Uh Oh! Is He Going To Get Gould-ed?

_{November 9, 2010

Intelligent Design}

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The word “borked” has entered our lexicon as a result of the treatment Judge Robert Bork received during Confirmation Hearings for Supreme Court Justice of the U.S. To put it mildly, he was not treated very well. When Stephen J. Gould came out with his theory of Punctuated Equilibria, he, too, was not treated well by the Darwinian establishment until such time as he made clear that his theory was firmly a part of Darwinian thought.

Now another geologist, Michael Rampino, has just set himself up for equal treatment. In a PhysOrg entry, Rampino points out what has been so obvious for so long a time: evolution is NOT gradual! It is episodic. He also seeks to go further back in time to Patrick Matthew, who predates Darwin and his notion of NS by thirty years or so. I think Michael has been reading far too much here at UD for his own good health (academic, anyway). It’ll be interesting to see how quickly he is gobbled up by the Darwinian thought police.

Comments

Mark: There does appear to a lot of literature about frameshift mutations and their ability to create novel proteins. I am not expert enough to evaluate them but isn’t the sdic gene another example? No. It is a completely different situation, mainly a chimera of two existing genes by duplication and retrotransposition and some minor mutations. No frameshift involved, as far as I can see.gpuccio_{November 15, 2010
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MathGrrl: I already had an interesting and rich discussion with Zachriel in the past on Mark's blog. That can certainly happen again. I am absolutely available, and I would really appreciate a direct confrontation with him, at least as much as is allowed by time and resources. And no, I will not post at PT or similar. First of all I really don't appreciate some attitudes very common there, especially the scientistic arrogance. But anyway, there is another simple reason why I have to post mainly here. I am one, and I can try to detail my positions here because I don't usually have (but sometimes it happens here too) to face the various objections of tens of people, some of them sincerely interested in a constructive discussion, some not. It is a fact that ID is a minority position, and that respect for it as a scientific theory is not common in the other field. This is the reality we have to deal with, and I can deal with it in a better way here. But sometimes I appreciate a confrontation in a neutral enough territory. Recently I have debated for some time on Niel's blog, but even there, with only three interlocutors, the huge variety of the objections and the scarce "cooperation" of at least one of the interlocutors forced me to go away at some point.gpuccio_{November 15, 2010
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gpuccio,
thank you for pointing to Zachriel’s comment about my posts. As you know, I really appreciate his contributions, which are always intelligent and respectful. I am really sorry that he can’t post here. Unfortunately, I don’t usually read in the place where he writes, because it is not at all an useful experience (except for a deeper understanding of the worst trfaits in human nature). Not Zachrile’s fault, obviously.
I would find a conversation between you and Zachriel to be very interesting. While I suspect you would get a warmer welcome than you think at The Panda's Thumb, if that's not your cup of tea, how about inviting Zachriel to a mutually agreeable venue. Perhaps Dr. Hunter would be willing to open a thread on his blog for the two of you.MathGrrl_{November 15, 2010
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gpuccio, I think you may find this link interesting: A New Guide to Exploring the Protein Universe "It is estimated, based on the total number of known life forms on Earth, that there are some 50 billion different types of proteins in existence today, and it is possible that the protein universe could hold many trillions more." Lynn Yarris - 2005 http://www.lbl.gov/Science-Articles/Archive/sabl/2005/March/02-protein-universe.htmlbornagain77_{November 15, 2010
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gpuccio, thanks very much for the link. If you don't mind I will also use your explanation for how they are grouped since it is very clear from your generous groupings as to exactly how much leeway is granted to Darwinists so as to give ANY plausible explanation, much less adequate explanation, for the origination of the many fundamentally different proteins that operate in tightly integrated fashion.bornagain77_{November 15, 2010
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#54 Gpuccio Of course Zachriel has no opportunity to respond to your comment here. I am in a rush right now but will try to create and opportunity for discussion on my own blog later today. On nylonase. It is interesting that evolutionary theory allows for specific hypotheses about how a gene came about - in this case disproved. Compare that to ID! There does appear to a lot of literature about frameshift mutations and their ability to create novel proteins. I am not expert enough to evaluate them but isn't the sdic gene another example? At least the paper is a detailed hypothesis about how a novel gene was created. As far as I know, In the course of its 20 years the ID community has not made a single proposal as to how a gene was created.markf_{November 15, 2010
