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
gpuccio, I can see that you have had enough discussion with me for now, and though I have more to say, I am content to rest my humble case as well. I am most grateful to you for pushing my brain so hard it seemed at times to threaten explosion. But it's still intact, and that is how we learn. Ciao, hasta la vista, bis später, AdelAdel DiBagno
April 12, 2009
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Adel: Happy Easter (or else) to you too! I must say that I find your last post very reasonable, and I don't think I have much to add. Our positions are clear and well expressed, I hope. But if I realize of something which is worthwhile to add, I'll come back after Easter. Otherwise, I am sure we will soon meet on some other thread. Again, a very happy Easter for you.gpuccio
April 11, 2009
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I will give you my counter arguments, but please consider that, if we find that we are repeating ourselves, we can stop any moment with full reciprocal respect. But as long as new interesting points come out, I am willing to go on.
Yes, repeating oneself is a pitfall of most discussions I have witnessed, even before the advent of the Internet! So, we should both feel free to call a halt at any time. Until then, I will try to keep my discourse interesting for you. And you are the judge of that.
Well, I will not spend much on this point. It is the usual “majority” argument. I have already stated that I am a minority guy. But I have to believe that my minority is on the right side, and in the case of ID I definitely do.
I was not saying that we must accept evolutionary explanations in biology because it is a majority view. My point was that it is the majority view because it has been fruitful. And more power to you for being a minority guy. All views are welcome in the marketplace of ideas.
Finally, you think that the great advancements in biology are due to evolutionary theory.
That was not my point and I don't recall making it. I said it was a 'participant' in those advancements. At the very least, it has done no harm. But more than that, I don't think the other contributions you mentioned would have the same value or would have been as strongly motivated in the absence of Darwinian hypotheses. (As Dobzhansky put it so nicely.)
I really don’t understand what is not clear in my use of the word “explanation”. I use it in a very trivial sense, the same sense it is always used in science. No deep philosophical assumption here. And it is not my invention that darwinian theory pretends to be an explanatory theory. It does. It is. A bad explanatory theory, IMO, one which does not work, but an explanatory theory just the same. Why? Because darwinian theory is not limited to the idea of “evolution” (common descent). It tries to “explain” why evolution happened. And the explanation is simple: ramdom variation (be it mutation, duplication, or anything else) and NS. That “is” an explanation. A model. And therefore, we can try to asses if it works or not. My point is simply that it does not work. First of all, the RV part and the NS part are never detailed. When does RV act, and at what point does NS act? The lack of any detail (even vague) makes it impossible to evaluate the two mechanisms quantitatively.
How can I respond without repeating myself? Perhaps I can't. So I will reiterate that the level of detail you are asking for may not be available, but its absence does not currently seem to be a hindrance to progress in the field. You are not satisfied, I think, because your agenda ("My only conclusion from that is that it is a shame for modern culture and science") is not the same as that of the workers in the field. This gets back to 'majority views.' The available levels of detail are evidently adquate to motivate continuing work among the members of that majority.
Cooption would be present if the same structure which was responsible for a previous function were “coopted” for a new function, independent from the previous one. That is very simply my point.
However, the idea of co-option is not restricted to a single structure. The term has been applied more broadly, as expressed by True and Carroll (2002) in the opening sentences of their abstract:
"Co-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both."
gpuccio:
The alternative is that any transformation in proteins and genomes is deconstructable in steps of 1 - 2 mutations, all of them selectable for reproductive advantage. Do you really believe that? And if you believe that, have you any evidence of that?
Not every change need be advantageous. Not every change need be a point mutation. Some neutral mutations might become advantageous when recombined with other neutral mutations. The function of a gene will also depend on the context in which it is expressed in the mileu of other genes that are expressed. It may be very complicated...
In ither models, the result is the same: the mutation which is not selected remain more or less confines to one allele and its propagation in the descendants, without any expansion.
But we are dealing with populations, so all kinds of genetic experiments can take place, especially by recombination in sexually reproducing species. Enjoy your Easter/Passover/Vernal Equinox holiday!Adel DiBagno
April 11, 2009
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Adel: Thank you for your answers and for the constructive tone of the discussion. I will give you my counter arguments, but please consider that, if we find that we are repeating ourselves, we can stop any moment with full reciprocal respect. But as long as new interesting points come out, I am willing to go on.
But it puzzles me that, despite that putative fundamental error, evolutionary theory should have been so successful as a participant in the spectacular advance of the biological sciences during the past century.
Well, I will not spend much on this point. It is the usual "majority" argument. I have already stated that I am a minority guy. But I have to believe that my minority is on the right side, and in the case of ID I definitely do. Poper, Kuhn, Feyerabend and others have really enriched our culture in philosophy of science, a subject too often overlooked and forgotten. But none of them has given a final standard for reality (and probably none of them would have wanted to do that). I can agree with you that evolutionary biology has been the majority option for a long time. That would be a variant form of the "majority argument", let's call it the "long lasting majority argument". But still I don't buy it. The long status of evolutionary biology may help convince you that the theory is good. My only conclusion from that is that it is a shame for modern culture and science. And an anomaly, certainly. Not the only one, I would say. Strong AI is a good companion. IMO, the only evidence these two theories give us id the evidence of how ideology and dogma have deformed and permeated the scientific thought in the last decades. Finally, you think that the great advancements in biology are due to evolutionary theory. That's a point on which we have to disagree. While I recognize with enthusiasm the great advancements of modern biology, and especially of molecular biology, I can't see how they are the product of darwinist theory (please remember that I recognize the value of the theory of common descent). The great advancements in biology, the discovery of the genetic code, of the role of DNA, of the mechanisms of transcription and translation, the studies about protein structure and function, the sequencing of genomes, the reevaluation of non coding DNA, the interest for epigenetics, and so on, and all the related technologies which have been developed, are a demonstration of the work and ingenuity of a lot of good scientists, but IMO they are in no way dependent on darwinian theory, although they have certainly been developed in the "light" (or shadow, according to points of view) of that theory. But let's go to more specific (and interesting) points. You say:
No, it’s not clear, because what you mean by the term ‘explanation’ is not clear.
