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,

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.

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!

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!

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.

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.

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.

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.”

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.

Please, read it again at #64.

And now, good night.