Signature in the Cell website now live

_{Paul Nelson

June 15, 2009

Intelligent Design}

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Steve Meyer’s new book from HarperOne, Signature in the Cell: DNA and the Evidence for Intelligent Design, will be in bookstores next week. The book’s companion website, www.signatureinthecell.com, is now live. Check it out.

Comments

Artificial selection is NOT natural selection. IC is an argument against natural selection and random variation only. Therefor to use a case of artificial selection as an argument against IC is dishonest at best and demonstrates ignorance of the debate, That Wisker keeps harping on this example demonstrtates the desperation of his position.Joseph_{June 19, 2009
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One other thing: cytoplasmic male sterility also has another fitness advantage: it encourages outcrossing by preventing the plant from self-fertilization. It increases the overall variation of the population by driving down its level of inbreeding.Dave Wisker_{June 19, 2009
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The third paragraph of my last comment should read:
Would such a gene be eliminated from the population by natural selection? If it had no effect on fitness, it woukld probably eventually be eliminated by genetic drift. Natural selection would eliminate it from the population if it had an overall negative effect on fitness.
Dave Wisker_{June 19, 2009
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joseph seems to think that T-Urf13 is detrimental because a population of all females couldn't reproduce. There is only one possible scenario for this the T-Urf13 gene becomes fixed in the population (i.e., 100% frequency). So let us consider this possibility. Does evolutionary theory predict that a gene which confers male sterility would become fixed in a population via natural selection? Anyone with even a rudimentary knowledge of natural selection would laugh and say "of course not". Would such a gene be eliminated from the population by natural selection? If it had no effect on fitness, probably. Natural selection would eliminate it fdrom the populatioin if it had a negative effect on fitness. So what are its effects on fitness? Well, we do know it leaves the plant with a heightened susceptibility to some diseases. But that is an environmentally dependent effect. But it also results in increased overall yields. That is an effect that <i.improves fitness by definition-- a population polymorphic for the gene (that is, at some frequency under 100%) would have more offspring than one in which the gene is absent. So, evolutionary theory would never expect the gene to rise to 100% frequency, but would predict a rise to some lower frequency and evehntually reach an equilibrium . So, one can see joseph's point about the population being all female is unrealistic, not what evolutionary theory would expect, and thus completely irrelevant. That he keeps bring it up shows very clearly that he has a scant understanding of the relevant biology.Dave Wisker_{June 19, 2009
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Dave Wisker: Specifically, his comment about male sterilization leaves oiut a critical piece of information: maize plants are hermaphroditic, meaning each plant possesses both male and female reproductiuve organs. T-Urf13 does not make the entire plant sterile, it simply renders the male reproductive organs sterile. Wisker leaves out a crucial piece of information- mainly that without males females will not reproduce And joseph fails to note that he has been coirrected on this point ad nauseum): populations polymorphic for cytoplasmic male sterility genes (like T-Urf13 have higher yields. Anyone with even a neophyte's understanding of evolution can see that a gene which confers higher fitness for its population is not detrimental by definition. I and others can explain this to joseph, but what we cannot possibly do is understand it for him as well.Dave Wisker_{June 19, 2009
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Mr Bruce David, Thank you for your thoughtful post. here are a few of the ideas it bring up for me. The mapping from genotype to phenotype is not linear. Small changes in the genotype can produce large changes in the phenotype. In large part this is caused by changing the pattern and timing of gene activation during development. This is the most basic challenge to any theory that demands that small changes must have small results. Thes kind of developmental changes are capable of opening and closing pathways between parts of the body, and these local changes can have a great change to the overall topology of the system. The comparative anatomy of all modern forms has to be taken carefully as a reading for what can and cannot have happened developmentally in the past. Birds are not the only animals with air sacs attached to the lungs. The feature appears in chameleons, some lizards, and snakes. This kind of wide distribution of a feature would argue that it is an old feature. In all cases, inhalation and exhalation occur due to muscles attached to the skeleton changing the interior volumes of dead end air sacs. The great innovation in birds is to separate gas exchange functions and localize them away from these dead ends. I think your ideas on IC are closely related to several topics in evo-devo. thank you for sharing them.Nakashima_{June 19, 2009
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Dave Wisker:
Specifically, his comment about male sterilization leaves oiut a critical piece of information: maize plants are hermaphroditic, meaning each plant possesses both male and female reproductiuve organs. T-Urf13 does not make the entire plant sterile, it simply renders the male reproductive organs sterile.
