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Natural Selection vs Artificial Selection

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gent-selecting-a-suit-1514073Stimulated by the nth discussion with Zachriel on this point, I would like to offer here some thoughts about the difference between Natural Selection and Artificial Selection.

First of all, the dramatic limitation of NS is the following: it works on one functional specification, and one functional specification only: reproductive advantage.

In a sense, that specification is the byproduct of the system: biological beings that reproduce, that use limited resources to do that, and that compete for those resources. So, NS is a selection made possible by the existence of a complex functional system, and it selects for improvement in a function critically predefined in that system: reproductive success. So, it is a byproduct of the functional complexity already existing in the system.

Now, the functional specification: “reproductive success” is rather generic. It can certainly include many sub-functions. That’s the point that neo-darwinists stress. They say: OK, NS can select only for reproductive success, but reproductive success can include any function, and everything which goes in that sense can be selected.

Well, this is a false reasoning, which takes into no account the nature of complex information. The simple fact is: the search engine to which NS can be applied is random variation, and only random variation (I exclude for the moment possible algorithmic adaptation mechanisms). So, NS works on variation that is random, and not purposeful. Can that mechanism build complex functional information?

The simple answer is: no. Simple functional variation can certainly be generated by random variation, and therefore selected by NS. Why? because a few bits of variation are in a search space small enough to be explored, even many times, by biological RV. Those rare instances where the variation can give an advantage, with a bit of luck, can certainly be selected. That is the case of simple forms of antibiotic resistance. We can call those cases “molecular microevolution”. The few examples we have of that are the only empirical examples of NS at work in biology.

But what about some function which can give reproductive advantage, but which appears only if at least, say, 500 bits of specific information are found?

Such a result is definitely beyond any resource of RV. Therefore, it will never be achieved, and therefore never be selected.

Neo-darwinists, like Zachriel, argue that gradual pathways exist that will build those 500 bits of specific information in small steps. That is simply a fairy tale, existing only in their imagination. Information does not work that way. If I need 100 specific aminoacids to make something work (a case very common), then there is obviously no pathway which goes to that sequence step by step. Why? Because those 100 AAs are specific to the function. Fragments of the sequence have no special meaning and function, unless the complete sequence is achieved.

 

What about AS? Let’s take the case of the ATP binding protein, quoted by Zachriel (IOWs the Szostak paper).

This is AS, as many times argued by me here. The designer starts by conceiving and defining a function: “I want a protein which can effectively bind ATP”. That is the functional specification, and it is a form conceived in the consciousness of the designer.

As anyone can see, the function is very different from the single function available to NS: reproductive success.

Then, the designer uses his cognitive understanding of protein biochemistry and lab techniques to devise a strategy to implement his goal.

First of all, he sets a system that measures and extracts those molecules which bind ATP.

This point is very important, and it shows one of the main reasons why AS is so effective, while NS is not.

AS can measure the function defined by the designer at any desired level of sensitivity. Instead, NS has a definite threshold, under which no selection happens: reproductive success must be present, and enough of it to ensure the fixation of the trait.

That means that our designer, if interested in ATP binding, can select molecules which bind ATP with any level of affinity. There may be practical limitations due to the technology used, bu in principle any level of binding can be detected.

The reason is simple:

1) In NS, the coupling between the new function and the selection is direct: it is due to the reproductive success conferred by the function itself.

2) In AS, the coupling between the new function and the selection is indirect and symbolic: it’s the designer of the procedure who connects two events completely unrelated, for example ATP binding and the selection and expansion process. (UB, are you there?  🙂 )

In our example of ATP binding, then the designer chooses to use some form of artificial RV (in that case, mutagenic PCR), and to apply it in rounds coupled to artificial selection again and again.

The results are powerful: he obtains, in a short time, a protein with strong affinity for ATP.

The important point is: while that protein satisfies well enough the functional definition for which it was artificially selected (ATP binding), in no way it confers a reproductive advantage. So, even at the end of the artificial selection procedure, still the protein is not in the range of NS.

So, to sum up, the main differences between NS and AS are:

1) AS can define any function, and select for it. NS works only on one function: reproductive success.

2) In NS, the coupling between function and selection is direct: it’s the function itself which confers the reproductive advantage, which is the reason for the selection itself. In AS, the coupling between the defined function and the selection process is indirect and symbolic: the connection is established by the designer, by definite procedures designed by him.