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#52 Pav Yet, I think of Behe’s work with the malarial parasite. Here is a premier replicator. And, if neutral drift is going to make these handy “intermediaries” available, it would be a great replicator. However, in TEoE (The Edge of Evolution) the malarial parasite took an estimated 10^20 replications to come up with the simply 2 amino acid solution that Chloroquine resistance required. My question then is: where were these handy “intermediates”? I am no expert on the mutations that lead to chloroquine resistance but a brief skim of the literature suggests that (1) Different populations of mosquitoes gained their resistance through different mutations (2) We don't know precisely what mutations were necessary in any of these cases (3) No one has investigated to see whether intermediaries do exist.markf_{November 15, 2010
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Mark: thank you for pointing to Zachriel's comment about my posts. As you know, I really appreciate his contributions, which are always intelligent and respectful. I am really sorry that he can't post here. Unfortunately, I don't usually read in the place where he writes, because it is not at all an useful experience (except for a deeper understanding of the worst trfaits in human nature). Not Zachrile's fault, obviously. I have read the two posts you link. They say correct things, but irrelevant. The first post is merely restating what I have stated many times: that RV + effective selection of each step works. I have just posted about that in another thread, restating the concept. My words are almost exactly like Zachriel's. So, I can see no disagreement here. In the second post Zachriel, maybe forgetting that he himself has used the wrong example of nylonase to support his claims about frameshift mutations, misses a good occasion to remain silent, and is forced to use a couple of theoretical model papers which really demonstrate nothing. Zachriel, I am waiting for a new "nylonase like" example. Maybe you will be luckier next time. In the meantime, be more cautious about what papers you boldly present as "evidence". :) His remark about possible translocation of motifs is obviously correct, but irrelevant to the origin of superfamilies (exon shuffling can certainly be a mechanism for multi-domain proteins). His statement that "random sequences can result in new proteins, including many of the stable folds found as the basis of protein superfamilies" is completely gratuitous and unsubstantiated. His admission/statement that "there may be more than a single ancestor for proteins families, but nothing suggesting design" is simply funny. Anyway, thanks Zachriel for the interesting contribution. Mark, going back to you, I accept your expanations for what (IMO) they are: honest, but completely unconvincing.gpuccio_{November 14, 2010
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Gpuccio I lack the expertise to continue this discussion. But it appears that Zachriel, who is one of the many with expertise banned from UD, does. He has made relevant comments on antievolution.org here and here I can only take a philosophers look at it. If there are no intermediaries between two proteins there are two possibilities: (1) They never existed (2) They existed but were removed My explanation for (1) is that there was a large change mutation. You say that the probability of such a mutation being viable is too small. Well that is a long discussion beyond my skill. Remember a translocation moves a viable piece of DNA which may well have been coding for usable proteins elsewhere. Also the resulting mutated DNA does not immediately have to be viable. It may not be expressed and can itself be subject to random variation, recombination etc. The true estimate of the probability of getting a usable result strikes me as a very hard sum even to an order of magnitude. My explanation for (2) is that the intermediaries were eliminated by natural selection. You consider that to be an ad hoc explanation but of course this is only an extension of the theory of allopatric speciation which has considerable theoretical and empirical support. Meanwhile what could be more ad hoc than an unknown designer of unknown powers and motives made it that way?markf_{November 14, 2010
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markf: In earlier posts you seemed to be relying on various functional intermediaries that just happen to be hanging around---and, hence, not requiring time to appear. Yet, I think of Behe's work with the malarial parasite. Here is a premier replicator. And, if neutral drift is going to make these handy "intermediaries" available, it would be a great replicator. However, in TEoE (The Edge of Evolution) the malarial parasite took an estimated 10^20 replications to come up with the simply 2 amino acid solution that Chloroquine resistance required. My question then is: where were these handy "intermediates"? Remember, Behe dealt with empirical evidence. These are raw facts.PaV_{November 14, 2010
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Whoa GP. Thanks.Upright BiPed_{November 14, 2010
