Uncommon Descent Serving The Intelligent Design Community

Co-option, Berra’s Blunder, and Speculation Presented as Fact

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In Bill Dembski’s thread, No Major Conceptual Leaps, I posted a comment about the evidential, logical, and probabilistic vacuity of the Darwinian co-option hypothesis. (I use the word hypothesis with reservation. A hypothesis in a domain such as this should at least be based on a minimal, mathematical probabilistic analysis.)

In response to my comment, another commenter offered this as a refutation.

This text from Deborah A. McLennan, of Evo Edu Outreach, is utterly embarrassing for her cause, because it makes the case for design, just as Tim Berra did with his infamous blunder.

Deborah writes:

The co-option of traits to serve new functions is not a difficult concept to understand. In fact, we ourselves do it all the time, which is why we speak about “new wine in old bottles” or “rebranding” for the repackaging of ideas, and more recently in keeping with the new management-speak, “repurposing”. We are forever finding new functions for old devices, using an old boot as a planter, a fishing rod to fly a kite, a magnifying glass to start a fire, a shell as currency, a berry or a root to dye cloth. The only difference between human and evolutionary co-option is that we purposefully change an object’s function, while evolution simply takes advantage of an opportunity with no direction, purpose, or forethought.

The only verifiable examples of co-option she presents involve agency. How about just one verifiable example of co-option that does not rely on agency? In addition, note the final sentence, which is pure speculation based on an assumed premise, but presented as fact. This is not how science works.

Berra’s Blunder:

If you compare a 1953 and a 1954 Corvette, side by side, then a 1954 and a 1955 model, and so on, the descent with modification is overwhelmingly obvious. This is what paleontologists do with fossils, and the evidence is so solid and comprehensive that it cannot be denied by reasonable people…

The point is that the Corvette evolved through a selection process acting on variations that resulted in a series of transitional forms and an endpoint rather distinct from the starting point. A similar process shapes the evolution of organisms.

Tim Berra, Evolution and the Myth of Creationism, 1990, pg 117-119

This is Phillip Johnson’s observation:

Of course, every one of those Corvettes was designed by engineers. The Corvette sequence — like the sequence of Beethoven’s symphonies to the opinions of the United States Supreme Court — does not illustrate naturalistic evolution at all. It illustrates how intelligent designers will typically achieve their purposes by adding variations to a basic design plan. Above all, such sequences have no tendency whatever to support the claim that there is no need for a creator, since blind natural forces can do the creating. On the contrary, they show that what biologists present as proof of “evolution” or “common ancestry” is just as likely to be evidence of common design.

Phillip Johnson, Defeating Darwinism by Opening Minds, 1997, pg 63.

It is illuminating that Darwinists, in many attempts to defend their blind-purposeless-undirected-chance-and-necessity hypothesis, draw on analogies from design and agency while trying to explain away agency and design.

It seems to me that this exercise should result in at least a modicum of cognitive dissonance.