in reference to my point about the difference between natural history (onserving that something has happened) and an explanatory model (building a causal model which explain why that thing happened, according to known laws and to a cause and effect model). I really don't understand what is not clear in my use of the word "explanation". I use it in a very trivial sense, the same sense it is always used in science. No deep philosophical assumption here. And it is not my invention that darwinian theory pretends to be an explanatory theory. It does. It is. A bad explanatory theory, IMO, one which does not work, but an explanatory theory just the same. Why? Because darwinian theory is not limited to the idea of "evolution" (common descent). It tries to "explain" why evolution happened. And the explanation is simple: ramdom variation (be it mutation, duplication, or anything else) and NS. That "is" an explanation. A model. And therefore, we can try to asses if it works or not. My point is simply that it does not work. First of all, the RV part and the NS part are never detailed. When does RV act, and at what point does NS act? The lack of any detail (even vague) makes it impossible to evaluate the two mechanisms quantitatively. a) RV must be evaluated quantitatively in relation to computable probabilities. Why? Because it is a mechanisms which invokes random events, and random events are governed by probability, and analyzed by probability theories. b) NS must be evaluated quantitatively in relation to the function which is supposed to be selected. Does that function exist? Is it capable of giving a reproductive advantage, and therefore to be selected? So, I mean with "explanation" exactly the same thing as darwinian theory does. The only problem is that darwinian theory gives an explanation which is easily falsified as soon as you try to detail and analyze it.
Why must the same sequence and structure explain both properties?
It must not. Indeed, I believe that it doesn't, as I have tried to explain. My point is that if different sequences and structures are responsible for the two functions, and if only the C terminal sequence is homologous to the other proteins in the family, and if that sequence is responsible only of the chaperone function, which is perfectly conserved, and other parts of the molecule (which are not homologous to the family of hsp) are responsible for the structural function, well then I don't see any cooption. Cooption would be present if the same structure which was responsible for a previous function were "coopted" for a new function, independent from the previous one. That is very simply my point.
What you disparage as ‘natural history’ has apparently been enough for empirical scientific purposes in biology and will remain so
I don't disparage natural history. It is an important part of knowledge. And it has certainly been useful for empirical research. But it does nopt explain why things happen, without an explanatory theory. Darwinian theory "is" an explicatory theory. And a very bad one. That's what I disparage. Natural history has all my respect, provided that it remains what it is: natural history.
Not OK, because it’s not clear why intermediate levels of B function could not have existed and have provided selective advantages short of the current level of function.
I am not saying that intermediate levels cannot exist. I am saying that I define coordinated mutations thgose which are necessary to pass from one level to another. You just show where the selectable trait appears, and I will do the computation form A to the new B. Maube it's 30 coordinated mutations. Maybe it's 15. Maybe it's 100. We have to see for each case. Unfortunately, darwinisn has not provided a single case, up to now (always excluding microevolution, of 1 - 2 coordinated mutations). The alternative is that any transformation in proteins and genomes is deconstructable in steps of 1 - 2 mutations, all of them selectable for reproductive advantage. Do you really believe that? And if you believe that, have you any evidence of that?
Since populations of the eukaryotic organisms in question are most definitely not clonal, I don’t follow you.
The issue of clonality is not important. I was thinking in terms of a bacterial model. In ither models, the result is the same: the mutation which is not selected remain more or less confines to one allele and its propagation in the descendants, without any expansion. You may say that sexual reproduction allows for genetic drift. True, but genetic drift is a random mechanism. It selects nothing. A "useful" mutation has exactly the same probabilities to be "expanded" as any other mutation. So, genetic drift does not explain anything.
But your argument founders on the issue of clonality.
No, as I have tried to show. My argument founders on the lack of expansion of the single mutations. The coordinated mutations have therefore to accumulate in the same isolated gene, wherever it is.
I value your willingness to continue this discussion, which I find challenging and interesting.
Me too!gpuccio
April 10, 2009
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Continuing,
But let’s consider now the problem of coordinated mutations. You say: "But why assume that all of those changes must have occurred simultaneously? Why could they not have occured incrementally, as Darwin proposed?" I use the term “coordinated” in a very specific sense (which is generally the sense all IDists use it), but that sense is probably not so intuitive, so I will explain it in detail. “Coordinated mutations” does not mean that “all of those changes must have occurred simultaneously”. The changes may well occur at different times. The meaning is that all those changes must be present at the same time in a single individual of the species to bear functional change.
(My emphasis)
The 30 changes are all necessary, and must all be present at the same time, otherwise the B function is not observable. OK? Now, the point is: you camnot have NS occurring on the intermediates. And the 30 changes must all be present at the same time in one individual.
Not OK, because it's not clear why intermediate levels of B function could not have existed and have provided selective advantages short of the current level of function.
To achieve that, it is not necessary that all the changes occur in the same individual. They can occur gradually. But the changes remain confined in the clone deriving form one individual.
Since populations of the eukaryotic organisms in question are most definitely not clonal, I don't follow you.
So, I mean with “coordinated mutations” a set of mutations which confers a functional advantage, presumably selectable, which cannot be achieved by a simpler mutation set, and for whom NS cannot be invoked as an intermediate causal factor.
But your argument founders on the issue of clonality.
I don’t know if you will accept my arguments, but I have tried. And I am always ready to discuss.
I have given my objections, which you may rebut. I value your willingness to continue this discussion, which I find challenging and interesting.Adel DiBagno
April 10, 2009
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I am happy we are discussing again.
I, also. And I apologize for my recent testiness.
And I explain. Again. Because, you see, the problem is always the same: you pass natural history for causal explanation. It’s not you fault, after all. You just repeat the fundamental error of all darwinian theory.
Your patience is exemplary, and I wish I could be as patient. Yes, the problem is always the same, because my error is the same as the error you perceive in evolutionary theory. I am grateful that you let me off the hook by placing me in the august company of those theorists. But it puzzles me that, despite that putative fundamental error, evolutionary theory should have been so successful as a participant in the spectacular advance of the biological sciences during the past century. You may remember Kuhn's argument that a scientific paradigm is successful as long as it provides a framework for progress in a scientific discipline. That has been the case for evolutionary theory. We can can expect, if the future follows the patterns of the past, that evolutionary theory will be replaced by a more fruitful theory when it no longer meets the needs of the laborers in the field. That time has not arrived, as best I can tell.