Wisker leaves out a crucial piece of information- mainly that without males females will not reproduce.Joseph_{June 19, 2009
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Dave Wisker:
joseph’s comments regarding T-Urf13 are misleading. He has been corrected on this before both by me and Art Hunt over on the ARN discussion board, yet inexplicably keeps repeating the argument here.
Wisker and Art are ignoranbt of ID's claims. They think their ignorance is some sort if refutation. That they think they can continue that here is amazing to say the least. Artificial selection is NOT natural selection. IC is an argument against natural selection and random variation ONLY. That neither Dave nor Art understands that just further exposes their ignorance. And now Dave can't even get my argument straight as he is continuing his lies. If lying is the best you have then why even bother posting?Joseph_{June 19, 2009
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Dave Wisker:
To use a biological example, are you saying a series of relatively small genetic changes could not produce an insect wing from a gill?
Do you have an example of an actual demonstration? Or are you just going to post the diatribe that speculates that such a thing happened? Speculation is meaningless without that demonstration. Gene duplication- again? In order for a duplicated gene to even get transcribed it must also have a binding site in its regulatory region. And yet we have a peer-reviewed paper that says just to get TWO specified mutations is close to impossible unless you have a very large population and they are fast reproducers.Joseph_{June 19, 2009
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Hi Bruce,
Imagine a factory that produces the famous WWII fighter, the P51. Imagine further that the QA folks, rather than simply rejecting any aircraft that doesn’t match the specifications, always test it to see if it might perform better in some way than those that do. If it does, then they change the specifications so that future models incorporate the accidental change. In this way the P51 slowly evolves. Will this evolutionary process ever be capable of producing a jet aircraft? The answer is obviously no, because there is just no way you can change a piston engine into a jet engine by a series of small changes, each of which results in a functional engine
To use a biological example, are you saying a series of relatively small genetic changes could not produce an insect wing from a gill? The two structures have completely different, unrelated functions.Dave Wisker_{June 19, 2009
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Hi Blu,
Hm, I might have misunderstood. I’m reading the paper now, it isn’t quite specific on the actual mechanism by which such a process occurs in a gradual manner…they are mostly talking about the probability of its occurence and its fixation within a population that necessarily requires selection against parts of the duplicate gene. But isn’t it that during that process occuring, the primary gene encoding for the protein would stop functioning? Kindly correct me if I’m mistaken. Trying to wrap my head around this as best as I can.
I have to apologize. The paper I cited was far more general, although it does discuss subfunctionalization. One focused on subfunctionalizatioin itself was published by two of the authors: Lynch M & A Force (2000). The Probability of Duplicate Gene Preservation by Subfunctionalization. Genetics 154: 459-473. Its available online as well (one of the great things about the journal Genetics. Figure 9 illustrates the process and paths very well. That <i.should answer your question, but if not feel free to ask for clarification.Dave Wisker_{June 19, 2009
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And...one more thing: You don't even need to observe the whole pathway, all that needs to be done is take any given system (within a larger system), define the maximum number of changes allowed/number of steps, observe the subsequent system, if there is no way to lead from A to B through creating to that system (where the limits and parameters are now being clearly defined due to the specific nature of the system and known allowable extentions). So you'd define all the things in the system that cannot be changed gradually, or at all. The structurally fixed points the change of which would cause the system to overload. then observe through those that you can change, out of those, you see whether given the number of steps allowed you can transfer any of those parts and their subsequent interaction that can affect the parts that cannot be changed. If the answer is no, then there's the limit. I mean...I'm not saying anything new here, just trying to clarify my thoughts by discussing and expressing them. But it seems to me that the darwinian, instead of figuring out ways in which to make things work by laying explanations on top of data, should observe and define the limits, and move from there...I think we'd find those limits to the simplest systems pretty fast. (the more complex systems get, the more interconnected and interdependent, the harder the change, and if an irreducibly complex structure exists...we all know what happens if you try changing one part...you'd need another structure taking over its function while not overloading the system to fully arise before changing it. I think...).Blu_{June 19, 2009