Comments
Adel: I don't like the term "nature" because it means different things to different people. We have debated that many times here. I can give you, for instance, the following different definitions of "nature": 1) All that exists. According to that defiition, even a God, if He exists, is part of nature. But I would definitely prefer the word "reality" for that meaning 2) All that exists and has phenomenic manifestations. That's more subtle, but requires some definite philosophical assumptions. But even noumenic realities have phenomenic manifestations, if they exists, so the problem remains. 3) All phenomena. But if noumena exists, and cause phenomena, the problem remains. 4) All that is material. That is very troublesome. What does "material" mean? Is consciusness material? Is consciousness part of nature? Are with, as conscious beings, part of nature? Is energy material? Is dark energy (whatever it may be) material? 5) All that can be explaine according to present laws of physics. That is at least clear, and probably the meaning many "scientists" give to the word. But you will concede that it is unnecessarily restrictive. How can we be sure that the present laws of physics can explain everything? Is consciousness explained by the present laws of physics? (it isn't, unless you are a dogmatic fan of strong AI). I think that "naturalism" is used at present as a form of "authority censorship" to deny existence to positions which are not "politically correct" according to the current ideology of science. Like ID. I don't appreciate that usage, so I don't appreciate the word. By the way, thank you for the link. I will do my homework. I do believe that progress will go on indefinitely using all methods available, however they are called,and I have great expectations from the studies about the network of transcription factors. The more we understand, the more it becomes easy to define what we still don't understand. False knowledge thrives only in ignorance.gpuccio
April 4, 2009
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I trust anyone reading the above understands that Greek letters, which abound in the quoted excerpt, are represented by question marks. I have not taken the trouble to insert the English words that correspond to those letters.Adel DiBagno
April 4, 2009
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gpuccio [74]: I gather from the above that no amount of information about the regulatory factors in crystallin gene expression will meet your stringent requirements. Nevertheless, I will point you to some relevant literature: http://www.ijdb.ehu.es/web/contents.php?vol=48&issue=8-9 is the contents page of the Vol. 48 Nos. 8/9 (2004) issue of The International Journal of Developmental Biology, which is loaded with free-access papers on Eye Development. So far, I have read only the one by Cvekl et al "Regulation of gene expression by Pax6 in ocular cells: a case of tissue-preferred expression of crystallins in lens." A quote from the abstract gives an indication of the complexities that had (up to 2004) been uncovered.:
Here, we review mechanisms of lens-preferred expression of crystallin genes by employing synergism between developmentally regulated DNA-binding transcription factors: Pax6, c-Maf, MafA/L-Maf, MafB, NRL, Sox2, Sox1, RAR?/RXR?, ROR?, Prox1, Six3, ?FBP-B and HSF2. These factors are differentially expressed in lens precursor cells, lens epithelium and primary and secondary lens fibers. They exert their function in combination with ubiquitously expressed factors (e.g. AP-1, CREB, pRb, TFIID and USF) and co-activators/chromatin remodeling proteins (e.g. ASC-2 and BP/p300).
I believe that the discussion in that paper addresses several of the points in your post above. Personally, I was deeply impressed by how much progress has been made in uncovering tissue-specific regulatory networks in only a couple of decades, and I see no reason why progress should not continue indefinitely using "naturalistic" methods. (Why don't you like such terms?)Adel DiBagno
April 4, 2009
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Adel: what I mean is IMO rather simple. 1) The genome is one in all cells of one organism (with the partial exception of the immune system). 2) The transctiptome (and therefore proteome) is different in each cell type, and in the same cell type in different situations. 3) Therefore, IMO, there must be somewhere in the genome the information which guides the implementation of specific transcriptomes in specific cell types and situations. 4) The idea that everything goes on because of feedbacks from the outer environment is, always IMO, rather silly. 5) So, as I have many times argued here, at present we understand the effectors in the genome (the protein genes), but we have practically no idea of where the procedures are: IOW, where is the information which tells a lymphocyte what genes should be transcribed to be a lymphocyte, and so on. That is a lot of information, if you consider how many different cell types and states exist, and how many different transcriptomes are possible, even form a pool of "only" 20000 protein genes. And another factor is the relative quantitative expression of each gene, the time sequence, and so on. 6) Even if we know that the final control network (which however is poorly known too) is the set of transcription factors (operating on specific DNA sequences), still that is not the real answer to the problem. Again, transcription factors may determine the transcriptome, but the problem remains of how the transcription factors are regulated, being those proteins too the same in the genome of all cells. So, we have gone back of one step, but we still don't know where the information about specific transcriptomes of transcriprion factors is written. And if we don't know where the information is, it becomes difficult to hypothesize if it could have arisen as a product of RV and NS. I would definitely say no, because regulating information (procedures) is probably even more complex and less "selectable" than effector information (protein sequences). But if we don't know, we don't know, and all discussions remain rather vague. That's why I prefer to restrict the quantitative arguments to protein coding genes, whose information is much better known. But let's remember that, in the human genome, protein coding genes are only 1.5%. 7) You ask if complete understanding of all that is possible by naturalistic methods. I don't see why not, but still that is only an assumption: if we don't know, we don't know. And, as I don't love very much the words "nature", "natural", "naturalism" and similar, let's say that if you ask if complete understanding of all that will be possible by application of what we already know (both in biology and physics), I will answer that it is possible, but IMO not likely. I personally believe that new approaches and paradigms will be necessary to completely understand this crucial point (so dear to our evo-devo colleagues), and that may include even new paradigms in biophysics. But, obviously, that's only a personal view.gpuccio