3) NS has a definite threshold of measurement: it can only act if enough reproductive success is present as to ensure the fixation of the trait. AS can measure and select any desired level of the defined function.

4) In NS, the only selecting procedure is tied to the reproductive success, and is in essence differential reproduction. In AS, any intelligent procedure can be used to isolate, expand and fix the desired function.

 

Comments
"If I need 100 specific aminoacids to make something work (a case very common), then there is obviously no pathway which goes to that sequence step by step. Why? Because those 100 AAs are specific to the function." Completely false. You could not be any more wrong.Alicia Cartelli
December 4, 2015
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wd400: Then I am afraid there is some problem in my way of writing, or in your understanding.gpuccio
December 4, 2015
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Zachriel:
You claimed there was no selectable pathway.
No. This is my statement: "But what about some function which can give reproductive advantage, but which appears only if at least, say, 500 bits of specific information are found? Such a result is definitely beyond any resource of RV. Therefore, it will never be achieved, and therefore never be selected. Neo-darwinists, like Zachriel, argue that gradual pathways exist that will build those 500 bits of specific information in small steps. That is simply a fairy tale, existing only in their imagination. Information does not work that way. If I need 100 specific aminoacids to make something work (a case very common), then there is obviously no pathway which goes to that sequence step by step. Why? Because those 100 AAs are specific to the function. Fragments of the sequence have no special meaning and function, unless the complete sequence is achieved." It is rather clear. No gradual pathway exists to a new function which requires, for example, 500 bits of specific sequence information to appear.
Unless you are claiming proteins are never subject to selective optimization in nature, then the point is directly relevant.
I did not claim that. Optimization of an existing protein is a possibility, probably even for NS. I have discussed that point many times, for example for the possible optimization of an existing active site, whose affinity can change with a small number of mutations. That's why, as you may have noticed, I always refer to protein superfamilies as examples of isolated functional islands. I have always kept an open mind for optimization or limited variation inside a family. Those examples should be evaluated case by case, according to the functional information necessary to achieve the transition. Axe has debated some aspects of that kind of problem.
gpuccio: An intelligently selectable path is not a naturally selectable path. That’s like saying we can’t study how salt dissolves in water in nature if we put salt and water in a beaker. Are you claiming proteins are never subject to optimizing selection in nature?
This comment of yours is really senseless. My OP is exactly about the essential differences between NS and AS. The way salt dissolves is the same in nature and in the beaker. But the process of selection and its modalities, powers and results are completely different in NS and AS, which is exactly my point. Bad metaphor, or simply bad trick? Regarding optimization, see previous point.
Therefore, we now know that highly-specified, complex structures can form through selection.
Absolutely not. As I have explained, that case is not the generation of a new highly-specified and complex structure. It is simply a case of partial retrieval from damage of an existing functional structure. The partial "optimization" (which remains however a strong reduction of function) is probably achieved through a few bits of variation, completely in the range of the probabilistic resources of that system. Try to explain why they do not achieve the wild type efficiency, or why, according to the authors of the ragged landscape paper, a starting random library of 10^70 molecules would be necessary for that result. We definitely don't know what you claim that we know.
gpuccio: As you know, I don’t discuss morphological issues, unless the molecular basis for them is known. Ignoring a primary line of evidence undermines your argument.
I am not ignoring anything, least of all a "primary line of evidence". My whole argument is based on the evaluation of functional complexity. We cannot evaluate the functional complexity of a variation whose molecular basis is not known. That would simply be very bad scientific methodology. I leave those kind of things to neo-darwinists, or to those who take a pluralistic view of evolution, suitable to a historical process.gpuccio
December 4, 2015
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I've read it. The four points just use more or fewer words to say the same thing: Breeders get to chose what to breed for. You can sub in "select" for "breed" if you want, I don't think it changes that point.wd400
December 4, 2015
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wd400 #16: The "big differences" are analyzed in detail in my OP. Did you read it? They are summed up in 4 points at the end, each different from the other. Have you considered them? And nowhere in the OP I refer to "breeders". I rather quote, as an example of artificial selection, a famous molecular experiment by a Nobel prize winner. Are you really sure that you read what I wrote?gpuccio
December 4, 2015