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BA: I always refer to the data in the SCOP (Structural Classification of Proteins) site, here: http://scop.mrc-lmb.cam.ac.uk/scop/ The SCOP classification is based on 38221 PDB (Protein Database) entries, for a total of 110800 Domains, and is at present updated at June 2009. Practically, it is based on all we know of the protein structures in the existing proteome. If you click on "Folds, superfamilies, and families statistics here. ", at the top of the home page, you will get a table (the most recent), which gives the total number of folds, superfamilies and families (and the number of them in each of the basic 7 biochemical types). The "folds" grouping includes at present 1195 entities, the "superfamilies" 1962, the "families" 3902. To get an idea of how that relates to primary sequence, you can go from the home page to another tool, by clicking in "Access methods" on "SCOP domain sequences and pdb-style coordinate files (ASTRAL)". In the ASTRAL page, click on "SCOP 1.75 Sequence Resources". You will get a tool which allows you to download a list of identifiers of genetic domain sequence subsets (IOWs, of basic domain types), grouped according to criteria you can specify. If you use the "percent identity" criterion, and set it at the smallest value (less than 10% identity), you get a list of identifiers. If you count them (you can easily do that by copying them and pasting them in Excel), you will see that they are 6258. If you do the same with the E-value criterion (which is more or less the probability that two sequences are unrelated) and you set it at the highest value of 10 (which means no significant similarity at all), you get 6041 values, which is more or less the same result. These are the broadest groupings you can have. The ASTRAL results are based on primary sequence, while the concepts of fold and superfamily are related to the 3D structure. As you can see, they are even more restrictive (there are proteins which have completely different primary sequence and similar 3D structures). If you use less restrictive criteria in ASTRAL, you can get higher numbers: for instance, if you set the percent identity to less than 20%, you get 7002 results. But the concept is very clear. However we group the proteome, we have at present at least 1000 different fundamental folds, 2000 "a little less fundamentally different" folds (the superfamilies), and 6000 totally unrelated groups of primary sequences. I generally use the superfamily number, because I believe it is the most representative. These are the basic "functional islands". That does not mean that in the context of a superfamily all is easy to explain for darwinists (not at all!). But there are priorities. The explanation of how the basic functional units came into existence remains, IMO, the main problem, at least at this basic "single protein" level of analysis. That's why Axe, for instance, is focused on that aspect too.gpuccio_{November 14, 2010
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gpuccio, do you have a good reference for protein superfamilies? I looked around a bit but seem to be getting numbers all over the place, from 'several thousand' to over 60,000.bornagain77_{November 14, 2010
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Mark: Maybe we understand a little better now. Just a few further remarks: a) I have discussed frameshift mutations because that was the only mechanism of "sudden big transition" for which (as far as I am aware) at least one explicit model (although wrong) has been suggested (nylonase). But any other mechanism (inversion, deletion, traslocation) can be treated in the same way. The problem is: such random events can certainly change a lot of aminoacids at a time. In the same way, random neutral mutations can change a lot of aminoacids sequencially, without any need of functional intermediaries expanding in the population. In the end, there is no difference. Thet are random mechanisms anuway. All these purely random mechanisms can certainly, in principle, determine a final functional transition of, say, 50 aminoacids. But the problem is that, being completely random, they must be evaluated by a probabilistic model. IOWs, by insisting for a model without functional intermediaries which expand for positive selection, you are practically dropping the darwinian theory in favour of a purely random model, which is a way to renounce to any explicatory power: a random model will not do, as we in ID know very well. It's not a case thyat darwinists constantly appeal to the necessity part of their model, NS, to defend themselves from the attacks of ID. But the intervention of positive NS is possible only if the deconstruction into functional intermediaries can be achieved (and it can't); and anyway, it raises the problem of the fate of the intermediaries. So, it's not me who want the intermediaries at all costs. It's the darwinian model which requires them! b) About the erasure of the intermediaries being "just one thing that happens sometimes". My model is about the emergence of superfamilies. I am explicit and detailed about that. We have 2000 superfamilies, not one. Each of them emerged at some point of natural history. For none of them are intermediaries known. Is that your idea of "sometimes"? In a superfamily, it's not so much that "intermediaries exist". It's just that the basic function in maintained throughout the whole natural history of the superfamily. Myoglobins remain myoglobins, both in the mosquito and in humans. Waht we observe is a continuity in the homology and differences at the primary structure level, which I have myself brought here as a good argument for common descent. But no new function is "discovered". In other cases, like in the recent article about nuclear receptors, we can find in a single suprefamily a variety of different sub-functions (in the context of the basic function which remains the same) which can be explained by slight variations at the active site level. These variety of subfunctions is usually in the range of microevolutionary transitions, so it can be potentially explained by a microevolutionary model. However, I don't believe that true intermediaries are knwon even here, but indeed, being the transitions small, they are not really necessary in this context. For protein families which are strongly different at primary level, even in the context of a same superfamily, a detailed analysis should be carried on in each case. But the fundamental question remains: how was the primary level of protein functional information (the 2000 superfamilies) generated? c) You say: "unless of course you are prepared to discuss how it is implemented and by whom – in which case it gets a little harder." I am certainly prepared to discussed that. So should be science. And hard does not mean impossible. It can be done. And, however hard it is, we can at least hope to find scientific explanations that way. But not certainly sticking to models which don't explain anything and which are falsified by facts.gpuccio_{November 14, 2010