April 3, 2009
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gpuccio [72]:
“Yes, I mean that the mechanisms which regulate the specific transcriptomes in different cell types are at present very poorly understood, and while some final detail of transcritpion control may be known, the general procedures which determine the individual transcriptomes in cells are still mysterious.”
I'm sorry, I gave you a reference that focused on cis-acting (promoter) elements, when the word "transcriptome" was staring me in the face. But your extended, and patient, further explanation may lead me on a more responsive path. First, a couple of clarifying questions: 1. You speak of "mechanisms which regulate the specific transcriptomes," "final detail" and "general procedures." Do you mean that if I cite some papers on what is currently known about lens-specific transcription factors such information would constitute only "final detail" and will not adquately address your concerns? 2. Please define "poorly understood" and "mysterious." Do you mean that complete understanding has not yet been attained (which should be no surprise to anyone) or that further understanding (employing naturalistic methods) is impossible? Or do you mean something else?Adel DiBagno
April 3, 2009
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Adel: I have read the paper (or at least, the expression part). I would like to make some quick comment, just to introduce further discussion, if you want. Please consider that the specific subject is completely new for me, and so I apologize if I am wrong in some of my impressions. First of all, I don't think that the paper, which is indeed detailed and very clear, says anything very different from what I had hypothesized. The expression section details many facts about the expression of different crystallin proteins in various tissues, and the highly preferential expression of some of them in the lens, and by means of deletion experiments it identifies many different regulation sequences in 5' DNA, acting both as promoters and enhancers, in different animal species. Well, that's interesting, but I don't think that it gives us a clear idea of how a "restriction" is working. It just tells us that some recognition sequences are implied in the process. I will be more clear. Take just as an instance the following paragraph: "Gel retardation and methylation experiments using oligonucleotides show evidence for selective binding of different chicken lens nuclear proteins to the proximal and distal regions of the mouse aA promoter (29). The proximity of the distal and proximal control elements suggests that the putative trans-acting factors physically interact when situated on their cognate sequences. Similar nuclear proteins (or protein complexes) appear to be present in chicken erythrocytes and HeLa cells (29),supporting the notion that the same or related proteins found in many tissues are necessary but not sufficient for expression of the mouse aA-crystallin gene." That illustrates well my point. Specific promoters or enhancers may well be necessary to realize the selective expression of a protein in a cell type, but they are certainly not sufficient for that. That is obvious form the simple fact that those sequences are the same in all cell types, like the rest of the genome. Therefore, it's not the recognized sequence in itself which accomplishes the "restriction". It is only an appropriate gignal which is used when the appropriate recognition apparatus in working. And the recognition apparatus (that is, the right balance of specific transcription factors) is determined by the specific transcriptome of that cell type, which means the control and regulation of mant different complex proteins (at least the final transcription factors). Otherwise, the "simple" DNA recognition sequence is useless. That's more or less what I had generically stated: "Yes, I mean that the mechanisms which regulate the specific transcriptomes in different cell types are at present very poorly understood, and while some final detail of transcritpion control may be known, the general procedures which determine the individual transcriptomes in cells are still mysterious." So, a variation in the genome which restricts a gene to a cell type can be determined by a variation in the recognition sequence, provided that a well organized recognition apparatus is working in that cell type. So, to have a detailed model of how credible it is that a random variation can restrict the expression of a gene to a specific cell type, and particularly to the cell type where it will work functionally, we should assess at least the following: 1) What genomic variations in promoter and enhancer sequences are necessary and sufficient to determine that step in a previous genome where the gene is not localized. 2) What are the quantitative probabilities that such a variation be achieved by random mutation. As you can see in the paper, long sequences of nucleotides are often involved, often more than one sequence is necessary, and distant sequences interact in the process, and the sequences themselves are different in different species. So, if we are building a quantitative evolutionary model, we should restrict our analysis to a specific acquisition of the restriction in one species, and hypothesize which regulating sequences were acquired that restricted the expression in a way which was not present previously, and then calculate how likely that coordinated mutation is, by RV and NS only. 3) Moreover, we should try to understand what is the specific transcriptome and set of transcription factors which allows the restriction in the lens, and if that transcriptome was already active in the previous genome where the restriction is supposed not to be present. And, if other specific changes were necessary to accomplish the restriction (for instance, the acquisition of a new transcription factor, or just a different regulation of the same in the lens), then calculate also the probabilities that such a necessary, but unrelated event could happen by those mechanisms. Now, I understand that point 3 is very difficult to deal with, and that's why I maintain that it's hopeless at present to make assumptions about events which are not understood, such as the emergence of specific transcriptomes. But I would be happy, for a start, of a quantitative evaluation of points 1 and two in a specific evolutionary model. And that's only a brief discussion about one single step of the evolutionary model suggested for the crystallins. All the other suggested steps should be quantitatively evaluated in a similar way, before they are suggested as credible by the proposed causal mechanisms.gpuccio