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Can't resist to add one more thing, What we have here are very specific driving factors, and they're all interrelated. 1- The number of steps allowed 2- The point at which a structure of a system cannot change due to its interconnectivity with itself and its environment 3- a gradual change that MUST translate into a change within the environment. The point I want to add is, the "number of steps allowed" is what allows the system to expand beyond its evolutionary funnel randomly. It is the free lunch so to speak to generate a particular multistep scenario that would allow the system to rise to a higher level of specificity/organization/function or to backtrack and create a restructuring shift that would in turn translate into fitness.Blu_{June 19, 2009
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Bruce... Yes! Yes!! That is -exactly- what I'm thinknig. And thats exactly where I think the line is ultimately drawn. Im pretty sure to state that the necessity of multiple beneficial mutations will actually weaken the evolutionary curve to a point where due to the specificity gained towards those functions, the system won't even be able to backtrack or move in any serious way. I'm not sure if I'm clear, I agree with you that its hard to formula, but it is quite clear and definitive and I think you'd agree. Here is what I personally am trying to do. I think, that by definition, necessarily a limit to darwinian evolution exists. It actually must, due to the fact that...as you state, systems have a nature and structure, and to each system there exists an end to its combinatory/evolutionary potentiality. The limit is expanded the more steps you're allowed at each stage (although, the more steps you're allowed, the (considerably) higher the improbability of getting specifices steps at once). So, to formulate this, here is what I'm thinking (and even though some fo these points might be simple, I'd appreciate it if the people here could expand/correct/clarify): 1- Define what a step is, and define its absolute limit. By absolute here I mean no matter how much time is given, you wouldn't for example get...3 protein binding sites in a row by a triple mutation that isn't extended from the combinatory possibilities of information already existing in a genome. So what I'm looking for here is the absolute limit of accumulating steps, not some probabilistic scenario (zapping radioactive slime from aliens in space excluded) 2- Define, for any given structure all the combinatory possibilities coupled with what is defined in point 1. These include all known recombinations, shuffling, etc. coupled with what would increase the function of a system. This will actually exhaust all possibilities that the system can move towards, and will show the dead ends of a given system because of the following point. 3- Define, at each stage when laying out the potentialities of a system's evolution, the points at which it can't step back. Where a particular change will not only be harmful, but fatal to the organism or to the particular system in question. The gradual accumulation will actually funnel the evolutionary pathway in a certain direction which it cannot gradually back up from to generate a higher structure. This isn't only because it will be fatal, but its because it will reduce the efficiency of the system it has just arrived at. Moreover, it is because certain indirect changes will not (and this is case specific) translate into a particular function that will be reflected int he environment. This is specifically clear when it comes to morphological and structural changes, or attaining higher information networks for cognition (this also blends in changing of behaviour by species to their environment, and whether this would happen if the brain was a mere algorithmic neuronal network, which I'm pretty certain it isnt). 4- Define, at each stage, the limits of the information accepting capacity from external sources through signalling out systems that would not/cannot change no matter how much information is derived from other sources by gradual means (lateral gene transfer, etc.) due to the same point in #3, and due to any factors that would resist particular insertions (and that, for certain systems, the information needs to be specific to the case, and is not generalizable, specifically considering the possibility space of biological systems this I believe is critical when it comes to developmental maps for multicellular morphologically novel organisms...if they exist at all). 5- Define a limit for the accumulation of neutral/random components, this ties into #1, in the sense that its important to clarify that any addition whatsoever that can add to a (however improbable) step must be accounted for, the entire effort is to reach what is impossible given a certain method, not just what is improbable and it is rationally and logically achievable as far as I can tell. After doing the above, you exhaust all the possibilities of a given evolutionary pathway. If the possibilities are breached, then the process cannot account for that pathway. So you either see if the process assumed is faulty, or look for another explanation. Now, making such a possibility tree, if you'd allow me to call it that, is for one evolutionary pathway a daunting task. But, nonetheless...such pathways necessarily and logically must exist. The limit is defined by the maxiumum number of allowed steps by each stage, and the necessity of accumulating gradual benefit. Now, one might argue that indirect pathways always exist, and they might. But indirect pathways will also be limited by the necessity of them being A- gradual, B- one step at a time (or whatever the limit is) 3-the necessity of an indirect pathway to translate into an interaction with the environment that will be beneficial