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

Hey Arthur, I've been thinking about the content and articles you wrote, and would appreciate your response on the following (plus the questions I asked earlier). What I'm having trouble with, is it seems that you're generalizing specific cases where a particular change "triggers" a possible combinatory sequence in an organism, but nonetheless...I don't see how this is generalizable to state that the addition of information in organisms is not difficult. While maize might reshuffle its mitochondrial genome and might be able to attain a protein coding gene (and I still don't see how you can make the speculation that it DID in fact happen sequentially and randomly, we have no epistemic ground to make that claim unless we emperically track down the probability of maize attaining a functional protein sequence and protein binding sites through direct observation...not secondary inference through homology studies. Only then we can we infer whether this is soemthign that generally happens or not)even considering the different protein sites required as you mention in your second essay as well as the underlying construction agent...which I will not profess to understand and would appreciate your clarification on. What worries me is that you seem to generalize certain cases across all organisms. So whereas an already information rich organism can contain combinatory/triggered changes within its already existing structure (to a certain limit), how does this extend to an organism like E Coli? Or a complex multifunctional integrated cell? Or a multicellular organism from a cellular organism? On what -empirical- grounds, across multiple species of the same "genre", are we making that extention? Moreover, it is clear that many changes require change within the developmental plan for the organism. If something like bacteria flagellum, excluding the new parts and IFT, was co-opted, a change would happen at the developmental level too. So how are we moving from the above, to the attainment of -functional- (as in, functional when other multiple changes occur) proteins is not difficult? If you could point me to a few empirical studies regarding maize, its probability of attaining a protein binding site, its probability of attaining a protein coding gene, and the extendability of those processes to create say...a new cell type. I'd appreciate it. And if could point me to empirical studies regarding the attainment of -multiple- sequential protein components in a simple organism that has added up over time to create a novel complex structure composed of multiple matching (and perhaps, irreducible) components...I'd appreciate that too. My difficulty isn't with attaining -a- protein, my difficulty arises when it comes to the building of a complex cell with thousands of proteins working together at multiple levels to generate one function. And to the limitations of a protein being functional and fixed -within the context of- a particular organism. If, for example, you require 20 proteins none of which are available within an organism, to have a function that would be beneficial and would only then remain fixed, and whereby there is no combinatory "room" within the organism to shuffle pre-existing structures (not talking about genome shuffling) in a slight direction here or there. On what basis are we claiming that is not difficult? What still bugs me is, how come E Coli, bacteria and malaria and even HIV still remain within clear boundaries regarding their internal structure and machinery. With HIV (-disputably-) attaining one viral protein site in its entire course of relationship with human history, with no constructive evolution to speak of. We can't simply dismiss that as negligble. I hope I was able to express myself properly.Blu_{June 25, 2009
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Hey Dave! What leads me to that conclusion is the high morphological specificity aquired by the organism, that same cell types in different organisms contain different morphological fields, its capacity for specified regeneration post development, and the fact that disturbing embryonic development in different way through different angels does not cause it to stop...but it continues regardless of its disturbing of equilibrium. There are other reasons I have, but they're not what you'd call currently academically acceptable. But they're strong nonetheless, I'd be happy to share them if you want. But they're just side points from personal experience. Regarding the rest, yes...its problematic, I think over time it will be found that most developmental sequences (don't really want to call them maps anymore) will be found to be highly polymorphic (I believe thats the conclusion reached for our genome in general), and that any distrubance prevents large scale evolution due to the interdependent, specified, and interconnected nature of the organism. Its problematic because it poses as a problem for how gradual structural changes occur over time. Mr. Nakashima, thank you for your posts. No offense taken! We're all (I think) trying to learn something here or expand in one way or another. You said: Every cell doesn’t come with a fixed 3D street address. it is better known by the sequence of cell types it has gone through before becoming fully specific. There are patterning factors such as noggin and chordin that establish the basic 3d axes of the embryo, but once the organogenesis stage is reached, all the overlaying morphogen fields become quite complex as the interact with the cell types. Some cells also are developed in one place, then migrate to another (a process which can be interfered with by the mother drinking alcohol during pregnancy, FAS). Alright, this