April 2, 2009
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gpuucio, Thanks, try this reference, which covers much of the issue, although it is a bit dated (Lens crytallins and their genes: diversity and tissue-specific expression, by J. Piatigorsky, 1989): http://www.fasebj.org/cgi/reprint/3/8/1933 (I hope the link works for you.) Expression is on pages 1936-1937.Adel DiBagno
April 2, 2009
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Adel: Yes, I mean that the mechanisms which regulate the specific transcriptomes in different cell types are at present very poorly understood, and while some final detail of transcritpion control may be known, the general procedures which determine the individual transcriptomes in cells are still mysterious. That's what I mean. I don't know anything specific about crystallins, and as I have said I would be glad to hear from you what is objectively known.gpuccio
April 2, 2009
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gpuccio, Thank you for the bump in your #66, but I can only access the Internet occasionally, hence this delay. You are amazing. In reply to my modest requests in my post #41, you have presented me with five posts totalling 3,000 words! And excellent words and sentences they are. Such generosity - you must have known that today is my birthday. Since this thread has already been pushed below the fold as you noted, we will have to search harder to find each other, so I will not try to drag things out in this location and I will not make any attempt to critique every one of your 3,000 words. (I don't have your strength.) So I would like to touch on a point or two before I am exhausted, beginning with the following, in which you refer to the deficiencies you perceive in the McLennan review on co-option:
It could try to discuss what kind of molecular changes could have given the reported changes, especially the changes in location, which IMO remain probably arbitrary even in a more detailed discussion like we could find in the original papers. And so on.
Before I start citing and quoting from the pertinent literature in an attempted counter, would you clarify your meaning in the above? Do you mean that you question whether science has any evidence about the mechanism of tissue-specific crystalline gene expression?Adel DiBagno
April 2, 2009
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Adel: As the thread is a little bit cold, I just mention here that I have answered your post. I hope you see the message.gpuccio
April 2, 2009
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Adel (continued): You say: "I am pleased to agree that it is a goal of science to provide credible causal explanations. Therefore, I ask you to present the alternative credible causal explanation of the origin of alpha crystallins based on design theory or any alternative theory you may prefer. (If my estimation of your character is correct, I am confident that you would not require evolutionary theory to meet a standard that your own theory does not meet.)" It's easy. The design of new species required that a protein with the characteristics of alpha crystallins were available in the eye, The designer used therefore the most easily available protein with a structure which implied the least modifications, duplicated the pertinent gene, resttricted it to the pertinent environment through a specific modification of the code which control the transcriptome in that kind of cells (whatever that code may be), and then operated a more or less gradual modification of that inactive code. When the functional result was ready, the new code was activated, and its regulation finely tuned to all the other changes that the designer had realized in the meantime in other structures. That is a model which makes specific previsions, which in time can be explored. But it is consistent, and it requires only the implementation of new information at specific points of natural history. And this is the end, for now. :-)gpuccio
April 1, 2009
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Adel (continued): Well, let's go back to serious discussion now. "Therefore, I ask you now to make the distinction clear by describing the alternative causal mechanisms established or envisioned by design theory. And it would be especially helpful if you would stipulate how one would go about deciding which explanation is the better one." Let's go back to our proteins A and B, of which we know all that is knowable. And still, it remains a mystery how B appeared out of A. Or, if you prefer, how A became B. But we know it happened, in a definite time, and it could not have happened by random variation, and it could not have happened by RV + NS. So, how did it happen? That's a legitimate scientific question, I suppose. Well, the answer can be as follows: the pattern of modification required was wxactly the correct one needed to implement a new function, and the new function was exactly the right one needed in the new species, the right one which, in coordination with 1000 other similar changes, makes the difference between the two species. So, our legitimate hypothesis is that there is a plan, a purpose in all that. Is that the end of our scientific reasoning? Absolutely not. We are just making an assumption: intelligent, purposeful information was implemented in the passage from A top B, and in the passage from A's species to B's species. But a lot of questions, scientific questions, remain: how did that happen? was it gradual or sudden? which physical laws allow conscious intelligent beings to manipulate material configurations so that they can express intelligent information, without apparently violating known laws of necessity? is that a quantum effect? or some other level of reality we still can't appreciate? who was the designer? was it one or many? can we infer anything about that from the design itself? can we infer something from other sources? what is the purpose of specific designs? was the implementation of design obtained by direct controlled variation, or by targeted random variation followed by intelligent selection, or by both? or by other strategies? And so on. And, as a collateral field of invewstigation: what is consciousness? how does it work? how does it interact with physical realities? and so on, and so on. You say: "And it would be especially helpful if you would stipulate how one would go about deciding which explanation is the better one." IMO, design at present is not only the best explanation for biological information: it's the only explanation available. That comes form my deep conviction that the actual alternative explanations (indeed, I know one only which has a minimum of structure: classical darwinism) are obviously false. But I can agree that not everyone seems to share my certaonty about that. well, I can live with that. I do believe in science. I am absolutely sure that, as our knowledge of facts increases, it will become increasingly obvious what is the best explanation. Indeed, it will become increasingly obvious that we have only one explanation, and that the others are daily losing any credibility. In that sense, while I do believe in science, I am not a fan of the definitions of science. All that stuff form Popper and similar, about falsifiability and predictions and method, is certainly interesting, but in no way a dogma, at least not for me. I am more a fan of Polanyi and Feyerabend: science is too rich a reality to limit it with our definitions. But science works: as knowledge about facts goes on, also reasoning about facts goes on. And intuition. And creativity. Physics has had its Einsteins, Bohrs, Diracs, Feynmans, and others. Biology is probably expecting its revolution.gpuccio