to the system. Two points to mention here, the nature of the systems accumulated by the gradual pathway will most likely differ from those that didn't (at least theoretically, you can specifically backtrack and see what led to what), and that there will be zones where no gradual pathway can reach. These zones will be defined by a particular organizational/hierchical/regulatory structures that requires multiple connections to function, but with a few steps would do nothing at all and with a few steps will not translate into a change within the system's fitness to get the ball going. Aka. fully irreducibly complex systems. (but here I'm not just talking about the systems themselves, but how systems fit together and can be integrated into a larger system). And again, the tendency of the step by step gradual benefit will create immense resistance to even an indirect pathway, since any evolutionary change that is beneficial must translate into a particular action that the organism activates and interacts with its environment. Limiting indirect pathways to pathways that must accumulate fitness and function. I think everyone who looks at the bacteria flagellum, intuitively senses that it lies within this boundary (especially if you consider the IFT, and who knows what else is lurking in the details). Or if someone looks at say...a mosquitos nervous system and its capacity for aerial navigation and pattern visual recognition, I believe something like that lies outside of the funnel. anyways, I'm writing too much already, the thought is still crystallizing within my mind, I have more thoughts about this, I look forward to hearing yours. I believe T-urf13 lies within the potential combinatory possibilities in question, and I'm not so certain that the information inherent therin arose by gradual accumulation that at one time translated into fitness (same with almost all organisms). (as a side note, irreducibly complex specified systems become not only hard to create, but hard to move away from)Blu_{June 19, 2009
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This discussion with Blu regarding IC is fascinating, and I look forward to its continuation. However, I would like to introduce an idea I have been thinking about for some time of which I am reminded by Steve Meyer's (and others') characterization of the challenge to Darwinism as the problem of the origin of biological information. Not to belittle that; I agree that it is a major stumbling block for the Darwinian paradigm. But in my opinion there is another equally serious problem that arises from the nature of systems, although it is deucedly difficult to make rigorous. Fundamentally, the problem is that complex systems (and all living things from single cells to large multicellular creatures are extremely complex systems) simply cannot be changed in any major way by a series of small incremental steps if you impose the requirement that after each step the system must continue to function at least as well as it did prior to the change. I will give an example from technology, because we understand technology better than we do living systems, and then relate it back to living systems. Imagine a factory that produces the famous WWII fighter, the P51. Imagine further that the QA folks, rather than simply rejecting any aircraft that doesn't match the specifications, always test it to see if it might perform better in some way than those that do. If it does, then they change the specifications so that future models incorporate the accidental change. In this way the P51 slowly evolves. Will this evolutionary process ever be capable of producing a jet aircraft? The answer is obviously no, because there is just no way you can change a piston engine into a jet engine by a series of small changes, each of which results in a functional engine. And even if you could, there are simultaneous changes that would have to occur in the aircraft as a whole to accommodate the vastly different engine: it would have to move from the front of the plane to the back, which would require re-positioning the wings to maintain proper balance; the air intakes would have to expand and a conduit for air into the front of the engine would have to be created, as well as a hole in the tail for the jet exhaust to escape; new cockpit instruments and controls would have to appear, etc., etc. Now the central dogma of Darwinian evolution is that many small, incremental changes to a species over geologic time will eventually produce genuinely new body plans, organs, organ systems, and processes (such as blood clotting or insect metamorphosis). But it seems to me that the same system problem that prevents a Rolls Royce Merlin engine from metamorphosing into a GE jet engine also prevents a reptilian bellows lung from metamorphosing into an avian circular one (for example), no matter for how many millions of years incremental changes keep occurring or even how directed the changes to the genome are, as long as the requirement that changes occur to only one or two (or even three) genes at a time is maintained. I think there should be some sort of theorem stating that in systems above a certain level of complexity changes above a certain size or degree are impossible to achieve by a series of small incremental changes each of which results in a functioning system. As you can see, I don't really know even how to frame such a theorem, much less prove it, but it does seem to me that when Darwinian theory proposes that an organism possessing a bellows lung can change into one possessing a circular lung via a series of small changes each of which enhances the fitness of the organism (to stick with our example), the burden of proof rests with Darwinism, not with those who point out that it appears to be quite impossible.Bruce David_{June 19, 2009