But why are you assuming that those changes can be explained by random mutations? That’s exactly the controversial point. That’s where you, and all darwinists, have no evidence at all. IOW, your evidence is just evidence that certain things happened. Not of why they happened. Is that clear?
No, it's not clear, because what you mean by the term 'explanation' is not clear. You go on to cite the crystallins.
Let’s go to the new, structural function. What evidemce have you that it is expalined by the same sequence and structure which gives the chaperone function?
I don't have any evidence regarding that question, but I don't understand why it should be an issue. Why must the same sequence and structure explain both properties? Protein molecules have domains, regions of structure that may perform different roles. One domain may provide the transparency function and another domain may provide the chaperone function. Or there may be overlap between domains and functions. I suspect that the literature may have information on such points, but that is not necessary to question the logic of your objection. And, please remember, if we don't know everything it doesn't mean we know nothing,
So, to show that they could happen as a result of random mutations and NS, you have to make an explicit model of at least some of those changes, of their complexity, and of the probabilistic resources necessary to achieve that result randomly.
Not at all. Neither I nor anyone working in the field has to meet those requirements. What you disparage as 'natural history' has apparently been enough for empirical scientific purposes in biology and will remain so until workers in the field encounter a need for potentially more useful explanations.Adel DiBagno
April 10, 2009
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Adel: I am happy we are discussing again. So, here are the answers to yopur questions, which point to fundamental issues. I will leave alone for the moment the thought experiment because it probably requires a longer discussion. So I will start with the other points.
As I understand it, random mutation changes the genetic information content of organisms. Take the crystallin example out of many. Changes in the regulatory regions and the protein-coding region occurred. The evidence also indicates that a gene-duplication event (which is an increase in genetic information) was involved. All empirical. Anybody can check it out. If this kind of evidence is not an adequate test in your mind, please explain.
And I explain. Again. Because, you see, the problem is always the same: you pass natural history for causal explanation. It's not you fault, after all. You just repeat the fundamental error of all darwinian theory. I will try to be more clear. If alpha crystallin is in the beginning only a small hsp expressed in all the organisms, and them in a more recent species it becomes (partially) confined to the lens, where it acquires specific characteristics which allow it to be also a structural protein of the lens and contribute to its refractory properties, while retaining its original function, and if we assume common descent (as I do), then it is obvious and trivial that, as you say: "Changes in the regulatory regions and the protein-coding region occurred.", passing from one species to another (from one without the lens to one with the lens, to be more clear). We agree on that. But why are you assuming that those changes can be explained by random mutations? That's exactly the controversial point. That's where you, and all darwinists, have no evidence at all. IOW, your evidence is just evidence that certain things happened. Not of why they happened. Is that clear? To be even more clear, I am not denying that random mutations happen. They do happen. So, my point is: random mutations happen, and certain functional changes do happen in natural history, but the functional changes are not explained by random mutations, and not even by any form of RV + NS. They can be explained only if we assume design, and therefore some source of guiding intelligent information. Is that clear? I will go into more detail, just to exemplify. Let's consider our beloved alpha crystallin. I argued (as a hypothesis, but the point could be certainly an object of inquiry) that the chaperone function can be attributed to the C terminal sequence of about 100 AAs. That's reasonable, because that is the sequence responsible for the homology with other shsps, IOW the conserved sequence. Well, that sequence is homologous in the family of proteins, but it's not the same. There are differences. As the function is conserved, I hypothesize that most of those differences are due to neutral mutations (some of them, obviously, could have some functional meaning). So, what can we say about that? We can say that the chaperone function has been expressed in that family form the beginning and that, nothwistanding many neutral mutations, and assuming the elimination of negative mutations by NS, the function is conserve up to alpha crystallin, where it is well present and expressed. Let's go to the new, structural function. What evidemce have you that it is expalined by the same sequence and structure which gives the chaperone function? Let's remember that the N terminal sequence varies abundantly in the family, and that quaternary structure is also important to determine the physical properties of a protein. IOW, the physical and refractory properties of alpha crystallin in the lens could well be explained by adjustments in both primary and quaternary structure of the protein which have been realized explicitly for its local utilization in the lens. So, while the neutral mutations in the C terminal sequence contributing nothing to the existing function (if not in not reducing or cancelling it), the supposed changes in primary sequence and in regulatory regions which did create the new function of transparency and refractory power had to be specifically restricted to a target space. So, to show that they could happen as a result of random mutations and NS, you have to make an explicit model of at least some of those changes, of their complexity, and of the probabilistic resources necessary to achieve that result randomly. So, for example, if you assume that a specific regulatory region of, say 100 nucleotides was created by random mutation, and that that change is responsible for restriction to the lens, even if we admit that isolated restriction to the lens of alpha crystallin is sufficient to be a selectable step (which personally I don't believe), still you should show that the assume modification of the genome could have taken palce by random events. IOW, shoe the starting genome of species A (where the protein is not restricted), show which changes in the genome in species B are responsible for the new function (restriction to the lens), and then let's compute the probabilistic resources, the available time and population size and reproductive time and mutation rate, and let's see if the observed result is even distantly compatible with our random model. That's what I call an explanatory model. Let's go to the other very important point. The coordinated mutations.
I have bolded the critical assumption here. It looks arbitrary to me. The only justification I can see is that it allows you to perform an elementary probability calculation: the number of ways 20 amino acids can be combined randomly, given 30 places, is 0.05 to the 30th power. The number I obtain is 9.3^-40, a very large number indeed, and adequate for your argument, but smaller than your number. (I am asking only for clarification: I wonder whether I have missed something that you included in your calculation.)
There are two different answers due here. The first is easier. Your calculations are right, I believe. But if you look at my original post, you will find, in the same part you quote, the following phrase: "(I am just giving numbers her, please don’t take them too seriously: it’s just to show the method)." Indeed, I was not trying to make any real calculation: I was just showing how a calculation can be made. I apologize if that was not clear enough. Your calculation is right and, as you say, adequate for my argument. But let's consider now the problem of coordinated mutations. You say:
But why assume that all of those changes must have occurred simultaneously? Why could they not have occured incrementally, as Darwin proposed?