April 1, 2009
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Adel (continued): So, your second point: 2) "Or, alternatively, how would you construct a “credible causal pathway” leading to the opposite conclusion?" Here comes the positive part: we were at a point where, in our well documented natural history, apparently magical events happen all the time. But wait a moment: are they really magical? No, not at all. They are magical only if we insist that their cause was random variation. RV cannot do those things, so if we believe it did we are believing in some kind of magic. And that could be a little uncomfortable for a scientist who has not yet embraced Harry Potter as his Bible. But what if we shift to another kind of explanation? We can definitely try necessity: but, alas, notwithstanding our repeated efforts, all our theories based on necessity don't work. Even worse is the fact that there are theorical reasons why it seems that no theory based on necessity will ever work: it's not just a question of our ignorance, it's the form of the problem which seems intractable to theories based on necessity. But... before we give up to utter despair, we are reminded of some vague memory: where did we see something like that really happen? Is there some empirical, real, observable context where improbable configurations of information emerge easily, and out of any known context of strict necessity? Yes, there is. We have always seen that happen. We have seen that happen while we were talking to our friends or writing a letter to our son. We have seen that happen when we tried our new program in C. We have seen it happen reading our favorite book, or seeing the last movie from our favorite director. We have seen that happen when our colleague from the near department of protein engineering has proudly told us of his new success, of his new artificial functional protein. And so on. Lots of information, Lots of magic. Everywhere. And what is the cause of all that magic? Conscious intelligent agents. Us. And the good thing is that it's not magic at all: it's nature. Consciousness and intelligence are part of nature. we are part of nature. Yes, that other colleague of ours from the AI department would object, but that's not a problem: his discipline has been now obsolete for many decade, after repeated failures to prove anything worthwhile, and is kept in the curriculum only for historical reasons... :-) And so, everything is bright again. Our despair vanished, we start on our new glorious scientific path. The mystery is solved. The magic has vanished. We have a theory. OK, it's just an hypothesis, we know that: after all, all scientific knowledge is made of hypotheses. Bu hey, this is a good one, at last! So, let's enjoy this perfect moment of provisional, but deeply satisfying, scientific attainment: we "know" how all that mysterious information came about. It's simple. Some conscious intelligent agent designed it! OK, we have now to understand who that agent was, how did he act, and many other details, but who cares? We are on the right path at last. In a sense, it was easy. We had just never thought of that. Well, it happens. That's the mark of genius: thinking of something that nobody has ever thought before. Never... But what is this other vague memory which is there, somewhere, in our subconscious?gpuccio
April 1, 2009
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Adel (continued): First of all a correction: your post was #41, and not #42. So, to go on, my point is that the confrontation between darwinian theory and ID is about causal explanation, and not about natural history. I want to be very clear about that: I don't personally accept darwinian natural history as a whole: I think that darwinists are very often declaring a gradualism which they badly need for their theory, and which is not supported by facts. But still, this is not the real important point. ID is perfectly compatible with gradualism, even if darwinian theory is certainly not at ease with saltation and "explosions". But the true point is causal explanation. Causal explanation means, as you well know, that if we have a theory about how something happens or happened, that theory must be first of all logically consistent, it must be as quantitative as possible, and finally it must explain known facts (and if possible future facts). Well, that's exactly what darwinian theory does not do. All the supposed "evidences" for darwinian theory are evidences (if and when they are) for a natural history, but they lack any explanatory power of that history. Why? Because the only explanatory mechanisms on which all the theory is built (RV and NS) are completely unable to explain the natural history which is provided by the theory itself, if we go a little into details and if we require a quantitative assessment. In other words, when put to test as explanatory models, darwinian assumptions invariably become just so stories. That's why we in ID insist on probability calculations: it's not just to confound people with high numbers, but rather because darwinists strictly avoid any convincing quantitative assessment of their own theory. And why should darwinian theory be assessed through probability calculations? it's very simple. Because that theory (and not ID) is based on random variation as the only engine of generation of new information (with all due respect to Allen MacNeill, who goes on counting engines which are not causal explanations of anything). IOW, a theory based on random events "must" count its probabilities, otherwise it's not a theory at all! So, let's see your two points: 1) "So, given the observation of sequence similarity between two genes, how would you go about disproving that they both derived from a common ancestor" by a darwinian mechanism? (obviously, the last part is added by me). It's simple: let's imagine that we have two genes in two different species, and that the two genes have a satisfying level of homology, so that both you and me agree that the second is derived from the first, and we have reason