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The Publisher Chronicles, Part:4? Mr. Burnett, Thanks for pointing out the connection between Zondervan and HarperOne. The important issue I see here is that the book is not published by the religious arm of the parent company, HarperCollins. That Zondervan features the book on its webpage seems a bit of a fluke, because I looked over the hundreds of publications on that site, and could find only a few that were not actually published by Zondervan. I have to stick with my original instinct that Zondervan features the book because of its possible interest to Christians. I don't think that HarperCollins, however is at all a religiously oreinted publisher - despite The Collins company's history as a publisher of Bibles and religious books. The merger of these companies suggests to me that the parent company desires to gain a niche in many different areas of publishing including religious, but not exclusively religious. The name of the game seems to be to earn a profit form various publishing ventures. I don't think that you can easily make a case for the religious motivations of a publisher, which is involved in commissioning a "no-holds-barred" autobiography from George Micahel, or the many other secular works they publish. It's a business, and as such, they need to diversify in order to survive - especially in this economy. What does that have to do with Dr. Meyer's book? You tell me.CannuckianYankee_{June 19, 2009
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Dave, Hm, I might have misunderstood. I'm reading the paper now, it isn't quite specific on the actual mechanism by which such a process occurs in a gradual manner...they are mostly talking about the probability of its occurence and its fixation within a population that necessarily requires selection against parts of the duplicate gene. But isn't it that during that process occuring, the primary gene encoding for the protein would stop functioning? Kindly correct me if I'm mistaken. Trying to wrap my head around this as best as I can.Blu_{June 17, 2009
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And by the way, so far we have subfunctionlization, and t-urf13...both of which have a lot of subtle issues to deal with. Are there other examples of known IC systems that arose experimentally, or maps that result into a known IC system in a reasonable detailed manner? Thank you.Blu_{June 17, 2009
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Hey Dave! Thanks for your response and the information regarding subfunctionlization. Thats interesting, I wonder if it would be a double edged sword in many instances though...I wouldn't exactly count it as an IC system (according to what I'm looking for), as it is increasing the parts of an already functioning structure rather than accumulating components and information to generate a new structure. I wonder if it could be used as a step stone in that direction...it seems to me that it could both increase and decrease the specificity of a certain process. Giving it possible problematic status in the future (in the sense that it might increase redundancy, reducing the flexibility of the system: a part of it that binds to another future addition will cause the protein in question to be dysfunctional, etc.). Regarding whether T-urf13 is beneficial or not. I agree that what "beneficial" is, is based on context. Again, this is a double edged sword...but thats not the point here. What interests me is what are the specific changes that occured that led to T-urf13, and do they lie within what we know is possible for process X, where process X is what we know is the way RMNS works. Now, this might raise a few hackles from the darwinian camp, I'm not suggesting a "poof" argument or whatever, but it follows logically that if X is capable of Y and not of Z, and Z happened, either our understanding of X must change, or some other process resulted into the change. Simply observing the arisal of that system does not necessarily entail that the system arose by RMNS (and again, nor by any other system). What were the steps? Why were they selected? Why was information retained? Was it simply reshuffling preexisting potentiality within the system? When? Did steps occur that had to restructure the foundation of the system thereby making it impossible to have occured gradually? etc. I look forward to hearing your thoughts.Blu_{June 17, 2009
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Hi Blu, Thanks for pointing out my essay. I think the comments by Khan and Dave are spot-on and don't need any more commentary from me. If our ID friends seem stumped or have questions that others care not to address, maybe I will be able to move things along. (Sure would be easier if my comments didn't languish in the moderation queue.) Along these lines, I would ask that if PaV is following this, (s)he might join in and recapitulate the gist of our conversation on Abbie Smith's blog some time back. Maybe that Art Hunter guy will stop by ...Arthur Hunt_{June 17, 2009
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Hi blu, You asked:
PS. Does anyone know any other supposedly irreducible complex system that arose experimentally or even hypothetically? I’ve yet to find one. And I discount vague assertions that do not map to the details or subtleties of reality…and the difficulties that arise with them when one attempts to construct such systems.