I use the term "coordinated" in a very specific sense (which is generally the sense all IDists use it), but that sense is probably not so intuitive, so I will explain it in detail. "Coordinated mutations" does not mean that "all of those changes must have occurred simultaneously". The changes may well occur at different times. The meaning is that all those changes must be present at the same time in a single individual of the species to bear functional change. So, let's go to my hypothetical model. We have protein A and protein B. Protein B expresses a new function (or some specific change in function) which we assume to be the selectable trait. Studying the two proteins, we observe that at least 30 AAs must change so that, starting from A, you can get the function in B. Please note that neutral mutations are not included in that computation. The 30 changes are all necessary, and must all be present at the same time, otherwise the B function is not observable. OK? Now, the point is: you camnot have NS occurring on the intermediates. And the 30 changes must all be present at the same time in one individual. To achieve that, it is not necessary that all the changes occur in the same individual. They can occur gradually. But the changes remain confined in the clone deriving form one individual. And, if selection does not happen, and the population is not expanding, the clone deriving form that individual will represent always approximately the same percentage of the total population. And even if some of those assumptions are not true, there is no reason that the clone with one, or two, of the required changes must expand in any significant way. Indeed, it could well become extinct. So, we are left with 30 successive changes which have to happen gradually practically in one individual clone (even if through many generations of that clone), and while the new changes accumulate any of the others already acquired can be lost. IOW, at any given moment any of the possible combinations of those 30 AAs can be present in the single clone, and any successive change is a random change, which can retain or lose any present aminoacid. IOW, if you have followed another busy thread here, there is no latching, neither explicit nor implicit, becasue there is no selection. Here, pure randomness reigns. Therefore, the probability of having the 30 aminoacids at the same time in one individual remains extremely low, approximately of the same order of having them at the same time in one generation (obviously, you can compute the probabilistic resources provided by having many generations and longer time: that is part of the computation). So, I mean with "coordinated mutations" a set of mutations which confers a functional advantage, presumably selectable, which cannot be achieved by a simpler mutation set, and for whom NS cannot be invoked as an intermediate causal factor.
My conclusion is that the underlying assumption of the thought experiment is wrong.
I believe the opposite. I don't know if you will accept my arguments, but I have tried. And I am always ready to discuss.gpuccio
April 9, 2009
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Correction: I said above,
the number of ways 20 amino acids can be combined randomly, given 30 places, is 0.05 to the 30th power.
I should have said "the probablity of a single outcome of 20 amino acids combining randomly."Adel DiBagno
April 9, 2009
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gpuccio, At last I have some free time. Thank you for your patience and your reference to your #64. I see that your #93, concerning "thought experiments" intervened. Let's look at that first:
Very simply, my imaginary experiment was intended go show a way in which an empirical test “can” be achieved, as our knowledge of the facts improves.
Maybe you showed a way, but I don't see it. Could you point it out?
I would just the same be curious to know how darwinists have tested their theory that RV + NS can generate biological information.
As I understand it, random mutation changes the genetic information content of organisms. Take the crystallin example out of many. Changes in the regulatory regions and the protein-coding region occurred. The evidence also indicates that a gene-duplication event (which is an increase in genetic information) was involved. All empirical. Anybody can check it out. If this kind of evidence is not an adequate test in your mind, please explain. Turning to #64,
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).
I have bolded the critical assumption here. It looks arbitrary to me. The only justification I can see is that it allows you to perform an elementary probability calculation: the number of ways 20 amino acids can be combined randomly, given 30 places, is 0.05 to the 30th power. The number I obtain is 9.3^-40, a very large number indeed, and adequate for your argument, but smaller than your number. (I am asking only for clarification: I wonder whether I have missed something that you included in your calculation.) But why assume that all of those changes must have occurred simultaneously? Why could they not have occured incrementally, as Darwin proposed?
What would be your conclusion? Mine would be that something is wrong in the model.
My conclusion is that the underlying assumption of the thought experiment is wrong.Adel DiBagno
April 9, 2009
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Adel (#96): Please, read it again at #64. And now, good night.gpuccio
April 7, 2009
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Adel: You say: "Pardon me if I do not bow to your opinion," Maybe you could just discuss my opinion with arguments. Who asked that you bow? "You are disagreeing with the views of the scientists who think that the literature I presented does support the concept of co-option." and: "especially in light of your unfamiliarity with the literature and your evident determination to deny that the evidence indicates that co-option has occurred. (If you admitted that, you would be admitting to your original mistake in post #18. Horrors!)" Yes, I am disagreeing. I thought that was still allowed. And maybe if you admitted that you are only using arguments from authority, you would be admitting that you are short of other arguments. And I beg your pardon, but is your only purpose in this long discussion to have me admit that I have made a mistake in post #18? A mistake I don't think I have made? Strange, I may be naive, but I thought we were discussing in order to have a sincere, passionate and constructive intellectual confrontation about our scientific views. But you see, sometimes I do make mistakes...gpuccio
April 7, 2009
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Very simply, my imaginary experiment was intended go show a way in which an empirical test “can” be achieved, as our knowledge of the facts improves.