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Zachriel, In your view, do you think there is any argument at all that can be made against evolution via NS&RM as the primary driving force of biological complexity? (regardless of whether it comes out of the evo or ID camp) Just wondering, thanks.computerist
December 4, 2015
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I wish I knew how to better articulate this, but it seems to me that a big problem with natural selection is that there isn't possibly enough time to "select" for all possible survival advantages from the population. There are just too many traits along an infinite scale of variation to make such a simplistic process work. I don't know if that makes any sense, so sorry for my stumbling.OldArmy94
December 4, 2015
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While a single binding protein isn’t as complex as ATP synthase, it is certainly complex. As we have seen, even random sequences can having selectable catalytic capability.
Natural selection didn't have anything to do with producing those random sequences. You are being dishonest at best.Virgil Cain
December 4, 2015
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Ignoring a primary line of evidence undermines your argument.
And continually spewing nonsense proves that you don't have one.Virgil Cain
December 4, 2015
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gpuccio: But ATP synthase and the genetic code are complex entities. While a single binding protein isn't as complex as ATP synthase, it is certainly complex. As we have seen, even random sequences can having selectable catalytic capability. gpuccio: As I said, the minimum requirement is reproducting entities which use limited resources to reproduce and which compete for them. Molecular replication entails competition for limited resources. gpuccio: I have purposefully avoided to discuss this aspect in this post, but you will agree that in general it does not seem to be the main component of biological evolution. These sorts of mechanisms are certainly important in the early evolution of life, and as your primary concern is evolution of metabolic processes, they are very relevant. Zachriel: There is ample evidence to support that selection can lead to complex functional adaptation, as can be seen with protein evolution, wherein simple selection can generate highly specified, complex, three-dimensional structures. gpuccio: What selection? What evidence? Hayashi et al., among others. gpuccio: I use neo-darwinist in a very general sense, and your arguments have always been much in accord with what I consider current neo darwinist theory We take a pluralistic view of evolution, suitable to a historical process. gpuccio: If you mean intelligently selectable, that is completely non relevant. You claimed there was no selectable pathway. Unless you are claiming proteins are never subject to selective optimization in nature, then the point is directly relevant. gpuccio: An intelligently selectable path is not a naturally selectable path. That's like saying we can't study how salt dissolves in water in nature if we put salt and water in a beaker. Are you claiming proteins are never subject to optimizing selection in nature? gpuccio: In brief, I have no problems that a random polypeptide which reduces the efficiency of an existing protein in an existing system can “improve” its behaviour in a highly efficient mutation selection system (phage infectivity). Therefore, we now know that highly-specified, complex structures can form through selection. gpuccio: As you know, I don’t discuss morphological issues, unless the molecular basis for them is known. Ignoring a primary line of evidence undermines your argument.Zachriel
December 4, 2015
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Natural selection could never produce the breeds of dogs artificial selection has created. And natural selection could never produce ATP synthase- only intentional design can.Virgil Cain
December 4, 2015
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These "big differences" are that breeders get to chose what to breed for? And selection just means differential surivial based on some trait -- that's true if it's artificial or natural.wd400
December 4, 2015
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wd400: You say: "Artificial selection shows that where there is genetic variance selection can rapidly generate phenotype change. And important point to make, I think." (emphasis mine) Well, why not: "Artificial selection shows that where there is genetic variance artificial selection can rapidly generate phenotype change. And important point to make, I think." That's what I mean by "neo darwinists go on trying to conflate the two things, which have completely different powers." You have made my case. If artificial selection can do something, it does not ensue that natural selection can do the same thing. Because, as I said, there are "big differences between artificial selection and natural selection". An important point to make, I think.gpuccio
December 4, 2015
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ATP synthase alpha and beta subuinits....
I'm sure these have hundreds of shared residues in these proteins, that's a very different claim that "100 specific residues" are required for a function.
The purpose of the post is to show the big differences between artificial selection and natural selection, because neo darwinists go on trying to conflate the two things, which have completely different powers.
Well, I don't think you've shown their powers are completely different -- only that natural selection only works on fitness. But no one has claimed otherwise. Artificial selection shows that where there is genetic variance selection can rapidly generate phenotype change. And important point to make, I think.wd400