is a rough sketch of the parts of some theories for how things work. But it hasn't been fully nor emperically tested, it gets very fuzzy at the "complex interactions" and "morphogens" stage, and even way before that. Anything we say now is merely speculation. The point I'm disagreeing with is that cells have a kind of 3D pattern, one of the reasons being if it was simply a cascade of interaction between cell types...the slightest disturbance in the process or prevention of a certain cell type to interact with its "preceding" sequence would cause cascade failure. And, because I do not believe that it is mathematically possible any interactions between cell types or underlying tissues or factors will specify the layered sequence due to the high degree of specificity found. To illustrate my thinking better. If you had a solid dot, and you placed in an equidistant manner some gell around it in suspended state. You'd get a sphere. But if you did that, and got a dot with equidistant spikes, and all that was underneath was the iron ball, you'd suspect something else is acting. Now if you got a 3D smiley face, you'd really start wondering. As the smiley face grows, you cut off a part -under- the growing gell, and the part regenerates and the growing gell continues to grow. You use a ruler to prevent one side of the gell interacting with another...and the form uses another side to grow the same structure. Highly flexible. These are all the marks of a system where the target or goal are primary, and the factors leading to them are secondary. I hope that illustrates what I (and many other embryologists) believe to be the problem. All underlying factors from that point are used not as the causal root, but as the tools utilized to bring the structure about. Noggin and chordin and the axis notwithstanding. (and I have to say...the idea of axis as developing the 3D structure has not been verified, they form a solid core for the structure to build on...kind of like metal wiring in a building, but I know of no empirical evidence to state that they result into the 3D form we observe.) This level of morphological stability and detail, and fields of organization that run through the body can be verified with our own bodies...in a sense. If you get a cut on your arm that scrapes a large portion off (hope that doesn't happen), and prevent the "primacy" sequence of different parts by placing an obstruction, the body will develop and heal the area from any angle possible. Moreover, the skin will return along with the exact same hair spacing and will be just like new. You might disagree, but this process, to this day...has not been fully defined nor settled. Now consider the same things happen in an embryo during development, when its overall structure hasn't even had a chance to settle yet...and, supposedly, the developmental process uses itself for its own development, making any effect in the regulator affect the regulated...and here the regulator and regulated are one and the same. Therefore the dilemma. Regarding your little folk anti-evolutionary claims list. I'm interested to hearing your next post before responding to the whole thing. Its an interesting list, but I think we both agree that the real difficulties are far more to the core...and perhaps with how much we can really know, regardless of what we can possibly find out. Looking forward to your next post PS. Arthur, I am still awaiting your response, would appreciate it when you have the time. Have a few thoughts and questions on T-urf13 too that I'd like to ask.Blu_{June 23, 2009
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Mr Blu, To prepare to answer your question, I want to share my little folk typology of anti-evolution claims. 1 - Evolution doesn't happen. This can either be the Genetic Entropy argument of BA77 quoting Dr Sanford or simply the flat denialism of Gil Dodgen. Often paired with frontloading to explain real world variety. 2 - Evolution is resource starved. The resource usually chosen is time. This is the one that bothered Darwin, because then current estimates of the age of the Earth were too low, he felt, to allow evolution enough time to work. Often displayed on UD by KairosFocus. Inverted by creationists who assume a short time period and therefore must have very rapid evolution instead of none. 3 - Evolution works, but only because of X. Not really a disproof of evolution, but a relabelling of what is important. This is unlikely to be cast as Newtonian angels pushing molecules around to cause mutation. More likely to be: - Evolution works but OOL doesn't (help at the start). - Alfred Russell Wallace's help at specific stages. - Evolution is like three card monte. Don't watch the cups, watch the ball (FSCI). 4 - Evolution might work in the abstract but there is no evidence for it here in the real world. Here on UD, often argued by Joseph until a Google search or Wikipedia article deflects into a demand for a pathetic level of detail. 5 - Micro-evolution, but not macro-evolution. The limited modified hangout option. Be magnanimous about anti-biotic resistance, but attack macro-evolution using one of the arguments above. 6 - Sure evolution works, but no civilized person would want to use that kind of thinking. 7 - Evolution is a social construct of a privileged elite. 8 - Evolution is a religion, but can be attacked for not being the right religion, or for claiming a privileged place in a supposedly religion neutral society. As I said, purely my own taxonomy, and probably incomplete. But it should help frame my thinking in the next post!Nakashima_{June 23, 2009
