Irreducible Complexity and TalkOrigins

Really? Where is the evidence for this? How much of a part is required? Does the rest of the protein linked to retinal matter or is it only retinal itself that forms part of the IC system? If we changed some structural features of downstream elements and the system still worked would that show that it wasn't IC? Just what is the irreducible part of the IC system?If the parts are so well matched how come the cGMP cascade is downstream of several other signalling pathways? And for that matter how come retinal is a component of dozens of different photosensitive proteins in varying organisms?Behe's argument falls down just as hard on the molecular biochemical level as it does on the gross morphological level. The blood clotting cascade for a start was a poor example given an extensive body of literature on the topic and a number of extant organisms with more rudimentary clotting systems. I agree, Behe has contributed to the scientific literature, but none of his contributions have offered any support for either ID or IC.TTFN,WK

Retinal is not part of the protein. It is a derivative of vitamin A that is bound to opsin, a G-protein coupled receptor (GPCR). The opsin is necessary as its conformational change as a result of the attachment or detachment of the light sensitive molecule determines whether it can activate the G protein transducin. The components of the systems must be specific, and in this case they are: transducin will activate phosphodiesterase via its alpha subunit, phosphodiesterase converts cGMP to 5'GMP, and cGMP no longer maintains cGMP gated channels open. By "change structural features" you mean change a few amino acids on the opsin molecule or the phosphodiesterase enzyme, it probably won't have much effect (although you'd be surprised how much change even one amino acid can cause: consider sickle cell anemia where the sixth amino acid on the beta chain changes from valine to glutamate). However, this would not disprove the highly specified nature of the parts involved, since even then the system would be IC. That all the components are necessary - the rhodopsin (retinal + opsin), transducin, GMP molecules and cGMP gated channels (incidentally other regulatory parts are required like guanylyl cyclase converting GTP to cGMP, opsin kinase and arrestin for reversing opsin state, and GTP and GDP in reasonable concentrations are naturally required for a G protein to work). Because it is the same parts in those signalling cascades that act on cGMP. Guanylyl cyclase produces cGMP from GTP and phosphodiesterase enzymes converts it to 5'GMP. Phosphodiesterases are themselves subject to activation and inhibition by several compounds and drugs, but the relative non-specificity of this one component does not undermine the specificity of the system (as yet, the parts before and after are specific and there are no other means, except externally, of influencing PDE). I'm not sure about varying organisms but there are different opsin molecules within the human retina (three cone opsins and one rod) which gives us the spectral preferences of the cones and rods. Despite this, the opsin molecules are not highly variable but this small degree of variability results in preferences for different wavelengths, and this does not detract from its specificty. There are other known opsin molecules in other regions but they are not involved in vision. I suppose you are referring to dolphins, whales, puffer fish etc. However Behe does say the blood clotting cascade is irreducible only after the intrisinc and extrinsic pathways meet (i.e. at the basic level of regulation, thrombin, fibrin, plasmin, TPA and probably a little beyond that, it is irreducibly complex; Doolittle attempted to show that mice did perfectly fine without fibrinogen and plasminogen but he misread the paper he was citing: http://www.arn.org/...mb_indefenseofbloodclottingcascade.htm)Edited by Suroof, : No reason given.

I know that, that is why I said 'the protein linked to retinal'. There is no evidence for this from what you have said. They only need be specific enough for the system to function. Clearly the components don't need to be highly specific since you yourself mention all the variation in the other vertebrate opsins, and that is without going anywhere near all the non-vertebrate opsins out there.You just keep reiterating various steps in the pathway, you don't demonstrate any particular specifity or any reason why such a system can't evolve. So there are only certain key residues that constitute the IC part of the system? Even if we could change 60% of the amino acids the few key interacting domains conferring specificity would be the IC core? So in fact in terms of specificity the only really specific element seems to be the photosensitivity of retinol to light just one of a number of signals which can activate different opsins and initiate downstream signalling. I suppose the particular elements involved in returning retinal to its original form might also be specific. So far Behe saying something is IC seems to be the only criteria out there. Once again saying the clotting cascade turns out to mean, certain elements of the clotting cascade form an IC core. Every time it seems to be a sweeping claim about a whole system which subsequently comes to rest on a few key proteins/elements, and at a further reduction potentially only on specific structural elements of those. I'm still not sure what implication can be drawn from this about the evolvability of any such IC system.Whether a modern mammal can survive without key elements of the clotting cascade tells us nothing about whether ancestors of that animal could have survived with a more rudimentary clotting system. I was also thinking of examples from more primitive organisms than dolphins or puffer fish since research suggests that key elements of the clotting cascade, probably those you identify as the components of the IC core of the system, are common to numerous vertebrates including teleost fish suggesting the origin of any such system would be before the divergence of tetrapods and teleosts (Davidson et al., 2003). I was thinking more of the fibrinogen like proteins found in lobsters and sea urchins and the lobster coagulation cascade.TTFN,WK