December 4, 2015
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wd400: ATP synthase alpha and beta subuinits. Triosephosphate isomerase. Phosphoglycerate kinase. Leucine--tRNA ligase Elongation factor G, mitochondrial isoform 2 Histone H3 For all of them, hundreds of AAs conserved between bacteria and humans, or fungi and humans (for histone H3). The purpose of the post is to show the big differences between artificial selection and natural selection, because neo darwinists go on trying to conflate the two things, which have completely different powers.gpuccio
December 4, 2015
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If I need 100 specific aminoacids to make something work (a case very common)
Common? Can you name some examples? The rest of this post seems to amount to a long argument that breeders can chose which traits to select for. Sure. So what?wd400
December 4, 2015
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GPuccio, Many Thanks!EugeneS
December 4, 2015
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And even if it can bind ATP, then so what? Just because there's binding doesn't means there's any activity. Right Zachriel?Mung
December 4, 2015
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Virgil Cain: Thank you for your comments. :)gpuccio
December 4, 2015
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EugeneS: Thank you for the kind comment! You ask: "Some time ago, I asked you a question but you might have missed it somehow. It was regarding repetitive sequences and the C-paradox. How can you characterize those in light of the design hypothesis?" Yes, I must have definitely missed it. OK. 1) Repetitive sequences: There are many kinds of them. I will comment essentially about transposable elements, which are the majority of non coding DNA. As you probably know, I am a big supporter of the concept that great part of non coding DNA is probably functional. That includes SINEs, LINEs, and other transposable elements. You may also know that I have many times defended here the idea that transposons are a tool for biological design. That is supported by many molecular data which are accumulating, where functional sequences seem to have origin from transposon activity. Therefore, one important possibility is tan transposons and non coding DNA are a "factory" for new functional information. But I also think that repetitive sequences have function in the epigenetic regulation of cell differentiation and of cell activity. They could be crucial in many processes, like the determination of chromatin 3d structure in different contexts, and the generation of functional non coding RNAs. Obviously, part of them can be non functional, as neo darwinists believe of the whole thing. 2) The C-paradox: Well, the number of genes seems to be rather similar in most metazoa: our 20000 genes are more or less the standard. So, what about C-value differences, which seem to defy any logic? I don't know. But I have no big problems with the fact. I suppose that we cannot understand anything until we have some detailed knowledge of the composition of the highest C-value organisms. I have not found many data about that. There is certainly a great variety of functional implementation in different species, and we still understand very little about that.gpuccio
December 4, 2015
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gpuccio:
As you know, I don’t discuss morphological issues, unless the molecular basis for them is known. Variation acts at the molecular level. Only there we can evaluate the complexity of some functional variation.
Dr Behe brings up that very point in "Darwin's Black Box" and evolutionists have never addressed it. They think that by ignoring that aspect of reality it will somehow go away.Virgil Cain
December 4, 2015
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Zachriel: Ah, I forgot mammalian ossicles. As you know, I don't discuss morphological issues, unless the molecular basis for them is known. Variation acts at the molecular level. Only there we can evaluate the complexity of some functional variationgpuccio
December 4, 2015
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Zachriel: Welcome to the discussion, which was anyway inspired by you! :) I find your comments very reasonable in general, but scarcely relevant. I agree with many things, so I will try to point at what I don't agree with.
Yes, but reproductive advantage may depend on molecular binding, or on the size of your teeth, or on how graceful you are when running.
This is a very good point, which I should have discussed more in detail, even if I have touched it briefly: "Now, the functional specification: “reproductive success” is rather generic. It can certainly include many sub-functions. That’s the point that neo-darwinists stress. They say: OK, NS can select only for reproductive success, but reproductive success can include any function, and everything which goes in that sense can be selected." You are right: reproductive success can depend on many different things. The point is, some of those "sub-functions" are simple, but many are extremely complex. Skin color variation can be a simple thing, in some cases it could depend on a single mutation. But ATP synthase and the genetic code are complex entities. Antibiotic resistance in its simple form often depends on one or two mutations, as discussed by Behe in his TEOE. But antibiotic resistance based on enzymes like penicillinases is complex, and can only be transmitted by HGT, it is never acquired, in empirical observations, by the emergence of a completely new functional protein. So, if in a software you need some ordering algorithm at some crucial point to improve efficiency, you will not get it by magic: you have to develop that subfunction, which has its own complexity, and then insert it in the right context. No blind step by step procedure will generate the ordering algorithm by gradual improvements of the original software. If you try to change your software by random search, and you can only measure the original software efficiency as feedback, you will never get a complex sub-algorithm which improves the original software. The concept is simple, and I am sure that you can see what I mean.