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#46 Gpuccio I am sorry. You are quite right you did attempt to address the "frameshift" argument. Although I think the way you address it fails. (1) Frameshift is by no means the only way that a protein can undergo a large transformation in one mutation. All the of the "chromosomal" mutations fall into this category - insertions, reversals etc. (2) You seem to be reverting to arguing about the probability of getting from A to B rather than why there are no intermediaries (i.e. the chances that a large change mutation will result in a fitness benefit). I think the large change/one mutation addresses the lack of intermedaries does it not? Let us stick to one issue at a time, and talk about the chances of a mutation being useful separately. Reverting to the second model for no intermediaries. I stressed (a) that this is just one way in which intermediaries might be removed - so not "each time" just sometimes and not as some kind of "law of nature" - just one thing that happens sometimes. (b) I believe there exist a good number of cases in which some or all the intermediaries exist! (In fact wouldn't a superfamily be a case where pretty much all the intermediaries exist?). So it is not the case that "the expansion (sic) of each intermediate, or of the final intermediate, was complete, erasing any trace of the process." on every occasion. It just happens sometimes. At the end you write. A good model, a credible and parsimonious one, is to affirm that each new superfamily arises independently of the existing ones, or through a rather sudden, designed treansition, Well of course - a designed transition can explain anything - unless of course you are prepared to discuss how it is implemented and by whom - in which case it gets a little harder.markf_{November 14, 2010
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Mark: I addressed your "single mutation - great variation" argument in my post #29. I paste here the relevant part for your convenience: "Let’s go to the possibility that one single variation event (inversion, frameshift mutation, or similar) may change completely one sequence into a different one. That is certainly possible. Frameshift mutations are perhaps the best example. In a frameshift mutation, a single aminoacid variation is the cause of a completely different reading of the existing information. The whole sequence changes. And so? From a probabilistic point of view, nothing changes. This is a simple point that darwinists have difficulties to understand. Let’s be more clear. You start from protein A and the final result is protein B. Both are functional, but they belong to different superfamilies, and are therefore unrelated at primary sequence level. That means that, to get B, most of the aminoacids in A must change. Let’s say that at least 50 aminoacids have to change exactly, which means a transition of 216 bits. As A is unrelated to B, any change can be considered as a random attempt at finding B. IOWs, the transition from A to B is a random walk. There is no significant difference if you change one AA at a time, or if you just “try” a completely different sequence. The probabilities of success remain practically non existent. The proff of that is that no frameshift mutation is known which has generated a new functional protein. As you may know, darwinists have blindly believed for years that such an example existed: Ohno’s theory about the emergence of nylonase. But obviously, serious research has clearly shown that such a theory was wrong. So, a sudden transition has no possibility to find a new isolated island of function, because it does not allow even the theoretical possibility that functional intermediates may make the transition possible." Proteins belonging to different superfamilies have no known intermediates. Protein belonging to the same superfamily or family do show continuity in natural history: they often keep the same function with differences in primary structure (probably the effect os neutral mutations), or may vary their function through small variations at the active site level (while the general folding and basic biochemical activity remain the same). Your suggested model is possible, but IMO it is definitely "ad hoc" and not credible. It implies many unlikely assumptions: a) That each time that a new superfamily arises, a subpopulation is constantly isolated, goes through the necessary functional intermediates, and finds the new protein structure in complete isolation from the original population, without any survival of the intermediate functional molecules. b) That this happened not once or a few times, out of some contingency, but always, as though it were a laws of nature. Indeed, all protein suprefamilies are isolated, and no intermediates are known for all of them. That