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Mr Blu, Let me focus on the following: If you disagree that you cannot make an estimate, and that it doesn’t have to do with cell types, could you tell me how the specific cells attain their specific location, merging into three dimensional form and organs and how many regulatory genes (if they were in fact responsible) it would take from early development till full expression for the expression of the eye? We, first I should apologize if I caused any offense. I'm very sorry. My estimate of the number of genes remains the same - 100 or less. Every cell doesn't come with a fixed 3D street address. it is better known by the sequence of cell types it has gone through before becoming fully specific. There are patterning factors such as noggin and chordin that establish the basic 3d axes of the embryo, but once the organogenesis stage is reached, all the overlaying morphogen fields become quite complex as the interact with the cell types. Some cells also are developed in one place, then migrate to another (a process which can be interfered with by the mother drinking alcohol during pregnancy, FAS). i'll take up your question of disproving NDE in another post.Nakashima_{June 23, 2009
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Back to the book: "Signature in the Cell"- my copy arrived this morning. I will dig in later today...Joseph_{June 23, 2009
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Hi blu, And I propose that the interactions themselves are not sufficient to explain the structure of organisms. What specifically leads you to this conclusion? (I'm now quoting from your other post) You’ll find that all major changes have been quite limited in morphological scope, and any attempt to create a major change has led to fatality. Is this problematic? Most mutations of large effect can be expected to be lethal. Ronald Fisher was pointing this out in the 1920’s. I'm not sure what your point is here. I mean new body plan major/serious change in size and shape that still makes the organism coherent, and isn’t merely replacing an antenna with a leg. etc.) Again, I’m not sure what you are getting at (I admit, it’s late, and I may just be too tired for the relevance to make it through). So I'll quit while I'm behind.Dave Wisker_{June 22, 2009
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And regarding your mention of fruit-flies (and any other experiments on the development of animals in general). You'll find that all major changes have been quite limited in morphological scope, and any attempt to create a major change has led to fatality. We know the same genes are used for the development of different organs, we know same organs use different genes and we know same organs embryologically develop from different parts of the embryo between different species, and when I say the same organs...I mean the exact patterns not some generalized similarity, Gavin de Beer raised this issue all the way back in the mid-late nineties. (and I don't want to get technical here to name an extra wing major, I mean new body plan major/serious change in size and shape that still makes the organism coherent, and isn't merely replacing an antenna with a leg. etc.)Blu_{June 22, 2009
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Mr. Nakashima, Heh, take it easy with the ignorance part. I gave the guess as the lowest concievable (on my part) estimate on what it would take, plus some of the numbers I recall from reading. If you disagree that you cannot make an estimate, and that it doesn't have to do with cell types, could you tell me how the specific cells attain their specific location, merging into three dimensional form and organs and how many regulatory genes (if they were in fact responsible) it would take from early development till full expression for the expression of the eye? This doesn't have to do with a cell type, it has to do with the where and the how. A bunch of cell types without specificed localization and organization and development isn't the point. A form is exactly that, a full form. Be it on the level of genes or their "interactions" no one really knows how forms come to be the way they are. We can signal correlations, but we don't know how it all fits together...and persume it to be one way or another. I wasn't focusing on plants, I was just responding to David's example to clarify what I mean by morphological development. If you know of a way that the venus flytrap's -shape- can arise from another organism (any other organism, evolution aside...even through genetic engineering), I'd be interested to hear it. The fact of the matter is...there are is no real theory of morphology, and generalizations simply won't do. Regarding the books, I did read Wallace's book, and if you noted the list I wrote to David earlier, you'll find that a few of those are technical. Finally, I invite your response to the other points...I do apologize as there were quite a few of them, but your response would be appreciated when you have the time. Specifically (and amongst them), if you were to try to disprove neo-darwinian theory, how would you do it and where would you start? What do you find weaknesses with?Blu_{June 22, 2009
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Mr Blu, First you hazarded a guess that the eye itself took 1000-2000 genes to build. I responded with an estimate based on cell types that was much lower. Now you say that you can't even guess. There is no need to retreat into statements of complete ignorance. You may be interested in reading The Shape Of Life, by Rudolf Raff, or The Origin Of Animal Body Plans, by Wallace Arthur. Both are more technical than the popular evo-devo books like Carroll's. i'm not sure why you have focused on plants, but sea urchins and fruit flies are very well studied models for development as well. With respect to the Venus Flytrap plant, I don't know if it has had its genome sequenced. I'm not sure why you think it couldn't be developed from modifying a more primitive plant. The trapping mechanism is not "irreducibly complex".Nakashima_{June 22, 2009