The minimum requirement is reproduction, which may be as simple as a molecular replicator.
No. As I said, the minimum requirement is reproducting entities which use limited resources to reproduce and which compete for them.
Random with respect to fitness is not pure randomness. For instance, according to endosymbiotic theory, bacteria invaded other cells. These cells responded by trying to isolate and minimize the effect of these invaders. Eventually, the bacteria were coopted and integrated in some lineages as mitochondria. Is that random? Certainly random mutation was part of the process.
OK. Some parts of this highly hypothetical and in no way understood process could also be what I call "possible algorithmic adaptation mechanisms". I have purposefully avoided to discuss this aspect in this post, but you will agree that in general it does not seem to be the main component of biological evolution. Anyway, any existing adaptation algorithm has its complexity, which must be explained.
There is ample evidence to support that selection can lead to complex functional adaptation, as can be seen with protein evolution, wherein simple selection can generate highly specified, complex, three-dimensional structures.
What selection? What evidence?
Not a Neodarwinist, as should be clear from above.
Well, I apologize. I use neo-darwinist in a very general sense, and your arguments have always been much in accord with what I consider current neo darwinist theory, maybe not strictly a-la-Dawkins, but almost. Maybe I miss something. Anyway, you can specify better you position, if you like.
We know that’s false because we can show selectable pathways from random sequences to highly specified proteins.
Naturally selectable? That's the whole point of my OP. If you mean intelligently selectable, that is completely non relevant.
The function was chosen because it is a common function in nature. Nonetheless, it still shows a pathway exists, contrary to your claim.
An intelligently selectable path is not a naturally selectable path. That's the whole point of my OP. Designed search overcomes rather easily the probabilistic barriers which are implicit in RV + NS.
This claim has some limited merit. The limitation is the assumption that we are starting with a random sequence, which may not be the case in nature. Nor are all random sequences of the same functionality. Some may have significant function and still be reasonably probable.
OK, but what do you mean by that? The point which I have made many times is that when a new complex protein superfamily appears in natural history, and that sequence is completely unrelated to what existed before, then what existed before is "random" with respect to the new functional sequence. Regarding the paper you quote, I have read the summary, and it seems similar to the paper about ragged landscape that I often quote. I could discuss it in detail, but I will not do that now, also because I should be able to read the whole article to do that well. In brief, I have no problems that a random polypeptide which reduces the efficiency of an existing protein in an existing system can "improve" its behaviour in a highly efficient mutation selection system (phage infectivity). The problem with these "function retrival" experiment is that no new function is generated: they simply "damage" the original function somewhat, and then the system acquires some "damage limitation" through RV + NS. The same happened in the ragged landscape paper, but there the authors inferred the very interesting result that it is impossible to retrieve the wild type efficiency by that kind of process, because we would need a starting library of about 10^70 random sequences to achieve that result. The abstract of the paper you quote seems to confirm that point: the initial "damage" reduces infectivity of six orders of magnitude, while the "evolved" protein shows only a 240-fold increase in infectivity. So, to sum up: a) The function is already present, and remains the same. Those experiments would not work at all if the function were suppressed. b) The function is only minimally restored by the RV + NS process. The wild type efficiency seems to be beyond the realistic capacities of such a system in nature.gpuccio
December 4, 2015
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Yes, but reproductive advantage may depend on molecular binding, or on the size of your teeth, or on how graceful you are when running.
And natural selection has nothing to do with any of those.
Random with respect to fitness is not pure randomness.
In a debate over if the mutations are directed or not, it is pure nonsense, though
There is ample evidence to support that selection can lead to complex functional adaptation,
Not natural selection. You are lying, again.
For a morphological example from nature, consider mammalian ossicles.
Right and there isn't any evidence that natural selection did it. Did you have a point?
