. 1). This newborn segment was expanded and then iteratively duplicated (perhaps by replication slippage or unequal crossing-over) to produce 41 tandemly repeated segments." A simple case of intron-exon recombination from the existing existing trypsinogen gene. No genetic information is created, once again but genetic recombinations expressed. Evolution needs swags of new information, if a microbe really did change into a man over several billion years. The additional new information would take nearly a thousand books of 500 pages each to print the sequence. Random changes cannot account for a page, or even a sentence, of this, let alone accounting for all of it. You have an incredible faith!
quote: Interesting pages. I'll go through them in detail when I have the time. You still haven't showed where Behe claims the unevolvability of metabolic pathways.
quote: Yes the immune system us highly complex... yet the idea of its evolution is hardly convincing. I know very little about it and Insha Allah (if God willing) will find out more from my library. Sorry for the long response... Regards,Ahmad
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