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(and as a side note, I'm not asking these questions in an argumentative manner. I'm genuinely asking for the answers, and really appreciate the time you take for your response. I think I kind of pulled the discussion in multiple angles, but I hope everyone here has the time and desire to continue with this conversation.)Blu_{June 22, 2009
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Arthur, Thank you for your response. I'll give what you mentioned some thought and do some research. Whats your take on Dr. Behe's Protein Science paper? From reading it, I understand arriving at multiple protein residues can be quite difficult. How would you suggest something requiring as many proteins and parts as the flagellum came about? And why would something as rapidly generating as E. Coli, Malaria or HIV not be able to generate constructive cellular functional proteins?Blu_{June 21, 2009
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Hey Dave, Right, when I said map out...I meant the extention of the interactions of the genetic material "out" into the organism. And I propose that the interactions themselves are not sufficient to explain the structure of organisms. And regarding randomness and chance, I understand that natural selection doesn't make it random per say, but I was using the word in its strongest sense. That is...that these forms can arise without some underlying principle (whatever that may be) that is aware of the context of the organism as a whole, where its heading and how to get there. Just like if you input a string of data representing dots on a screen to a computer program, through trial and error the computer will be able to refine its existing code to perhaps simulate an organism moving right/left when dots appear on one side of the screen or another (even that would require quite a bit of information), but it would never reach a point where it recognizes what...say, a square is. I look forward to hearing your response. (and Mr. Nakashima's, Arthur's, Bruce's and everyone else who might take interest)Blu_{June 21, 2009
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Hi blu,
I’m rambling again…it is exciting stuff. But wouldn’t you say its important? Here we have an entire civilization stating something or another is a fact about how things came to be, when we haven’t even begun to understand what the thing in question -is-. Do you think forms of this degree of efficiency could come about by random mutation+chance?
I am enjoying our conversation as well. I’ll start by making sure we are both clear about evolution not being just random mutation and chance. Variation has a chance element to its generation (and even then it isn’t random in the mathematical sense). Much of that randomness is constrained by natural selection, which is the antithesis of random.
Beyond correlations between control genes and expression in multicellular organisms, there is simply very little in the way of knowledge that anyone has on how genes map out into specified 3D shapes of -extreme- specificity along multiple stages (not just in terms of general morphology, but in terms of cell type X at point Y), and can regenerate/form regardless of the primacy of the cells neighbouring them, or any mapping hypothesis. What is even more disturbing is the fact that the same organs/limbs across different species (and lineages) arise developmentally from different areas during development.
Let me throw this out to start. Strictly speaking, genes do not “map out” into anything. They merely specify the structure (and resulting functionality) of the individual proteins for which they code. The morphology and control of the morphology is actually more a function of the interactions between the proteins coded by the genes. That is, the true complexity of an organism does not lie in the information carried by its genes, or even in the individual proteins themselves. Instead, the complexity lies in how those proteins interact not only with each other, but the environment as well. It is the biochemistry of the organism that is complex, not the information carried in its genome, and it is the biochemistry which determines morphology and form. That’s all I have time for at the moment. Take cae.Dave Wisker_{June 21, 2009
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Hey Dave, I wouldn't say I'm any kind of expert on the matter. You might even know more than I do! If I do have to contribute something to the discussion, its simply to state whats actually missing...and to state what my own personal reflections on the extents of any reactive system is...which I've done quite a bit of thinking and discussing on. Beyond correlations between control genes and expression in multicellular organisms, there is simply very little in the way of knowledge that anyone has on how genes map out into specified 3D shapes of -extreme- specificity along multiple stages (not just in terms of general morphology, but in terms of cell type X at point Y), and can regenerate/form regardless of the primacy of the cells neighbouring them, or any mapping hypothesis. What is even more disturbing is the fact that the same organs/limbs across different species (and lineages) arise developmentally from different areas during development. I've read quite a bit of books on the subject though, and a lot of articles. The books that, amongst others that come to mind are: From DNA to diversity and Endless forms most beautiful, Biological Physics of the Developing Embryo, How the Leopard changed its spots, Biased Embryos and Evolution, The Art of Genes, From Embryology to Evo Devo, Origination of Organismal Form... Sheldrake's books, which I still consider scientifically worthy (and its always good to stir things up a bit) offer some very interesting points. In summary, evolution is the theory of how life came to be the way it is. Yet, we do not know how forms become the way they are, we do not exactly know how they stay the way they are and that they don't Butterfly Effect apart from changes and spiral out of control. To imagine the sheer volume of the task, image a machine that generates itself, maintains itself, organizes itself, regulates itself...