Fine. Please post it again. And now, good night.Adel DiBagno
April 7, 2009
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Adel: Who has decided that the main function of the alpha crystallins is to provide a refractive matrix? Where is that written? Where is written that the chaperone fucntion has become secondary? Or has been lost? Eye. 1999 Jun;13 ( Pt 3b):403-8.Links Lens alpha-crystallin: function and structure. Horwitz J, Bova MP, Ding LL, Haley DA, Stewart PL. Jules Stein Eye Institute, UCLA School of Medicine 90095, USA. horwitz@jsei.ucla.edu alpha-Crystallin is a major lens protein, comprising up to 40% of total lens proteins, where its structural function is to assist in maintaining the proper refractive index in the lens. In addition to its structural role, it has been shown to function in a chaperone-like manner. The chaperone-like function of alpha-crystallin will help prevent the formation of large light-scattering aggregates and possibly cataract. In the lens, alpha-crystallin is a polydisperse molecule consisting of a 3:1 ratio of alpha A to alpha B subunits. In this study, we expressed recombinant alpha A- and alpha B-crystallin in E. coli and compared the polydispersity, structure and aggregation state between each other and native bovine lens alpha-crystallin. Using gel permeation chromatography to assay for polydispersity, we found native alpha-crystallin to be significantly more polydisperse than either recombinant alpha A- or alpha B-crystallin, with alpha B-crystallin having the most homogeneous structure of the three. Reconstructed images of alpha B-crystallin obtained with cryo-electron microscopy support the concept that alpha B-crystallin is an extremely dynamic molecule and demonstrated that it has a hollow interior. Interestingly, we present evidence that native alpha-crystallin is significantly more thermally stable than either alpha A- or alpha B-crystallin alone. In fact, our experiments suggest that a 3:1 ratio of alpha A to alpha B subunit composition in an alpha-crystallin molecule is optimal in terms of thermal stability. This fascinating result explains the stoichiometric ratios of alpha A- and alpha B-crystallin subunits in the mammalian lens.gpuccio
April 7, 2009
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gpuccio, We seem to be posting at the same time, so I missed your #91. I'm sorry to disappoint you, but I disagree that I have not responded to your arguments. If that were the case, why have there been so many replies from you? If it seems to be a monologue, maybe it's because you say so much? I'll give it a rest for now and let you catch up.Adel DiBagno
April 7, 2009
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Adel: Just read your #90. The following is from Wikipedia: Thought experimentation in science Scientists tend to use thought experiments in the form of imaginary, "proxy" experiments which they conduct prior to a real, "physical" experiment (Ernst Mach always argued that these gedankenexperiments were "a necessary precondition for physical experiment"). In these cases, the result of the "proxy" experiment will often be so clear that there will be no need to conduct a physical experiment at all. Scientists also use thought experiments when particular physical experiments are impossible to conduct (Carl Gustav Hempel labeled these sorts of experiment "theoretical experiments-in-imagination"), such as Einstein's thought experiment of chasing a light beam, leading to Special Relativity. This is a unique use of a scientific thought experiment, in that it was never carried out, but led to a successful theory, proven by other empirical means. Relation to real experiments The relation to real experiments can be quite complex, as can be seen again from an example going back to Albert Einstein. In 1935, with two coworkers, he published a famous paper on a newly-created subject called later the EPR effect (EPR paradox). In this paper, starting from certain philosophical assumptions, on the basis of a rigorous analysis of a certain, complicated, but in the meantime realizable model, he came to the conclusion that quantum mechanics should be rejected as "incomplete". There were of course influential people, e.g. Niels Bohr, who refuted Einstein's analysis immediately. However it took decades, until the error in Einstein's paper was located by a real experiment. This means that finally, after decades, there was a decision. The outcome: there was no error, neither in Einstein's analysis nor in his model, but the above-mentioned philosophical starting assumptions were falsified (e.g. by the optical real experiments of Alain Aspect). This was only possible after the Bell inequalities had been published in 1964, another rigorous theoretical paper. Very simply, my imaginary experiment was intended go show a way in which an empirical test "can" be achieved, as our knowledge of the facts improves. I would just the same be curious to know how darwinists have tested their theory that RV + NS can generate biological information. But perhaps only you decide where the ball goes...gpuccio
April 7, 2009
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gpuccio [85]
And you have not answered my basic objection that the literature you cited does not bear any support to the concept of cooption, as the main concept seems to be that alpha crystallin is a small heat shock proteins which has retained its main function while acquiring a supplementary structural function, which probably depends on other (non conserved) parts of the molecule. Again, that has nothing to do with cooption.
You are disagreeing with the views of the scientists who think that the literature I presented does support the concept of co-option. Pardon me if I do not bow to your opinion, especially in light of your unfamiliarity with the literature and your evident determination to deny that the evidence indicates that co-option has occurred. (If you admitted that, you would be admitting to your original mistake in post #18. Horrors!) Your rationale above has it backwards. The concept in question is that the main function of the alpha crystallins is to provide a refractive matrix for the vertebrate lens. None of the other members of the small heat-shock protein family have anything to do with lenses. Their job is to protect cells from heat shock.Adel DiBagno
April 7, 2009
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Adel: What do you mean? I am playing no game. I have given you a lot of arguments. You have given me quotations which did not prove your points. I have commented about them in detail. You have promised many time to comment on my comments, but I am still waiting. You have promised to show me an elephant and heal my eyesight. I am still waiting. You have changed arguments many times, passing from defense of unguided cooption to logical errors to generic requests of fruitful heuristic, whatever that means, to sudden repositioning of the ball. So, who is playing games? If you are just tired of the discussion, just say it. You have no obligation to go on. I hope you have enjoyed it as much as I have. But if you want to go on, please say something, and be my ophthalmologist. I am here, ready to consider what you say. But at present, this looks ever more as a monologue.gpuccio
April 7, 2009
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Ah, we are lucky. I have another few moments free. So, a brief question: I had written:
Nor do you have a way of testing your hypothesis.
You responded in #85:
Why not? Great part of my previous discussion was about that. Do you remember the imaginary experiment about observing with certainty that something happened which could not have happened unless it was designed? I don’t remember any comment from you about that. Must I repost it?
Yes, please. And while you're at it, please explain how an imaginary experiment is an empirical test.Adel DiBagno
April 7, 2009
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gpuccio: Just had a moment to catch this:
And obviously ID offers a better paradigm for working scientists. We will discuss that after you explain what is the utility of the darwinian paradigm, and which are its testable predictions.
Please don't play games. You have already dismissed modern evolutionary theory as credible (your post #86, etc.), so it is clear that nothing I can say will satisfy you, which places the ball logically in your court.Adel DiBagno
April 7, 2009
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Adel: Please take all the time you need. If your elephant is evidence which makes non design theories of biological information credible, I will be happy to see what you can provide: I have never found anyone up to now who has given me (or others) something like that. So I am waiting for the fruitful heuristic of darwinian theory (or of any other similar theory). And obviously ID offers a better paradigm for working scientists. We will discuss that after you explain what is the utility of the darwinian paradigm, and which are its testable predictions. And please, one important disclaimer: evidence for common descent (with which I do agree) will not be considered by me evidence for darwinian mechanism: we are discussing causal explanations here, and not simple natural history.gpuccio
April 7, 2009
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gpuccio, My time is currently limited, and will be for a couple of days, so I will be brief and ask for your patience until I can reply at greater length. Your #86: I am delighted at your agreement that the argument for design is not deductive. This is an important clarification for me. But I would remind you that if it is inductive, it must provide a fruitful heuristic for further advances in understanding. It must make testable predictions. It must offer a better paradigm for working scientists than the existing evolutionary theory. (Thank Kuhn for that.) In sum, I don't see that it's worth anything scientifically. I would be pleased if you will provide empirical evidence (not argument) to the contrary.