to agree on which is the oldest, and the two proteins coded by the genes have different structure and function, and the functional difference can be shown to be due to a difference in primary sequence of at least 30 aminoacids, all ot them necessarily different so that the new function may substitute the old, and that we can experimentally show that no intermediate protein between the two has any improvement in the originary function, or any detectable level of the new function, so that it could have been selected by NS. Although those assumptions may appear a lot, it is perfectly reasonable that while our understanding of proteins and their function increases (and it is increasing!) we will be able to verify many of those things in real cases. So, let's go on with our imaginary experiment. So, let's say that we have all the reasons to infer that a coordinated mutation of at least 30 aminoacids is necessary to pass from protein A to protein B. And we know that "natural history" did indeed pass form protein A to protein B, when the second species appeared. and we can determine with enough precision how much time passed from A to B. And the maximum rate of mutations for those species in that period. And then, with all that knowledge available with enough detail and precision and credibility, we make our probability calculations and... the probability of the proposed coordinated mutation in that period of time, even taking into account all possible functional variants, is, say, 10^-200. (I am just giving numbers her, please don't take them too seriously: it's just to show the method). What would be your conclusion? Mine would be that something is wrong in the model. Well you can say that probably some of our assumptions is mysteriously wrong. But then we repeat our reasoning for other cases, with fresh new data, always more detailed, always more credible, and the result is the same: very unlikely events (indeed, completely unlikely events) seem to have happened all the time in our perceived "natural history". What would that leave you with? Maybe with magic. Or, more reasonably, with the evidence that a causal theory is wrong. Our assumptions were not wrong. It is our causal model which is wrong. And what is wrong? Is NS wrong? No. We know that NS can work, given the right context, we have a few models of that, real models like antibiotic resistance. It's RV which cannot work. Or, at least, it cannot do those things. It's the "engine" which is wrong. Another break.gpuccio
April 1, 2009
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Adel (#42 and 59): Thank you for mentioning your previous post: indeed I had completely mussed it, in the complex flows of information here at UD... So, I will try to answer as much in detail as I can. Indeed, detail is exactly what I like in discussions about ID and darwinian theory. Ans so I am happy that you raise so many pertinent and constructive point which could well give rise to a very constructive discussion. Let's begin... You say: "In any case, how would you have dealt with the shortcomings you perceive in the McLennan review? Please help me understand what kinds of arguments McLennan should have given by providing an example of what you consider to be a more correct approach." Well, that's not really a very important point, so I will not spend much time on that. My reaction to that paper was probably due more to the context it was presented here, as evidence of a concept which I really dislike, than to its intrinsic merits or demerits. Let's say that, where it suns up: "Molecular analysis indicates that ? crystallins are homologous with heat shock proteins" it could have given a few more details on the level of homology, and where it says: "Phylogenetic and functional analyses indicated that ? crystallins originated following two duplication events" it could give at least an elementary explanation of why these duplications are inferred, and where it says: "In the first event one of the copies of a heat shock protein (copy 1) retained its plesiomorphic function (protection against damage) and plesiomorphic location (throughout the body), while the other (copy 2) added a change in function (focusing light) to the old function of protection from degradation in the plesiomorphic location." It could try to discuss what kind of molecular changes could have given the reported changes, especially the changes in location, which IMO remain probably arbitrary even in a more detailed discussion like we could find in the original papers. And so on. But again, the point is not the quality of the review. I think that what I find arbitrary in that review is probably arbitrary in all darwinian literature, and so I used that review just as an example, probably mixing up what was untold just because it was a summary review (which is bad but forgivable) and what was untold because it is always untold (which is bad and unforgivable). I will try to detail better this last concept in the following part of my post. You say: "I thought you understood that there is no “established truth” in science. Correct me if I’m wrong, but I thought you wrote that very thing on another thread. All scientific inferences are hypotheses, are they not? " I understand that and I absolutely agree. That's one of my most important convictions about science. "So, given the observation of sequence similarity between two genes, how would you go about disproving that they both derived from a common ancestor?" That's a very important question. First of all, I don't want to disprove that. I do believe that in many cases homology between proteins is strong evidence that they derive from a common ancestor. I have probably expressed badly my opinion about that. I don't believe that homology, of any level, is evidence that one protein derived from another through darwinian mechanisms. But I do believe in common descent, and even if I have sometimes vague doubts about universal common descent of all living beings (it's an issue about which I am really curious, and open to all possibilities), I have no doubt that very similar proteins have a common descent. And when two proteins are really similar, and the function is the same, the observed differences in species can really be due only to random variation, and reflect the natural history of those species. And yet, I would not accept a general rule that homology always implies direct derivation, and I would never accept that it implies derivation through darwinian mechanisms. First of all, homology can sometimes just imply similar function, even if direct derivation is not true (that is similar to the difference between the concept of common descent and the concept of common design). I do believe that homology can mean both things (similar function or derivation), and probably it is possible in principle to distinguish between the two. I stop a moment here, and I will go on in the next post (just a trick to avoid being accused of posts too long).gpuccio