should mean something, or not? c) That those isolate small population retained sufficient probabilistic resources to effect the transition through all the necessary steps, even with its reduced number of replicating individulas. d) That the expansion of each intermediate, or of the final intermediate, was complete, erasing any trace of the process. This is particularly unresonable. It's not what we observe in nature. Even in humans, a lot of strongly negative mutaions do survive: human mendelian diseases are a good example of that. And many of them are even dominant, and not recessive. In sexual reproduction, alleles usually survive even if "negative", and freely circulate in the population. So, if even negative, and certainly neutral variants of a functional protein do survive, why should all those very functional intermediates of the transition, which were selected and expanded for their intrinsic functionality, be completely erased from the genetic memory? And this every single time? While, as we know, the original starting protein, the least functional of all, does survive? IOWs, this is a very, very bad model to explain what we observe in protein superfamilies. A good model, a credible and parsimonious one, is to affirm that each new superfamily arises independently of the existing ones, or through a rather sudden, designed treansition, which does not require the intermediates, ar at least does not require their expansion in natural populations. That explains well why we find the individual superfamilies, and no trace of intermediates.gpuccio_{November 14, 2010
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Gpuccio #40 OK - I have some time now. On rereading, I realise we got sidetracked into answering a different question from your original one - which you repeat in #40. Then, why can’t we find any trace of those molecular functional intermediates in the present proteome? If it is true that each of those intermediates had to be selected, fixed and expanded if the model is to work? I believe that in many cases there are functional intermediates between two proteins - right? However, I am sure there are also many cases where there are no such intermediates. I imagine there are several reasons why this might be the case. I offered just two. The first was that single mutation could actually cause a very large number of changes in a protein i.e just because two proteins differed in a lot of amino acids it does not mean there were actually a lot of intermediates. You did not address this. But let us turn to the second reason. In essence I am saying that if there was a transition from protein A to protein B via X, Y, Z etc and protein B had very significant fitness advantages over A, X, Y, Z ... etc then you would expect X, Y, Z etc to be eliminated by natural selection. The interesting question is why A still exists. The answer is that the transition from A to B happened in an isolated population. So the population with A was not exposed to competition from B. If at some stage the populations are no longer isolated the population with protein A will also have moved on - but in a different direction quite possibly adapted to a different niche - so two populations with quite different proteins and no intermediates live side by side. A second question is what is the probability in an isolated population of getting from A to B?And, closely linked, - does this require that each intermediary become fixed in all or most of the population? This is complicated. I believe it is the subject of population genetics and I am not an expert in this area - but it will be fun to make a inexpert stab at it in another comment.markf_{November 14, 2010
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PaV: Thank you for the information. I agree with you that the paper is absolutely irrelevant to the subject which was being discussed.gpuccio_{November 14, 2010
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PaV you state: 'just as another student author picked up on the vpu protein in HIV—if you remember that incident.' Who could ever forget 'that incident', or the 'lady' behind 'that incident'? I believe she could have made a sailor blush :)bornagain77_{November 14, 2010
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Well PaV on the bright side, hopefully when Dr. Behe is done correcting the students papers, they will learn first hand not to trust what their BioLogos teachers are telling them as to the 'unlimited edge of evolution': OT: I found this gem from Stephen Meyer that I had somehow missed earlier this year: Higher Level Software Design In Cells - Stephen Meyer http://www.metacafe.com/w/5495397bornagain77_{November 14, 2010
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BA and gp: I have access to Science magazine. I've read the paper. But, I have very little background for assessing it. However, I can make a few points: (1) They are dealing with "permanent" binding sites; not transitional binding sites which are involved in metabolism. ["In a cell, permanently associated proteins guarantee mechanical integrity, wheras transient associations are indispensable for metabolism and the regulation thereof.] (2) We're basically dealing with structural proteins, proteins involving repetitive structures which the authors call 'symmetries'. (3) Because of the symmetric nature of these proteins, the effect of any ONE mutation in the binding site is therefore 'multiplied'; hence, a 'single' or 'double' mutation is sufficient. However, when the symmetries are high enough----NO mutations are necessary (which I'm not clear on why this is so) (4) The introduced mutations bring