-to the nanobot-, in a way more complex than a Transformer would (and I do look forward to the second movie). And then imagine that it would have to do so reactively (and by chance, over time)...I don't see how that can be possible, a regulating agent that has an informational blueprint of the structure as a whole (and this is just my personal view on thinsg) must exist. This presents a challenge to the current evolutionary paradigm. How does a cell know where it is? How does the body know where its components are? How does it maintain temperature regulation with such a varying degree of chemical reaction? How do cells split into daughter cells from a contextual perspective? When and how does the body know when to activate a component or another, and how does it regain equilibrium when the entire system is disturbed? How does an embryo or body regulate when its very organizational and regulatory features are themselves in constant regulation (even the brain is now known to continuously rewire itself). I'm rambling again...it is exciting stuff. But wouldn't you say its important? Here we have an entire civilization stating something or another is a fact about how things came to be, when we haven't even begun to understand what the thing in question -is-. Do you think forms of this degree of efficiency could come about by random mutation+chance? One last point I'd like to add, is that brain/informatino system's evolution is also being currently ignored. This is another elephant in the room. Lets take the bat example. If someone had a computer program capable of even some complex coding features, could it ever arrive at a 3D layout from getting sound signals without having prior information on what 3D is, how to interpret the signals, how to understand relationships between them, how to signal out noise. -massive- amounts of information...we employ the same degree of complexity in our 3D hearing or seeing. I think most have an idea regarding cognition as a bunch of wiry nerves that randomly move about...step by step increase in complexity and then kind of...blllaaah...an emergent order arises. But out of my reflection on the matter, you can't increase the information of a program by randomly putting strings in its code, nor by giving it feedback yes/no. It will reach a high degree of efficiency and refinement at its current level of information (if the noise isn't strong), but won't exceed that. I'm glad to be discussing this with you, I hope to hear your feedback soon. What would you say are the difficulties for the current evolutionary scenario? If you were to try to disprove it, where would you start and what would you find problems with?Blu_{June 20, 2009
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Dave Wisker:
T-Urf13 had a natural origin in maize. How could it arise by artificial selection? Selection–artificial or otherwise— does not generate the variation.
Artificial selection allowed for the development of the gene. Without artificial selection no corn no Turf-13. It's pretty basic actually. MY POINT has ALWAYS been that this (Turf-13) is NOT an example of IC being formed via RM and NS.
Then don’t bring up minor points–especially if you cannot take correction of your errors on them gracefully.
Your point about Turf-13 being IC has been soundly refuted and neither you nor Art took the correction gracefully. As a matter of fact both of most likely still think it is an example of IC coming about via random mutations and natural selection.Joseph_{June 20, 2009
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Hi Blu, Thanks for your interest. You asked:
1- The specific gradual changes that occured, their order and timing of their occurance
Several recombination events occurred (I don't recall the exact number, but it was more than five). The order is not known. I don't know what you mean by timing.
2- Whether they were in fact gradual ( did the arisal happen with what we expect for how many “steps” are possible for this particular organism, and did it occur with what we probabalistically expect to be reasonable), or arose at once. And if they did arise gradually, why was each step selected.
The series of recombinations was probably sequential (is this what you mean by gradual?). Plant mitochondria do this sort of "shuffling" of their genomes pretty regularly (relative to an evolutionary time scale).
3- Whether the origin of the gene is recent or whether it was already present in the information and combinatory potentiality of the genome.
The gene originated in the 20th century, as part of breeding programs focused on making new and improved corn hybrids.
4- Whether the gene was triggered by some environmental trigger, and existed within the combinatory potentiality of the genome.
??? Are you asking if the gene itself is under regulatory control? Or if the recombination events were triggered by environmental signals? In any case, this gene came from sequences that have or had no protein-coding potential or history.