Hayashi et al., Can an Arbitrary Sequence Evolve Towards Acquiring a Biological Function?, Journal of Molecular Evolution 2003: “The infectivity assays of the clones revealed that the first generation comprised a population with selectable variation in view of infectivity.”
Those "arbitrary sequences" were designed.Virgil Cain
December 4, 2015
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EugeneS: NS is passive, AS is active. NS does not select for a future function (but rather from among existing functions), AS does. NS crucially depends on there being a functional replicating system. AS has no such limitation. Good point. Artificial selection can look forward to a future state, or in gpuccio's nomenclature, to envision the goal in the conscious mind. However, traditional artificial selection didn't look towards the distant future, but only considered change on a generation-to-generation basis. Indeed, the traditional concept that selection was meant only to bring out the "true form" is contrary to the evolutionary idea that progressive change being possible.Zachriel
December 4, 2015
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gpuccio: First of all, the dramatic limitation of NS is the following: it works on one functional specification, and one functional specification only: reproductive advantage. Yes, but reproductive advantage may depend on molecular binding, or on the size of your teeth, or on how graceful you are when running. gpuccio: So, NS is a selection made possible by the existence of a complex functional system, and it selects for improvement in a function critically predefined in that system: reproductive success. The minimum requirement is reproduction, which may be as simple as a molecular replicator. gpuccio: The simple fact is: the search engine to which NS can be applied is random variation, and only random variation (I exclude for the moment possible algorithmic adaptation mechanisms). Random with respect to fitness is not pure randomness. For instance, according to endosymbiotic theory, bacteria invaded other cells. These cells responded by trying to isolate and minimize the effect of these invaders. Eventually, the bacteria were coopted and integrated in some lineages as mitochondria. Is that random? Certainly random mutation was part of the process. gpuccio: So, NS works on variation that is random, and not purposeful. Can that mechanism build complex functional information? The simple answer is: no. ... huge hand wave, then conclusion... gpuccio: Such a result is definitely beyond any resource of RV. Therefore, it will never be achieved, and therefore never be selected. There is ample evidence to support that selection can lead to complex functional adaptation, as can be seen with protein evolution, wherein simple selection can generate highly specified, complex, three-dimensional structures. For a morphological example from nature, consider mammalian ossicles. gpuccio: Neo-darwinists, like Zachriel, ... Not a Neodarwinist, as should be clear from above. gpuccio: ... argue that gradual pathways exist that will build those 500 bits of specific information in small steps. That is simply a fairy tale, existing only in their imagination. Information does not work that way. If I need 100 specific aminoacids to male something work (a case very common), then there is obviously no pathway which goes to that sequence step by step. Why? Because those 100 AAs are specific to the function. Fragments of the sequence have no special meaning and function, unless the complete sequence is achieved. We know that's false because we can show selectable pathways from random sequences to highly specified proteins. gpuccio: The designer starts by conceiving and defining a function: “I want a protein which can effectively bind ATP”. The function was chosen because it is a common function in nature. Nonetheless, it still shows a pathway exists, contrary to your claim. gpuccio: AS can measure the functioned defined by the designer at any desired level of sensitivity. Instead, NS has ha definite threshold, under which no selection happens: reproductive success must be present, and enough of it to ensure the fixation of the trait. This claim has some limited merit. The limitation is the assumption that we are starting with a random sequence, which may not be the case in nature. Nor are all random sequences of the same functionality. Some may have significant function and still be reasonably probable. In any case, per the claim, if we were to replace a functional sequence in a living organism with a random sequence, then it should not be able to evolve a replacement because the initial level of function would be too low to be selectable. However, in this experiment, the phage with the inserted random sequence exhibited varying levels of reproductive success, meaning the modified trait is selectable. Hayashi et al., Can an Arbitrary Sequence Evolve Towards Acquiring a Biological Function?, Journal of Molecular Evolution 2003: "The infectivity assays of the clones revealed that the first generation comprised a population with selectable variation in view of infectivity."Zachriel
December 4, 2015
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GP, Nice post! NS is passive, AS is active. NS does not select for a future function (but rather from among existing functions), AS does. NS crucially depends on there being a functional replicating system. AS has no such limitation. Some time ago, I asked you a question but you might have missed it somehow. It was regarding repetitive sequences and the C-paradox. How can you characterize those in light of the design hypothesis? Thanks!EugeneS
December 4, 2015
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