about binding, however, the binding sites have their problems since the globular protein is affected (negatively) (5) The mutations selected were 'designed' based on certain rules they had detected in the protein polymers that normally form. Here are some quotes that come from the end of the paper: "Symmetry is an important factor in protein association because it enhances the multiplicity of a single point mutation . . . . The highly symmetric Rua octamers with a contact mulitplicity of 8 form complexes after merely one or two mutations, and the 16-fold contact of Myp-A required no designed mutations at all. On the other hand, high multiplicity is hazardous for evolving organisms tha tneed to avoid detrimental mutations. [My emphasis]. . . . To what extent did our constructs follow the design? . . . The available high resolution of Uro-A revealed that the novel contact deviated slightly from the design but was so strong that it caused the opneing of a large, surprisingly weak interface within the protein partners. . . . Because this Rua-B complex can be explained by the influence of teh side-chain mobility, the mobility is probably an important factor in contact design. Our experiments demonstrate that the production of aparticular contact is quite feasible, whereas high precision seems difficult to achieve."[My emphasis] Very typically, in critiquing Behe, Darwinists want to use these structural type proteins as an argument to defeat his claims. However, when it comes to 'life', it is the truly 'life-giving' functions that matter; not so much the structural. We know that lipids in water form membrane-like structures (only in the most basic of ways); this is due to strictly chemical interactions. [Notice that the multiplicity which allows a single mutation to have a larger effect also introduces a grave danger.] It seems to me that when it comes to determining the power of NS to bring about positive changes that these structural kinds of interactions are only trivially important. It would seem our student author picked up on this study, just as another student author picked up on the vpu protein in HIV---if you remember that incident. I wonder if the Darwinists like to use students to carry their water: it eliminates the need to put their reputation on the line in any confrontation with Behe, and, additionally, should the student prevail then it would be an instance where some 'wet behind the ears' student knew more than one of the key propenents of ID. They can't resist this. But it strikes me as rather cowardly.PaV_{November 14, 2010
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Mark: I am sorry, but it's you who are making a mistake, maybe non classic, but a mistake just the same. I have never said that mutations in the darwinian model are towards something. But you must remember the reasoning we followed to understand my point. I has suggested an example of a darwinian explanatory model which could use the concept of RV and NS to make a transition of 50 aminoacids possible through 20 functional intermediates which represent steps towards the final transition. All the model is nased on that assumption. But it is not an "a priori assumption" (mutations did not happen towards the final result), but rather an "a posteriori" assumption (for the explanatory model to explain anything, it must have happened that mutations brought to each of the intermediate steps, otherwise we are again with a 50 aminoacid impossible variation to be explained). If you read carefully all my reasonings in the previous posts, you will see that there is no other assumption than that. So, I maintain that my reasoning in this example is completely darwinian and orthodox. You say: "They don’t need to be established widely in the population (although the mathematics of genetic drift does allow for neutral mutations to become widely established)." But it is you who miss the real point of darwinism. The expansion of a mutation is exactly what positive NS does. In brief: a) negative NS eliminates negative mutations. In this way, it "fixes" functional mutations, either existing or new. But the functional mutation, although fixed, remains limited to the descendants of the individual where the mutation happened. In this way, the probability of any further useful mutation in that clone has to be multiplied to the probability of the first useful mutation: IOWs, we are still in the field of pure randomness (except for the "fixing" effect). To be more clear, if the original population is of 10^15 bacteria, and a first useful mutation (with a probability of 10^-15) happens in one of them, the probability that a second similar mutation may happen in the general population is still of 10^-15, while the probability that the same mutation may happen in the single clone with the first mutation is of 10^-30. That's because, if the clone does not expand, its probabilistic resources (number of reproductions) are 10^15 times lower than those of the general population. That's why expansion of each selected tract is so important to darwinian model: it offers the way to "tame" the probabilistic barriers. b) positive NS is supposed to expand the positive tract. That is the real trick. You cannot do anything in a darwinian model, without that expansion. All darwinian examples, and reasonings, about microevolutionary models (antibiotic resistance), selective pressures, fitness functions, competitions, and so on, IOWs all the mythology of darwinism, is based on the concept of expansion of the fittest at the expenses of the less fit. So, to sum up: in a darwinian model, NS can only eliminate negative mutations and "protect" functional