April 1, 2009
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ScottAndrews,
He writes of “descent” but means two entirely different things in relation to the car and to the fossils. If the two were really comparable, we would have to conclude that either the fossils were manufactured or that the cars reproduced.
I frankly don't see why you make such a claim. He's merely saying that, if you have those examples, and if you know the time they were produced, you have enough to infer a relationship of descent. That's all. In fact, I'd go further. Let a person examine twenty Corvettes of different dates over thirty years or so. Only reveal the dates of three cars: one toward the beginning, one toward the end, and one somewhere in the middle. I bet that alone is enough information for an intelligent examiner to put the 17 other cars in approximately correct order. That's the kind of thing Berra is talking about in the chapter. If you read the whole chapter you'll see that Johnson's charge is about an argument that Berra does not use the example to make.David Kellogg
April 1, 2009
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The Corvette people would disagree with you.
I would disagree with them as well, but I know that they were using the word "descendant" metaphorically. Obviously Berra doesn't mean to say that one Corvette literally descended from another. But he says
If you compare a 1953 and a 1954 Corvette, side by side, then a 1954 and a 1955 model, and so on, the descent with modification is overwhelmingly obvious. This is what paleontologists do with fossils.
He writes of "descent" but means two entirely different things in relation to the car and to the fossils. If the two were really comparable, we would have to conclude that either the fossils were manufactured or that the cars reproduced. It's a verbal shell game. The analogy is intended to make Berra's point. But it raises the question, how does understanding why the Corvettes are similar tell us why the fossils are similar? I don't like making analogies because they are so easy to pick apart. But in this case it's the underlying premise that's flawed, not the details.ScottAndrews
April 1, 2009
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gpuccio, I would very much appreciate your kind attention to my post number 41 dated 03/30/09, 1:28 PM. Yours in collegiality and scientific rigor, AdelAdel DiBagno
April 1, 2009
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Here's another quote, this one about the engine:
The basic Chevrolet small-block V-8 design has remained in continuous production since its debut in 1955, longer than any other mass-produced engine design in the world auto industry, though current versions share few if any parts interchangeable directly with the original. Descendants of the basic small-block OHV V-8 design platform in production today have been much modified with advances such as aluminum block and heads, electronic engine management, and sequential port fuel injection, to name just a few improvements over the 54-model-year design life of the engine concept to date.
Link Of course, the word "design" is here too. But again, Berra is not arguing against design in the chapter where he uses the analogy. He's arguing about evidence for descent with modification. That's the point of the analogy, and it holds. There's no blunder at all.David Kellogg
April 1, 2009
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ScottAndrews [57],
But no Corvette has ever been known to descend from another Corvette, with the second Corvette having modifications (or not.)
The Corvette people would disagree with you. From a General Motors press release:
Equipped with a 377 kW LS7 V8 engine and built on a lightweight chassis, the Corvette Z06 is a road going descendant of the championship-winning Corvette racing programme that includes the Le Mans 24-Hour race in its annual schedule. With its racing-inspired powertrain and suspension features, the Corvette Z06 delivers exceptional levels of capability and technology.
We even know its ancestor:
The original 1953 Corvette is a direct descendant of the one-of-a-kind prototype LE SABRE, a multi-million dollar research project hailed in 1952 as “The Car of the Future.” Many elements of the LE SABRE were incorporated in the production version Corvette, including the wraparound windshield and subtle tail fins.
Of course it's an engineered descent, but Berra never denies that. His point holds. There's no "blunder," because he's not arguing about the mechanism.David Kellogg
April 1, 2009
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He is simply saying that the Corvette evolves “in the sense of ‘descent with modification’”
But no Corvette has ever been known to descend from another Corvette, with the second Corvette having modifications (or not.) It works an illustration of what the effects of descent with modification would look like. But to illustrate descent with modification, he should have used something that descended and modified.ScottAndrews
April 1, 2009
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This is an old issue, but I've got the book now. I asked for some context of Berra's analogy. If he's talking about naturalistic mechanisms, Johnson has a point. If he's just talking about common descent, I would argue that Johnson is both wrong and misleading. Having read the chapter, it is clear that Berra here is simply talking about descent with modification. He is definitely not talking about a naturalistic mechanism at this point, nor is he making a "claim that there is no need for a creator" (as Johnson puts it). He is simply saying that the Corvette evolves "in the sense of 'descent with modification'" (page 118, in a passage Johnson does not quote). Does Johnson say Corvettes didn't evolve in that sense? I would say they did. Does Johnson say Berra's analogy doesn't work to illustrate the mechanism of naturalistic evolution? So what? Berra doesn't use the analogy for that purpose.David Kellogg
April 1, 2009
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Scott: Correct: instantiation is not analogy. (Case in point -- the cell's DNA, RNA, ribosomes, enzymes etc instantiate a re-programmable, digitally stored data, coded, algorithm-implementing information processing system, i.e a computer. [And, what do we know from the observed causes responsible for computers whose origins we directly see?) Further to the original post, Berra's blunder was to try to compare a claimed spontaneous process tracing to chance + necessity only, to a known designed process. He only succeeded in showing that common design can account for apparent evolutionary sequences. This has a lot of implications for many claimed evidences and icons of evolution, as we see here how they fail to distinguish themselves from common design. Thus also we see the censoring significance of the recently imposed rule of methodological naturalism, which in effect rules out a priori the ability to raise this point, and still be deemed -- note the reference to an authority -- "scientific." (For, methodological naturalism changes science from the pursuit of the truth about our world based on evidence, to the best evolutionary materialistic account of our world. Big difference.) Thus, much of what has been going on in recent years is plain for those willing to look. Sadly GEM of TKIkairosfocus