That's why I'm asking the questions, isn't it? Again, Behe isn't really talking about "irreducible" complexity at all, is he? He seems to be talking about "improbable" complexity. The height of the hurdles is irrelevant unless he/you can show that they're insurmountable, not just inconvenient.In Message 59, I asked you to

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Give us some examples, please - specific examples of which functional groups need to be moved where and why it's "implausible" without an intelligent nudger.

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Again, in the examples you gave - the cilium and the blood clotting cascade - which functional groups need to be nudged intelligently because they can't find their own way? Hurdles don't count when you're claiming barriers.

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Disclaimer: The above statement is without a doubt, the most LUDICROUS, IDIOTIC AND PERFECT EXAMPLE OF WILLFUL STUPIDITY, THAT I HAVE EVER SEEN OR HEARD.

Let us look at one IC system - the blood clotting cascade. In his book, Behe describes quite extensively the cascade and the consequent regulation. Despite describing the entire cascade he says "Leaving aside the the system before the fork in the pathway, where some details are less well known, the blood clotting system fits the definition of IC". The component parts are fibrinogen, prothrombin, stuart factor, accelerin, plasminogen and tPA, and this is leaving aside the control of stuart factor by the two pathways and tPA itself. [a breif sketch: after a wound certain factors are activated and via a cascade activate stuart factor; prothrombin is inactive and requires activation by being converted to thrombin; however thrombin is available in very small amounts; small amounts of thrombin activates accelerin and together with the now activated stuart factor, accelerin, activates more prothrombin; thrombin activates fibrinogen creating clots; fibrin (active form of fibrinogen) are bound together by FSF and eventually after healing has taken place FSF are broken down by plasmin the activated form of plasminogen - activated by tPA]The question is: could this have evolved in a Darwinian fashion? Yes it does seem that way because people generally overlook Behe's above statement. For example, Doolittle in response to Behe wrote "In particular, we noted that fish should not have both Hageman Factor and prekallekrin, two of the factors described in Behe's outline of blood clotting in his book." (Home - Boston Review) But the problem is Behe did not say Hageman Factor and prekallekrin formed part of the irreducibilty of the IC system. It is in that same article (in the last paragraph) where Doolittle makes the mistake of misreading a paper and assumes mice are healthy with plasminogen and fibrinogen knocked out. Behe refers to this paper as well as a similar paper by Doolittle in the same year (2003) in his Afterword "Ten Years Later" (2006). The two papers, as Behe wrote, "compares sequences...sequence comparisons can give an interesting overall picture of what proteins came first and second, and of who is related to whom, but can't even begin to tell what is the driving process". The two papers make the assumption Darwinian evolution had taken place in creating the clotting cascade, and the comparisons are used to highlight it but not to show a step-by-step pathway of how it took place.In an article defending the ICness of the blood clotting cascade, Behe said a better definition of IC would be: the number of non-advantageous unselected steps before the selected step are too many to occur at random (http://www.arn.org/...mb_indefenseofbloodclottingcascade.htm). For blood clotting to evolve, an explanation must give a selective advantage of each step, and not just a sequence comparison of the various proteins. The reason this can't be done (by Darwinian evolution) is because it works gradually, and therefore all the proteins I mentioned above (which have to appear simultaneously) could not have come about except by several unselected steps.Edited by Suroof, : expandEdited by Suroof, : No reason given.Edited by Suroof, : No reason given.