information from degeneration ("fix" it). That is completely insufficient to solve the problem of the probabilistic barriers. Only positive NS, which in theory can expand a functional mutation in the population at the expenses of the old population, can give the probabilistic resources to bring the model at least in the wide range of credibility. And that expansion has to happen each time a functional step is found, otherwise that functional step would behave exactly like a neutral mutation, and there would be no real gain in the model. That's exactly the reason why neutralists have had to use the concept of genetic drift to "mend" their theory of the absence of an expansion mechanism. But the "cure" is worse than the "disease". It is true (perhaps) that genetic drift can expand neutral mutations, but it certainly expands them randomly, and confers no advantage in the model as to probabilities of a certain outcome. Instead, the darwinian model can work in theory. What a pity that, in order to work, a very simple premise should be true which instead is false: All complex functions should be deconstructable into a series of simpler, functional, selectable, fixable and expandable steps All my reasoning here was hypothetically "accepting" such a premise for a hypothetical "real case". See my premise at post 20, which is the basis for my whole discussion here: "Therefore, our darwinian friends have to deconstruct the transition into intermediate functional steps, just to be credible, so that NS cam enter the scenario. Let’s pretend they succeed (they never have, but just for discussion…)." So, the purpose of my discussion is: a) If it were true that complex functions are deconstructable into a seiries of functional intermediates (which would allow the darwinian model to work). b) Then, why can't we find any trace of those molecular functional intermediates in the present proteome? If it is true that each of those intermediates had to be selected, fixed and expanded if the model is to work? So, please, re-read all my arguments here in the light of these clarifications (if you like, and if you have the time :) ).gpuccio_{November 14, 2010
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#35 Gpuccio I am sorry but you are making a classic mistake. The mutations in the population are not mutating towards anything. They don't need to be established widely in the population (although the mathematics of genetic drift does allow for neutral mutations to become widely established). There will be a number of strands of cumulative mutations with little impact on the phenotype going on - most of which lead nowhere. Then one will happen to stumble upon a fitness advantage. There could have been many other potential destinations that provided a fitness advantage - that population just happened to stumble upon that one.markf_{November 13, 2010
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gpuccio, I fully agree with you that neo-Darwinism has far more severe problems than quibbling about a few binding sites, but none-the-less I look forward to Dr. Behe's response. It seems every time they try to refute the severe limit he has established for evolution that they end up with egg on their face and the limit grows even more severe than he had originally laid out in his book. notes: "The Edge of Evolution: The Search for the Limits of Darwinism" http://www.amazon.com/Edge-Evolution-Search-Limits-Darwinism/dp/0743296206 The Edge Of Evolution - Michael Behe - Video Lecture http://www.c-spanvideo.org/program/199326-1 An Atheist Interviews Michael Behe About "The Edge Of Evolution" - video http://www.in.com/videos/watchvideo-bloggingheads-interview-with-michael-behe-4734623.htmlbornagain77_{November 13, 2010
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BA: Unfortunately, the paper is not free, and the abstract really says too little. I cannot comment on that basis. I have not commented about the arguments on protein binding sites in the biologos piece for two reasons: a) I don't remember exactly what Behe says, and I could create confusion. b) In general, I find the argument irrelevant and boring. Protein binding sites can certainly be more or less complex, but most of them are certainly more complex than two AAs. So, the two AAs threshold determined empirically by Behe is still an unsurmountable barrier for most of them. Moreover, you well know that for me the true "impossible problem" for darwinism is the emergence of protein superfamilies and basic domains, which require usually at least 200 - 300 bits of complex information in most simplest cases. Why should I care about simple protein binding sites, when there is so much more to explain?gpuccio_{November 13, 2010
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BA: I'll look at that paper later, and answer.gpuccio_{November 13, 2010