One example that I have seen involves the process known as subfunctionalization. This is where a gene duplicates, and then both copiues undergo a series of complementary degenerative mutations such that each contributes an essential piece of the complete protein. That is, a protein that was once coded by one gene now relies on two (or more) genes to supply different elements of it before it can be fully functional. In other words, an IC system evoilved by Darwinian means. The process is described in this paper (which I believe is online) if you Google the title: Lynch M, M O'Hely, B Walsh & A Force (2001). The Probability of Preservation of a Newly Arisen Gene Duplicate. Genetics 158: 1789-1804.Dave Wisker_{June 17, 2009
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Maybe Art Hunter can comment more when he gets a chance on this relationship to what Behe outlined in his book. It seems that a three element system is not one that should be described as irreducibly complex. I will have to get Behe's book out to see just what he said.jerry_{June 17, 2009
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blu, joseph's comments regarding T-Urf13 are misleading. He has been corrected on this before both by me and Art Hunt over on the ARN discussion board, yet inexplicably keeps repeating the argument here. Specifically, his comment about male sterilization leaves oiut a critical piece of information: maize plants are hermaphroditic, meaning each plant possesses both male and female reproductiuve organs. T-Urf13 does not make the entire plant sterile, it simply renders the male reproductive organs sterile. In other words, it turns the plant into a female. This has led some people (joseph especially) to declare T-Urf13 to be a deleterious mutation. Somehow, he has the idea that if the mutation were to become fixed in the population, then the population would become extinct. On the surface, this sounds like a reasonable argument. However, those familiar with basic evolutionary biology know that such a mutation would not become close to being fixed for the very same reason joseph thinks it is deleterious. However, that does not mean that it is reduces the fitness of the population (which is the definition of a deleterious gene) necessarily. It may be beneficial to the population if it remains at some frequency below fixation for two reasons: first, male sterility promotes outcrossing (prevents the plant from self-fertlizing), which reduces teh elevel of inbreeding, and second, maizet populations with male sterility genes (T-Urf13 is one of several that do this) show higher yields. The last thing one would expect a deleterious gene to do is increase yield of a population. Finally, T-Urf13 may confer a susceptibility to disease, but only under certain specific conditions. In niches where the disease isn't present, the increased yield would grant populations polymorphic for T-Urf13 increased fitness. So, as you can see, the situation with T-URF13 is not as cut-and dried as joseph seems to think.Dave Wisker_{June 17, 2009
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jerry,
The specific importance of Turf-13 is that is an ion channel between the inside and outside of the cell and that is not a trivial capability but does not rise to the level of an IC system.
if we compare it to an example used by Behe himself it is: (from the PT article)
Those who have read Darwin’s Black Box might recall Behe’s description of a gated ion channel. On pp. 108-110, Behe describes the signal recognition particle (SRP)-mediated transport of proteins (footnote 3) as a gated transport process. In so doing, he asserts (among other things) that “(b)ecause gated transport requires a minimum of three separate components to function, it is irreducibly complex”. The three components he describes for SRP-mediated protein translocation are the signal peptide, SRP, and the transport channel. The T-urf13 gated ion channel also consists of three components – the fungal toxin (footnote 4) is analogous to the signal peptide, the toxin binding site is analogous to SRP, and the ion channel is analogous to the protein channel. In case this comparison has hidden the bottom line, it is this – T-urf13 is irreducibly complex in exactly the same way that Behe asserts for SRP-mediated protein transport.