I should also add the following, you mention in the last part of the essay that functional proteins are not difficult to attain, if I’m understandnig you correctly. Would you state that as a general rule?
Yes.
Are you saying achieving coherent functional proteins beyond specific combinatory potentialities within the organism’s already existing structure (how those potentialities came to be is another issue) isn’t difficult? And that it isn’t case specific?
Yes. Of course, by "difficult" I would mean possible well within the limits places by population sizes, and the frequencies of occurrence of the many processes that contribute to the origination of new protein-coding genes. I discuss this here, here, here, and here.
Moreover, (and this might be an ignorant statement on my part) isn’t the entire effort based on observing homologies between 2 parts with proteins in other corn genome, and the third part’s homology is not found? How much can we certainly and accurately extrapolate from that?
The sequence similarities involve parts of the maize mt genome that do not encode protein. We know that plant mt genomes undergo all manner of recombinational shuffling, so we can be fairly certain as to how the T-urf13 gene came about.
And! (Finally, I promise), what is the basis for accurately and certainly stating that the origin of the gene is recent? (this doesn’t bear much, but it is nonetheless relevant)
It occurred (quite randomly) as a part of breeding directed at making new and improved corn hybrids. I don't know exactly when the Texas cytoplasm was released, but this event was clearly a 20th century event, probably in the 40's or 50's.Arthur Hunt_{June 20, 2009
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Hi blu, I'm off to work now, but I thought I'd at least acknowledge your comments. Given the nature of your questions, I'm reluctant to contribute much more, since developmental biology is way outside my area of expertise (I'm trained in Ecology, Population Biology, and Genetics). You seem to have done some research on the subject, so I think it would help if you gave some indication of what level of study in developmental biology (courses, textbooks, etc) you have taken. That way I'd know if I don't have much to contribute to the discussion and should just shut up and listen ;)Dave Wisker_{June 20, 2009
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And! (Finally, I promise), what is the basis for accurately and certainly stating that the origin of the gene is recent? (this doesn't bear much, but it is nonetheless relevant)Blu_{June 19, 2009
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Moreover, (and this might be an ignorant statement on my part) isn't the entire effort based on observing homologies between 2 parts with proteins in other corn genome, and the third part's homology is not found? How much can we certainly and accurately extrapolate from that?Blu_{June 19, 2009
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I should also add the following, you mention in the last part of the essay that functional proteins are not difficult to attain, if I'm understandnig you correctly. Would you state that as a general rule? Are you saying achieving coherent functional proteins beyond specific combinatory potentialities within the organism's already existing structure (how those potentialities came to be is another issue) isn't difficult? And that it isn't case specific?Blu_{June 19, 2009
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Hello Arthur, Good to hear your response! Would love it if you could join in on the other points in the discussion too if you have the desire. The essay was very well written, thank you for sharing it, and frankly provides the only IC system that I'm aware of that has been "observed" to arise live so to speak. What isn't clear to me, as with most cases with studies of this sort. Is the following: 1- The specific gradual changes that occured, their order and timing of their occurance 2- Whether they were in fact gradual ( did the arisal happen with what we expect for how many "steps" are possible for this particular organism, and did it occur with what we probabalistically expect to be reasonable), or arose at once. And if they did arise gradually, why was each step selected. 3- Whether the origin of the gene is recent or whether it was already present in the information and combinatory potentiality of the genome. 4- Whether the gene was triggered by some environmental trigger, and existed within the combinatory potentiality of the genome. The main point is I'm trying to ask: Did it in fact arise randomly and gradually? I'm not saying it did or didn't, simply asking what we do and do not know.Blu_{June 19, 2009
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I don't mean to reiterate, but I would really appreciate it if someone could aid me with this question. Its probably a very basic question for a lot of people here, and its important for me to get a clear answer: "For now, I have a question for the experts here…it might seem like a silly question but I ask your indulgence. How many steps can we expect to happen at once? Can we give a number. If there was no selective cleansing going on (where a mutation that wasn’t beneficial wouldn’t move forward) is there a limit to how many new steps/components an organism can have laying around? Or does the number increase indefinitely over time till something “clicks”(again, presuming that no selective cleansing pressure exists and the organism keeps reproducing)?"Blu_{June 19, 2009
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Out of curiosity, did T-urf13, and the breeds before it undergo any artificial genetic modification?