Therefore, and in the absence of any other credible hypothesis, at present our best explanation for biological information is that it was designed by one or more intelligent beings.
Of course you are not seeing the elephant in the room. I hope to be your ophthalmologist.Adel DiBagno
April 7, 2009
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Adel (#84): Here you really disappoint me. But you have probably not read the many past detailed discussions about that "argument" which I have entertained with others here at UD. But it's late, so just a few tips: 1) The design argument is not a syllogism, and not a logical deduction. It is an empirical inference, a search for the "best explanation", like all empirical science. How is it that when darwinists are short of empirical arguments, they invarialble resort to ill inspired logic? 2) You say:
Some improbable configurations of information are/were designed and created by intelligent beings. Living beings are improbable configurations of information. Therefore, living beings are/were designed and created by an intelligent being. The conclusion does not follow; there is a hidden premise: All improbable configurations of information are designed and created by intelligent beings.
Wrong. The right reasoning is as follows: a) All improbable configurations of information which we know of, with the only exception of biological information (which, I believe, is the object of our hypotheses)are/were designed by intelligent beings. b) Biological information shows the same type of improbable configurations of information, with the same formal properties. c) Therefore, and in the absence of any other credible hypothesis, at present our best explanation for biological information is that it was designed by one or more intelligent beings. It's not exactly the same, do you agree? And c) does follow from a) and b): not like a mathemathical theorem follows from its premises (again, that is not a deductive reasoning), but exactly in the same way as all empirical inferences follow from existing data, and are considered good, or best explanations in empirical science. So, I have repeated that for the nth time. Who will be the next?gpuccio
April 6, 2009
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Adel (#83): Well, now the discussion is becoming hotter! Good.
The task that I set myself was to provide links to the scientific literature bearing on the issue of co-option with respect to lens crystallins.
And you have not answered my basic objection that the literature you cited does not bear any support to the concept of cooption, as the main concept seems to be that alpha crystallin is a small heat shock proteins which has retained its main function while acquiring a supplementary structural function, which probably depends on other (non conserved) parts of the molecule. Again, that has nothing to do with cooption.
Literature that you seemed to be unaware of when you derided the idea of co-option back in post #18.
True. But I did not deride anything, I "criticized" the idea, and I still do. And I stated that there was not evidence in the original paper in support of the idea. Which was true. Just like now I state that there is no such evidence in the further literature which you graciously let me know, and for that I am really grateful.
So I am satisfied that I have made a good effort to reduce your ignorance of the empirical basis for some examples of the concept of co-option.
I am satisfied too, although not for the same reasons. You have certainly reduced my ignorance, and I am happy of that. But I can't see how you reduce my ignorance "of the empirical basis for some examples of the concept of co-option". For that empirical basis, I am still waiting.
It’s not clear what you find lacking. For example, the sequence alignments in de Jong’s Fig. 1 indicate that many mutational events have occurred between members of the small heat-shock protein family. There is no reason to think that those mutational steps were non-random with respect to fitness.
And so? Who is denying that random mutations happen? They do happen, and they are usually neutral (the really bad ones being usually eliminated by negative selection). I don't see what you are inferring from that alignment. We have different member of a same family. The function is the same. The function remains the same. There are neutral mutations which do not affect the function. And so? What you had to show was how "positive" mutation could have produced the function form something which did not have it. How that 100 aminoacids sequence, in any of its functional implementation. could have been "found" in the search space of 20^100 sequences, starting from... what? A different protein? A differnet function? A coopted function? You choose... And again, what has that to do with cooption? Alpha crystallin "is" a small hsp. The function of those 100 aminoacids remains the same, even with some random modifications of the sequence.
Perhaps you’re asking for a mutation-by-mutation account of those changes, and how they affected the function of each organism in whose genome they occurred.
What I am asking for is an explanatory model which deserves the name of scientific hypothesis. Something that darwinists never want to give. It needs not have all the details. But at least some detail would be appreciated.
I doubt that much relevant data are available yet.
I doubt too.
We are shocked, shocked (heat-shocked?) to observe that there are gaps in the evidence.
"You" are shocked. I am rather cool about that. In my view of reality, it's very normal that there are gaps, huge gaps of evidence in a wrong theory. Indeed, let's say no evidence at all.
If and when gaps are filled by data, I expect that they will be published. Without additional data, further hypothesizing seems unproductive.
I would emphasize the "if". And we are not hypothesizing, we are only discussing the existing evidence for existing hypotheses. At least, that was my impression.
However, you have generously filled in those gaps with your preferred alternative hypothesis (though with rather scanty detail)
My generous nature is one of my weaknesses! :-) And scanty details are better than no detail at all.
An excellent and entertaining hypothesis, but you are not the designer (as far as I know - do you claim otherwise?)
No, it was obviously a narrative tool. I am sure you had understood that.
and there is no evidence for the existence of a designer.
I suppose you mean "no evidence for the existence of a designer of biological information". I must have missed something. Wasn't that exactly what we were debating? Are you jumping to conclusions? Is our debate over? In case that was not clear, my point is that biological information itself is evidence of the existence of a designer.
Nor do you have a way of testing your hypothesis.
Why not? Great part of my previous discussion was about that. Do you remember the imaginary experiment about observing with certainty that something happened which could not have happened unless it was designed? I don't remember any comment from you about that. Must I repost it?
Your scenario is fanciful
I take that as a compliment.
A fable.
I do like fables.
A “Just-so Story.”