Khan_{June 17, 2009
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Joseph, Jerry...thank you very much for your response. Joseph: As far as I understand, even though corn was the product of artificial breeding, the selection here was merely adding environmental selective pressure rather than genetic modification (correct me if I'm wrong here), so in that sense, one could imagine the plausible scenario where some environmental pressure led it to that direction (ok, highly unlikely...but what we're trying to see is the internal capacity to generate an IC system from within, and if such minor exceptions exist what are they and where does one draw the line.) Jerry: I believe Art Hunter is Arthur Hunt, the person who wrote the article. If T-urf13 is the result of genetic recombination, can genetic recombination within certain systems result in an IC system? Again...just trying to draw a line here. To get as specific as I can in my own mind. I know a line exists for sure, I have a rough zone, but its not specified yet. You mention it doesn't rise to the level of an IC system, could you kindly elaborate on that? What do you consider a proper IC system and how would we define one in relation to minor situations? Another point of interest, is in the fourth point in the footnotes, Art mentions: 4. The toxin made by C. heterostrophus race T is a polyketide. It is beyond the scope of this essay to detail this class of compound, or the fascinating enzymes that synthesize them. Suffice to say that these enzymes add another layer of “complexity” to this subject, in that a rather complex set of activities had to evolve, along with the maize mitochondrial genome, to “assemble” the IC T-urf13 system. What I wonder is whether those enzymes too, arose "de novo", or whether they were present in some dormant state before. If they did arise, what selective advantage existed that would confer the amount of successive mutations necessary (if I'm understanding the situation correctly), and if none was available is it due to the capacity of systems to retain some dormant combinatory possibilities in its underlying enzymes, or whether its something else? I would appreciate the input of the experts here on this! I believe its possible to clearly and definitively demarcate an edge if a contextual understanding arises (at least...for me!). I also have a few followup points and questions...so look forward to your response. PS. Does anyone know any other supposedly irreducible complex system that arose experimentally or even hypothetically? I've yet to find one. And I discount vague assertions that do not map to the details or subtleties of reality...and the difficulties that arise with them when one attempts to construct such systems.Blu_{June 17, 2009
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Blu, I am not sure they know for sure how Turf-13 came about but Art Hunter who comments here occasionally has written on it will know. I believe and he can correct me, that is arose from recombination. If this is so then they should be able to identify the origins of it. I would let Art or someone else familiar with plant biology describe it if they see your comment since I am in no way knowledgeable on this. The specific importance of Turf-13 is that is an ion channel between the inside and outside of the cell and that is not a trivial capability but does not rise to the level of an IC system. Again, someone with expertise could explain it better. Since it is found only in corn and corn is a recent phenomena due to natural selection, the origin of Turf-13 is relatively recent.jerry_{June 17, 2009
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Blu, Turf-13 is found in maize- ie corn. Corn is a product of artificial selection, not natural selection. IC is an argument against natural selection and random mutations. Also Turf-13 leads to disease and male sterilization. Not quite the thing evos should hang their hat on. That they do just further exposes the desperation of their position.Joseph_{June 17, 2009
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HarperOne and Zondervan are both publishing divisions of the News Corporation (Rupert Murdoch's outfit).Paul Nelson_{June 17, 2009
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Ok, here's a few of the more significant things Dr. Ruse had to say: ___________________________________ Well, I think Steve’s a really nice guy. I’ve known Steve for many years. I think he’s a bit of a sweetie, but as Winston Churchill once said, I think pretending that intelligent design theory has nothing to do with religion is what Churchill called, what was it, “a terminologically inexactitude.” In other words, it’s a great big fib." And: "I think he’s not appealing to scientific ideas. I think he’s appealing to religious ideas for all that he’s saying that this is not religiously driven, I think that it is. But also, and I trust we’ll get into this, I think it’s also part of a general social cultural agenda which I would, in fact, link with the creationists." and: "First of all, I don’t think your motives are dishonest. I think you know me well enough now to know that I don’t think that in dealing with you people at the Discovery Institute or indeed with the people at the Institute for Creation Research that I’m dealing with a bunch of crooks. Because I don’t think you are. I think you’re profoundly mistaken, I think you are often more religious than you let on, I think that you do try strategies to get around the separation of church and state, I think all of those things. But I think that you are deeply sincerely, if misguided evangelical Christians. So that is very much where I come from, and that’s where I feel at least we can meet there. Now let’s get back to the science." ________________________ So quite quickly after Dr. Meyer explained that he was not a Creationist, all Dr. Ruse does is reinforce this idea without an ounce of proof or reference. He does not at all engage anything that Dr. Meyer Stated.CannuckianYankee_{June 17, 2009
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"CannuckianYankee" (#11) wrote: "The book is published by HarperOne, not by Zondervan. Zondervan carrys the book on its website perhaps as a publication of interest to Christians. I found this out simply by opening their “about the book” link. The two are completely separate entities, and I can find no link between the two. HarperOne is out of New York, and Zondervan is out of Grand Rapids." "Zondervan is an international Christian media and publishing company located in Grand Rapids, Michigan. Zondervan is a founding member of the Evangelical Christian Publishers Association (ECPA). ... According to Zondervan's website, the company was bought out by HarperRowCollins Publishing in 1988 and has continued to be its parent company's Christian bookselling outlet." - http://en.wikipedia.org/wiki/Zondervan_Publishing So it's pretty clear who Signature in the Cell is aimed at, both in its primary religious publisher and its associated "Christian bookselling outlet" - i.e., it's not intended for the mainstream science publishing market at all.PaulBurnett_{June 17, 2009
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