No.
And, as I mentioned earlier…I don’t think anyone has a clear idea on what the gradual changes leading to T-urf13 were, why they were retained, etc.
So what is it that is unclear about the figures and discussion in this essay?Arthur Hunt_{June 19, 2009
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Hi Dave, Thanks for your response. Your example is a good example for the discussion, and perhaps might make me clarify my position further. Just like in the other examples Mr. Nakashima generously provided, the genes here act like a switch, press play, press stop. What I was referring to is the structure of the plant itself. Plants...are tricky. But, I believe you'd agree with me that all changes have maintained a plant's inherent structure and form within a defined boundary. Consider the venus flytrap. The boundary I'm talking about is if you get a plant, and change its genes as much as you want, you'll never get to a venus flytrap. The morphological form itself, and underlying structure requires additional factors. DNA, from my study and reflection, provides in multicellular organisms three components. (and again, plants are tricky...and as with all things...demarcation lines aren't black and white). The first is the raw material, or more specifically an intersectional point of energetic transformation (from one kind of energy/chemical to another), the second is it provides the switches themselves. Note...I'm not saying it does the switching, I'm saying it contains switches that can be utilized to turn other things on and off. The third, is it might have a yet unknown property that functions as an organizational force in the cell, allowing it to be an intersectional point for that too. Now the last one might seem a bit woo-woo, but time will tell. Imagine a painter using a brush, palette and has a bunch of materials to make her canvas. If you change the kind of brush, its tip, its curve, or if you change the colours, or the material of the canvas she uses, the painting will come out different. Or if the painter needs some signals and ques to start painting one part or another, and those cues change...the result will differ. Nonetheless, none of these agents were the sole responsible factor for the generation of the painting. If you search the literature...you'll find an immensely scarce supply of information on the generation of form and morphology. The best you can find are on plants, and its still not clear how things work. The critical point is: How does an organism recognize its spatio-temporal position in relation to the rest of the structure? The question's difficulty becomes compounded when you realize that shifts done to the entire structure (whatever it is considered to be dependent upon), doesn't change the direction of development nor the form taken, and that the same cell types take widely varying forms within the same organism. Its quite astounding and awe inspiring...if you look at for example, the development and branching out of the nervous system during development. To respond to Mr. Nakashima, I frankly have no idea how any number of control genes can direct any course of development to the degree of flexibility we observe. I am unable to generate or find a concept that applies. Multiple theories were provided in the past, cells get their developmental motion from the primacy of other cells. Ok...but if you change the other cells, everything goes fine, moreover if you change the angle of a developing embryo, it will contniue in its proper morphological trajectory. Cells attain a sort of chemical equilibrium: too general, doesn't account for specificity of form or ist generation, and if you disturb the equilibrium in different ways you get the same result. Mathematical models account for the growth of cells, ok...but mathematical models would need to be highly specified and would change over developmental time...they don't just accumulate one on top of another, and so on. So for now, I'll choose silence. I think you'd both agree with me that the question: "How do forms arise?"...respectable opinion notwithstanding, is poorly answered. We understand -correlations- between the availability of switches in genes and their expressions. Gene controls in the past was actually used as a metaphor...now, its become the Word. Out of curiosity, did T-urf13, and the breeds before it undergo any artificial genetic modification? If it did, regarding what I mentioned earlier...a particular genetic change could have expanded its evolutionary funnel and allowed it to progress in a direction it otherwise couldnt've. This isn't a point against the ICness of the system. And, as I mentioned earlier...I don't think anyone has a clear idea on what the gradual changes leading to T-urf13 were, why they were retained, etc. And, a question to those who lean more to the side of the darwinian side of things. How do we deal with changes in organisms that require massive amounts of coordination, across multiple factors within the organism? Like what we spoke about before. See...the difficulty is, no one knows exactly how a neural network changes its structure, how a lung takes its shape...this is why there's so little talk on these issues, and so much on how gene controls inhibit this, or activate that, and on how shifts on the reactive components of an organism result in others. But if a change in an organism required shifting its skeletal structure, muscular structure, neural networks, associated information in the brain, surpassing thresholds of pain to account for the transformation, change of weight and accustomed to balance, behaviour and habits, metabolic pathways and habits. Or something as radical as bats echolocation (imagine the first "random neuron" starting in the alleged pre-bat, making him see flashes whenever a sound arose...how useful would that be). 