That is probably less of a compliment! Let's see: my scenario lacks some detail, that's true. But is it a "just so story"? Has it really no explanatory power? (that is my idea of a "just so story"). What did I say? Ah, yes: "I am the designer" Well, I think we agree that is nopt literally true. "and I am planning a new organ, the eye, and in particular the lens." Well, the eye did emerge in natural history, or not? My hypothesis is that it was designed, so it is perfectly natural that I hypothesize that the designer at some point planned it. You know, that's what "design" means. "I have special constraints there: I need many functional proteins to protect the tissue from light stress." I though we agreed on those points. It's also in your literature. "Among them, I decide to use a type of small heat shock protein." Well, a type of small heat shock protein is in the lens. My hypothesis that the designer decided to use it becasue it was useful (and you do agree that it was useful, don't you?) ia a very logical inference, if we are in a design scenario. "But I also need the lens to be transparent, and to have a specific refractory power." I think you should agree on that too. "So, I slightly adapt one of the existing small hsps, so that it can serve as a structural protein, while preserving its more complex biochemical function as a chaperone." Here I am just describing your natural history, and pointing out that it in no way is a history of "cooption", but rather of added function. And I am pointing out a very trivial concept, that adding a new function, which is needed in the context, to an existing fucntion, which is also needed in the same context, is a rather trivial example of how a designed sequence usually appears. Just so story? I don't think so. Just a simple example of how the design hypothesis "has" explanatory power of the observed natural history. A fanciful scenario and a beautiful fable which is also a very good explanation.gpuccio
April 6, 2009
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gpuccio, In your post #63 you presented an argument for the existence of a designer of living beings. Some excerpts:
Is there some empirical, real, observable context where improbable configurations of information emerge easily, and out of any known context of strict necessity?
Lots of information, Lots of magic. Everywhere. And what is the cause of all that magic? Conscious intelligent agents. Us.
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.
This is an argument of the form: Some A have property B C is an example of A Therefore, C has property B The conclusion does not follow. There is a hidden premise: All A have property B Your argument: Some improbable configurations of information are/were designed and created by intelligent beings. Living beings are improbable configurations of information. Therefore, living beings are/were designed and created by an intelligent being. The conclusion does not follow; there is a hidden premise: All improbable configurations of information are designed and created by intelligent beings. In any case, if your conclusion is only an hypothesis, how can it be tested?Adel DiBagno
April 6, 2009
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gpuccio [82]:
I don’t think so. You have shown, with satisfactory details, some of the tools acting to (partially) localize crystallin expression to the lens. Now you should give a model of how those tools were acquired by RV and NS form an ancestor where they were not present. For instance, ho dd the cis regulatory elements emerge? And what was the pobability ot their emergence by random mechanisms, before they could be selected? Ans so on. What you have done up to now is to show the existence of mechanisms which restrict the expression of those protein (partially)to the eye. Well, we know those mechanisms exist (after all, the expression of those proteins “is” partially restrticted to the eye. But your task was to give an explanatory mechanism, or at least amodel, of how those mechanisms were acquired.
The task that I set myself was to provide links to the scientific literature bearing on the issue of co-option with respect to lens crystallins. Literature that you seemed to be unaware of when you derided the idea of co-option back in post #18. So I am satisfied that I have made a good effort to reduce your ignorance of the empirical basis for some examples of the concept of co-option.
And again, nothing in the quoted literature shows how that could have happened by RV + NS.
It's not clear what you find lacking. For example, the sequence alignments in de Jong's Fig. 1 indicate that many mutational events have occurred between members of the small heat-shock protein family. There is no reason to think that those mutational steps were non-random with respect to fitness. Perhaps you're asking for a mutation-by-mutation account of those changes, and how they affected the function of each organism in whose genome they occurred. I doubt that much relevant data are available yet. We are shocked, shocked (heat-shocked?) to observe that there are gaps in the evidence. If and when gaps are filled by data, I expect that they will be published. Without additional data, further hypothesizing seems unproductive. However, you have generously filled in those gaps with your preferred alternative hypothesis (though with rather scanty detail):
I am the designer, and I am planning a new organ, the eye, and in particular the lens. I have special constraints there: I need many functional proteins to protect the tissue from light stress. Among them, I decide to use a type of small heat shock protein. But I also need the lens to be transparent, and to have a specific refractory power. So, I slightly adapt one of the existing small hsps, so that it can serve as a structural protein, while preserving its more complex biochemical function as a chaperone.
An excellent and entertaining hypothesis, but you are not the designer (as far as I know - do you claim otherwise?) and there is no evidence for the existence of a designer. Nor do you have a way of testing your hypothesis. Your scenario is fanciful. A fable. A "Just-so Story."Adel DiBagno
April 6, 2009
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Adel et al: Sorry for the many typos above (old age, I presume). I rewrite the last part here: g) So, to sum up: I am the designer, and I am planning a new organ, the eye, and in particular the lens. I have special constraints there: I need many functional proteins to protect the tissue from light stress. Among them, I decide to use a type of small heat shock protein. But I also need the lens to be transparent, and to have a specific refractory power. So, I slightly adapt one of the existing small hsps, so that it can serve as a structural protein, while preserving its more complex biochemical function as a chaperone. That is not cooption, not even guided cooption. It is rather direct utilization of an existing function in a different environment, with appropriate adaptation to serve also in a different, simpler function (structural). And again, nothing in the quoted literature shows how that could have happened by RV + NS.gpuccio
April 5, 2009
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Adel (#80): "Now, if you are willing, I would like to go back to the original topic of this thread: co-option." Happy to do that. "In the two references I have given so far, Piatigorsky (1989), and Cvekl et al. (2004), there is information on the cis- and trans- acting factors, respectively, that are responsible for preferential expression of crystallin genes in vertebrate lenses. So I have addressed the “change in location” issue." I don't think so. You have shown, with satisfactory details, some of the tools acting to (partially) localize crystallin expression to the lens. Now you should give a model of how those tools were acquired by RV and NS form an ancestor where they were not present. For instance, ho dd the cis regulatory elements emerge? And what was the pobability ot their emergence by random mechanisms, before they could be selected? Ans so on. What you have done up to now is to show the existence of mechanisms which restrict the expression of those protein (partially)to the eye. Well, we know those mechanisms exist (after all, the expression of those proteins "is" partially restrticted to the eye. But your task was to give an explanatory mechanism, or at least amodel, of how those mechanisms were acquired. But let's go to the more interesting part: the proteins themselves. You say: "Turning to the evidence for the origination of crystallin genes by duplication and functional modification, I offer this paper by de Jong et al." Well, I have read with great interest that paper (a very good paper, by the way), and have trued to deepen my understanding of the subject by other sources too. I will therefore make some comments, apologizing in advance if I have misunderstood something, and always open to further discussion. 