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Mark: The problems: 1) A small population has small probabilities to find useful mutations. The samller the population, the smaller the probability. 2) You say: At some stage the isolated population after extensive divergence which gives little fitness advantage stumbles upon a mutation which gives significant fitness advantage. At this point the intermediary versions in the isolated community will quite quickly be eliminated by competition. But for the mechanism to work, the "divergence which gives little fitness advantage" should instead be a series of related intermediaries each of which expand to cover the whole population (or most of it). The reason is simple. The population is small in the beginning. So letg's say that the forst "favourable mutation", which is also a step in the diorection of the final result, is in itself already difficult to achieve. If that first mutation does not expand at least to almost all the original "subpopulation", there will be practically no chance that a second mutation in the samme direction can happen in the same subclone where the first mutation happened. Expansion is essential for that. Remember that we have created our 20 intermediaries in the model exactly because the transition from A to B was too big. But each of the intermediate transitions nis not completely easy to obtain. I has supposed a deconstruction of a 50 AAs transition into 20 steps, just to stay broadly in the limits of "the edge of evolution" (two or three coordinated mutations per step). Such a result woul be extremely difficult to attain even in a large, rapidly reproducing population. In a small isolated subpopulation it is reALLY a challenge. In a singular clone which does not expand, it is impossible. That's why each intermediate step must be favourable enough to expand and substitute the original subpopulation. And that must happen 20 times. And I suppose that the final "b" population will than expand, and that a subset of it will be again segregrated to start the process again towards some new species "c", through sone new 20 or 30 functional intermediates of which no trace will be left. Can you see how absurd all this is? Darwinists are forced to stick to unmeaningful vague concepts like "extensive divergence which gives little fitness advantage". That is senseless. A random divergence which is not really functional will produce what we often observe: diversity of expression of the same functions, without any new functional information accruing. That diversity will go on co-existing in the same pool. There will be no expansion of a trait which can only be the basis for further accumulation of function. If the steps don't expand, the general probabilities remain the same, There is no sense, then in deconstructing a transition into a series of intermediates. You still have to explain how a probabilistically impossible transition happens thousands of time, without any reasonable path to it, but only by sheer luck.gpuccio_{November 13, 2010
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gpuccio, I've just heard that Dr. Behe will be responding to BioLogos in a few days.bornagain77_{November 13, 2010
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#30 Gpuccio I am sorry. I was not clear enough. My model goes like this. They key difference is that there is no mutation required before isolation. Isolation might for example be geographic. Stage (1). We have a species a with protein A. A subset of that species gets genetically isolated for some reason i.e. there is no gene flow between this subset and the rest of the species. It does not have to be particularly large- in fact the process is likely to happen quicker in a small founder community. Orginally it shares the same gene pool as the main species, but because it is isolated it is almost certain to start diverging - the environment may be different or may simply be genetic drift. There is nothing freakish about this process. Subsets of species get genetically isolated all the time and some divergence would almost inevitably happen - we see this in small human communities. Stage (2). At some stage the isolated population after extensive divergence which gives little fitness advantage stumbles upon a mutation which gives significant fitness advantage. At this point the intermediary versions in the isolated community will quite quickly be eliminated by competition. These two stages are the only essential stages to answer your question. There is nothing ad hoc about them. Stage (3). Optionally (!) sometime later the barriers may be removed. If the communities can interbreed we have two significantly different races of one species. If they can no longer interbreed we have speciation. If the barriers are never removed then we can only guess whether they are same species or different races. Perhaps the difference in the phenotype will be so large it is obvious - maybe not.markf_{November 13, 2010
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Thanks gpuccio for bringing clarity, Do you have any comment on her 'designed' protein side-chain argument that she used?? i.e.
Finally, in a study by Gruenger, protein sequences were altered and engineered in order to determine the necessary alterations required to form higher order protein complexes. In many cases, changing just one side chain of a protein resulted in a new protein-protein interaction and the development of a new multi-protein complex. Although these mutations were designed by humans, the fact that we can develop a new high-order protein complex simply by changing one side chain shows that Behe’s assumption is egregiously erroneous. One or two, rather than four or five, amino acid changes can produce a new significant protein-protein interaction (Grueninger et al, 2008).
here is the abstract: Designed Protein-Protein Association http://www.sciencemag.org/cgi/content/abstract/sci;319/5860/206 That is the one study that caught my eye gpuccio. Though it is clearly a designed change, I was wondering exactly how far they were able to push the change before they ran into a road block,,, BioLogos also has two other students who are to present their critiques of 'The Edge' in the near future. Hopefully Dr. Behe will address them on ENV, or here on his blog on UD, but if not I may be back to ask you your opinion again :)bornagain77_{November 13, 2010
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