3D internal holographic generation from sound signals is something even we haven't mastered! And when we say, skeletal, muscular, nervous, brain, etc. Imagine the amount of complexity required to carry those things out by subtle biochemical changes. When considering the necessity of coordinated change of this kind, how do we expect these changes to happen randomly again, and again, and again. And across different branches of species, numerous times. Across some very clear defined boundaries sometimes too, like insect metamorphosis, shifts in ways of oxygen intake, joint restructuring, cognitive maps, and many more (and joints are very location specific, slightest deviation will lead to a lock or a loose joint). Couple that with the fact that a lot of these features appear quite fully formed with all their information networks from the beginning (Cambrian), without any indication of a precursor...and I start getting pretty skeptical really fast. I look forward to hearing your response.Blu_{June 19, 2009
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joseph, T-Urf13 arose naturally in maize. No it didn’t. It arose due to artificial selection. T-Urf13 had a natural origin in maize. How could it arise by artificial selection? Selection--artificial or otherwise--- does not generate the variation. Male sterility- more susceptible to fungal infections- yeah I would say it is more detrimental than beneficial. Given your level of actual knowledge on the subject, and the evidence available to easily rebut it, your saying so doesn't cut much ice. But again that is only a MINOR point. MY POINT has ALWAYS been that this (Turf-13) is NOT an example of IC being formed via RM and NS. Then don't bring up minor points--especially if you cannot take correction of your errors on them gracefully.Dave Wisker_{June 19, 2009
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Hi Nakashima, We can take your example one very impressive step further. If we assume a very simple model, whereby each and every cell in a human body (all 1 trillion of them) is specified by a unique combination of gene switches (say, transcription factors), the we would need only 40 or so such proteins to completely and uniquely define each and every cell.Arthur Hunt_{June 19, 2009
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Mr Blu, Thank you for inviting my further comments. Lets think about all the different cell types in the human body. The Wikipedia list of cell types is about 210 distinct types of cells. But to be safe from our own ignorance, lets double that, and round up to 500. Now lets double that again to cover all the cell types that might exist during development, but not in the final adult body. So human development takes 1000 cell types. Wow! How many gene switches would it take to regulate all those? 10. 2^10 = 1024. OK, our bodies might not be that efficient in terms of using switches, so double it. 20. Maybe each signalling gene needs 3 other genes to work right. 80. Lets round up and say that to be safe our original estimate of 10 was off by an order of magnitude. 100. So the body uses 100 genes to build the eye. It uses the same 100 genes to build every other cell type. That is cool.Nakashima_{June 19, 2009
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And one more refutation- Turf 13 provides only ONE component. I don’t know any IDist who says that undirected processes cannot account for ONE component.Joseph_{June 19, 2009
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Dave Wisker:
It doesn’t matter one iota that maize is a cultivated plant.
Maybe not to you but to the IC argument it matters a great deal.
T-Urf13 arose naturally in maize.
No it didn't. It arose due to artificial selection.
T-Urf13 is a CMS gene.
So what? That is irrelevant. This discussion is about IC not male sterility. The WHOLE point of Turf-13 is that it allegedly procuced an IC system. The part of it being detrimental is just a small part of that. Male sterility- more susceptible to fungal infections- yeah I would say it is more detrimental than beneficial. But again that is only a MINOR point. MY POINT has ALWAYS been that this (Turf-13) is NOT an example of IC being formed via RM and NS. And that much is obvious.Joseph_{June 19, 2009
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Joseph, But corn is the result of ARTIFICIAL selection. And via artificial selection male sterility in a hermaproditic plant population can most definitely occur. What part of that don’t you understand It doesn't matter one iota that maize is a cultivated plant. T-Urf13 arose naturally in maize. It wasn't artificially introduced. T-Urf13 is a CMS gene. CMS can arise in natural populations and can be maintained in them. Thus your attempt to argue that T-Urf13 is a detrimental mutation is rendered impotent. Why did you try and argue that T-Urf13 is a detrimental gene, joseph? Why did YOU bring it up? That is what I am responding to-- YOUR point. And when I do you divert the conversation by sudennly announcing its all about IC now. Why bring up the point about it being a detrimental mutation when all you REALLY want to talk about is IC?Dave Wisker_{June 19, 2009
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