1) If I understand well, we are discussing alha crystallin, and its relation to the family of small heat shock proteins. Other crystallins are not at stake here. 2) If I understand well, alpha crystallins "are" heat shock proteins. This is the concept which I find everywhere. They are members of the family, they are even named as heat shock proteins, and their function "is" to work as molecular chaperones, like all other small hsps. 3) Alpha crystallin is made up of two chains, A and B. While chain A is more (but not absolutely) restricted to the lens, chain B is well expressed also in other tissues (heart, muscle, kidney). 4) In addition to its function as a chaperone and heat shock protein, "alpha-Crystallin has a structural function in the lens, contributing to the extremely high protein concentration, up to 50%, in the lens fiber cells, which warrants proper refractive properties and transparency" My conclusions: a) Where is the cooption? b) Alpha crystallin is and has always been a heat shock protein. c) It is higly expressed in (but not absolutely restricted to) the lens, because it is necessary there for its function. d) Having to contribute to the structural function of the lens, it is finely tuned to give, together with the other proteins in that tissue, the necessary "proper refractive properties and transparency". This is an additional function, which coopts nothing, but which is added to the original function. e) I quote from the conclusions in the paper: "The recruitment of a-crystallin as a major lens protein now becomes understandable. Not only does its intrinsic structural stability makes it suitable for residing life long, without turnover, in the ens; but, by preventing undesirable protein interactions and restoring unfolded proteins, a-crystallin would contribute to the maintenance of lens transparency and integrity. In fact, the constitutively high level of crystallin in the lens cells would make them permanently stress tolerant." And: "Logically, the functioning of a-crystallin as a stress protein in various tissues must have preceded its recruitment as an abundant lens protein." And: "Whether the dual function of a-crystallins-as ( 1) stress proteins in and outside the lens and (2) structural lens proteins-imposes additional evolutionary constraints is yet uncertain." f) Finally, let's remember that the common sequence in the family of hsps (the C terminal 100 AAs sequence) is only part of the molecule: the N terminal part is very different in different molecules, and that part could well contribute different specificities and functions, while the C terminal part would be responsible of the hsp chaperone function (probably, more is known today about this: thatpaper is not very recent after all). g) So, to sum up: I an the designer, and I am planning a new organ, the eye, and in particular the lens. I have special constraints there: I need many functionl proteins to protect the tissue form light stress. Among thm, I decide to use a type of small heat shock protein. But I also need the lens to be trnspsrent, and to have a specific refractory power. So, I slight adapt one of the existing small hsps, so that it can serve as structural proteins, while preserving its more complex biochemical function as a chaperone. That is not cooption, not even guided cooption. It is rather direct utilization of an existing funtion in a different environment, with appropriate adaptation to serve also a different, simpler function (structural). And again, nothing in the quote literature shows how that could have happened ny RV + NS.gpuccio
April 5, 2009
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gpuccio [79]:
Empirical science is enough for me.
Agreed. Now, if you are willing, I would like to go back to the original topic of this thread: co-option. You will remember that in your post #18, you asked:
For instance, how was the “change in location” achieved? By a random mutation in the rehulatory, and vastly unknown, procedures which determine the emergence of specific transcriptomes in different cells?
In the two references I have given so far, Piatigorsky (1989), and Cvekl et al. (2004), there is information on the cis- and trans- acting factors, respectively, that are responsible for preferential expression of crystallin genes in vertebrate lenses. So I have addressed the "change in location" issue. Turning to the evidence for the origination of crystallin genes by duplication and functional modification, I offer this paper by de Jong et al. (1993), "Evolution of the [alpha]-crystallin / small heat-shock protein family:" http://mbe.oxfordjournals.org/cgi/reprint/10/1/103 I should like to call your attention especially to the sequence alignments in Fig. 1, which provide compelling evidence for genetic relationships within this gene "family;" the phylogenetic tree that was deduced from the foregoing data (Fig. 2); Table 1, which compares the known (as of 1993) functional and structural properties of the alpha-crystallins and the small heat-shock proteins; and the statement on page 112:
The 5’ flanking regions of all analyzed small-hsp genes and of the [alpha]B-crystallin gene contain one or more heat-shock elements. As a consequence, these genes-but not the [alpha]A gene-can be induced by elevated temperatures and various other types of stress...
(My emphasis)Adel DiBagno
April 5, 2009
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Adel: Empirical science is enough for me. That means any serious attempt at understanding the nature of reality through objectively sharable methods and approaches. Empirical science as it is currently practiced is OK, but empirical methods and their conceptions could change in the future. Why shouldn't they? We are not certainly at the climax of empirical knowledge or of empirical philosophy. Moreover, there is a tendency today to deny the empirical status of important observable realities like consciousness and all its activities. I completely disagree with that. Future empirical science will have to consider consciousness as an empirical fact, and to investigate it appropriately. Finally, while empirical investigation is today very satisfying, epistemology, methodology and philosophy of science are IMO in great crisis, and very badly understood and practiced especially by scientists. That is a problem which must be faced, if we want empirical science to be able to meet its most important challenges. Contemporary science is gathering a lot of interesting data, but is often interpreting them in a very biased way. That "is" a problem, and we have to remember that true scientific culture is something which goes far beyond mere technology, and has deeper cognitive implications. Please, note that your phrase: "I see no reason why progress should not continue indefinitely using “naturalistic” methods." interpreted in the light of your clarification, becomes: "I see no reason why progress should not continue indefinitely using the methods of science as currently practiced". IMO, that is not true. Science has never been that way, and never will be. Science changes: in its methods, in its vision, in its perspective, in its philosophy, in its culture, in its morality, even in its errors. There is no reason that science will be, in 200 years, any more similar to current science than current science is to science of 200 years ago. Science is not the final truth, not the final culture, not the final model of everything. And yet it is precious, even more so for its weaknesses and limits. Science idolatry is IMO the greatest enemy of science itself.gpuccio
April 4, 2009
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gpuccio, Concerning "naturalism," you are of course entitled to you aversions. I was using the term "naturalistic methods" to encompass empirical science as currently practiced. Please suggest an alternative term that you prefer.Adel DiBagno
April 4, 2009
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