This doesn't follow. The fact that we can't document functional molecular intermediates doesn't mean that they can't exist, just that we don't know what they are.Look at the nonsensicalness of the statement For the blood clotting cascade to evolve requires no explanation at all, all this says is that we can't fully describe the evolution of the cascade. How is this anything other than a classic argument from ignorance?TTFN,WK

The question is: what functional intermediates could there be? As Behe wrote there are other simpler ways of stopping blood flow from a wound like platelet aggregation and constriction of blood vessels but the clotting cascade could not have arisen from these for obvious reasons. The simplest blood clotting system imaginable might be just a single protein that randomly aggregated when the organism was cut. However this has several problems: no triggering of clotting factor, non-directional, unregulated - all of which would result in low perfusion and ultimately death. So, what exactly is the functional intermediate?"One could imagine a blood clotting system that was somewhat simpler than the real one - where, say, Stuart factor, after activation by the rest of the cascade, directly cuts fibrinogen to form fibrin, bypassing thrombin. Leaving aside for the moment issues of control and timing of clot formation, upon reflection we can quickly see that even such a slightly simplified system cannot change gradually into the more complex, intact system. If a new protein were inserted into the thrombin less system it would either turn the system on immediately - resulting in rapid death - or it would do nothing, and so have no reason to be selected. Because of the nature of a cascade a new protein would immediately have to be regulated..." (Behe) This is not an argument from ignorance. The idea of IC and ultimately design has a positive and negative element. The negative argument is that such interactive systems resist explanation by the tiny steps that a Darwinian path would be expected to take. The positive argument is that their parts appear arranged to serve a purpose. Richard Dawkins in his Blind Watchmaker makes a clear case for design, that biological systems clearly look designed (of course, he goes on to say Darwinian natural selection can account for design). Hence, the positive argument is in a nutshell: 1. we infer design whenever parts appear arranged to accomplish a function, 2. the strength of the inference is quantitative and depends on the evidence; the more parts and the more intricate and sophisticated the function the stronger is our conclusion of design 3. aspects of life overpower us with the appearance of design (Dawkins) and 4. since we have no other convincing explanation for the strong appearance of design, Darwinian pretensions notwithstanding, then we are rationally justified in concluding that parts of life were indeed purposely designed by an intelligent agent (Darwin's Black Box, pg. 265)Edited by Suroof, : No reason given.

And that is a classic argument from ignorance - we have no convincing explanation (yet), so there is none. You might as well be saying that we have no convincing explanation for birds flying, so we're "rationally justified" in concluding that it's Intelligent Buoyancy.

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Disclaimer: The above statement is without a doubt, the most LUDICROUS, IDIOTIC AND PERFECT EXAMPLE OF WILLFUL STUPIDITY, THAT I HAVE EVER SEEN OR HEARD.

Please see: Message 1Behe's problem is that we do see a particular kind of design. It is exactly the wrong kind of design for your argument. We do NOT see the kind of design that we know results from intelligence. We DO see the kind of design that results from unguided, unintelligent processes.

That was not the argument. The argument was: we have no OTHER convincing explanation, and the explanation of an intelligent agent is the best explanation of IC available. Hence, there is a negative element that Darwinian evolution cannot account for these systems, but there is also the positive element that a purposeful arragnement of parts to serve a function (which varies in the clarity of design - i.e. some systems are more clearly designed than others) requires an intelligent designer.Edited by Suroof, : No reason given.

Let's take a look at functional intermediates, shall we?In the only paper Behe has published in the last 10 years, Simulating Evolution by Gene Duplication of Protein Feature that Requires Multiple Amino Acid Residues, Protein Science (2004), Behe claims "this may well be the nail in the coffin [and] the crumbling of the Berlin wall of Darwinian evolution."The following is from the court transcripts from Behe's testimony at the Dover trial: Now let's take a look at Ed Brayton's summary of Behe's testimony. (All quotes from Page not found | ScienceBlogs.)Are you starting to get the picture?Even using Behe's definitions, even using Behe's absurd limitations, a supposedly IC system evolves in less than 20,000 years.

And (see post Message 69 it is a wrong explanation because it produces the wrong "kind" of design. So we have clear evidence that life does not have an intelligent designer.

I don't know much about evolutionary algorithms and how they create design or complexity in biology but the ID proponent, mathematician Dembski, appears to contest the idea that EA can account for IC systems (which he says is biological SC): http://www.antievolution.org/...19990913_explaining_csi.html

So when Behe doesn't support your position switch to the next source. Kinda like the Texas Two-step.

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Immigration has been a problem Since 1607!

And just what does he say about it?And noting what Jar had to say, you've decided that Behe is wrong now?A quick glance at the paper shows that he is NOT talking about the evolution of complex structures but about the origin of life.What we now KNOW is that once we have living things evolutionary algorithms CAN generate a "kind" of design. It is exactly the kind of design that living things give the appearance of and it is exactly NOT the kind of design that intelligence produces.If you want, now to argue about the origin of life you will have to go to another thread for that. You will also have to know just what Demski is saying. Edited by NosyNed, : added a bit