April 1, 2009
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David Kellog:
You mean there’s no analogy between things produced in nature and the alleged activities of the designer?
That's not what I said, but it's an accurate statement. You can't draw an analogy between something and itself. There is no analogy between a Jetta and a car because a Jetta is a car. But that wasn't the point. A good analogy sheds light on one or both of its subjects, helping others to understand them better. Comparing deliberate changes in a the design of a car to unintended variations in animals caused by undirected breeding doesn't shed light on either. If someone accepted the premise, his understanding of at least one of its subjects would be diminished, not increased. All analogies break down, but they should impart something useful first.ScottAndrews
March 31, 2009
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skeech plus: I still can't follow your reasoning. You point #1 is common descent, which I do accept. So please, at least with me, don't bring again evidence of common descent: I agree. But where is your evidence of gradualism? Especially at the molecular level? Where are the pathways which bring from one protein to a different one with coordinated mutations of not more than two or three aminoacids (the only realistically achievable ones), and all the intermediate states selectable? Please, answer that, and give specific examples.gpuccio
March 30, 2009
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I hope this comment doesn't go into the moderation queue like all of the others I've submitted today. Clive, If you read the entire thread, you'll see that the designer hypothesis has a huge problem whether or not common descent is true. In any case, like it or not, the evidence points overwhelmingly to common descent. Take another look at Douglas Theobald's point about the accuracy of the phylogenetic tree:
…the standard phylogenetic tree is known to 38 decimal places, which is a much greater precision than that of even the most well-determined physical constants. For comparison, the charge of the electron is known to only seven decimal places, the Planck constant is known to only eight decimal places, the mass of the neutron, proton, and electron are all known to only nine decimal places, and the universal gravitational constant has been determined to only three decimal places.
If phylogenetic trees based on independent traits converge with that kind of stunning accuracy, then we can be logically certain that either a) there is no designer, or b) the designer exists, but he chose a design method that makes common descent appear absolutely, overwhelmingly true. Contrary to your repeated assertions, I do not claim to know why a designer would choose such a strategy (indeed, I see it as a purely academic point since there is no reason to think that a designer exists in the first place). Is it because he wants to remain hidden? I don't know. Because he wants to test our faith? Can't say. Because he is constrained to design this way in order to achieve some other, unknown goal? Who knows? It doesn't matter for our purposes. The question is not why a designer would design that way. Our task is to determine which explanation is most economical and best fits the data. You asked for an examples of design schemes that would not conform to neo-Darwinian expectations. That's easy. I could design a set of cars so that if you tried to infer a "phylogenetic tree" based on the types of engines used, you'd get one tree, but if you did the same based on air conditioners or radios or fuel injectors you would get completely different trees that bore no resemblance at all to the first tree. We don't see this in nature. Real phylogenetic trees are amazingly consistent. The evidence points overwhelmingly to common descent. And as I pointed out to gpuccio earlier in the thread, conceding the truth of common descent doesn't solve the problem. See my earlier comments for details.skeech plus
March 30, 2009
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Ray, I didn't write what you credit me with in your quote. I was quoting Skeech, he wrote it. I know faith is based on facts. I have facts that back up and support my faith in my friends and family. It's no different with any person--what we deal with when we are dealing with a person or a personality is faith; we have faith in them based on facts. The more we know the person, the more faith we may have in our assurances in how they'll deal with us, and whether we believe them in their actions.Clive Hayden
March 30, 2009
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Scott Andrews,
There’s no analogy between living things producing offspring over multiple generations and someone repeatedly producing new objects from raw materials.
You mean there's no analogy between things produced in nature and the alleged activities of the designer?David Kellogg
March 30, 2009
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Clive Hayden (#33): "To insist that there is a designer is to abandon science and resort to faith." Error. Faith is based on facts---that's why we have faith. Your use of the word "faith" assumes as true a pro-Atheism corruption of the concept. RayR. Martinez
March 30, 2009
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Skeech, I reject common descent. Therefore the Designer isn't denied his design in light of it. And I'm really skeptical of what we should "expect" from the Designer, as far as knowing what he would or wouldn't do, which is what you're implying, even though you say you're not implying it. I'm not sure what you mean about literally millions of possible design schemes that do not produce the appearance of common descent, gradual change, and consistent phylogenies. What are just a few of these literal millions? Do you mean a design appearance that doesn't show common descent? I think that's what we have. Do you mean a design that doesn't show gradual evolution? That's exactly what we have too. Again, we cannot get into the motives of the Designer, which is what you do, even though you say you don't. And again, by your scheme, the conclusion that there is no Designer would be wrong, even though he tried to hide himself.Clive Hayden
March 30, 2009
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