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Commenter nails the problem with neutral theory of evolution

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Comment of the day (re Darwin’s natural selection acting on random mutation vs. neutral evolution/genetic drift:

The real problem is not that they are “mutually exclusive”. Obviously, they are not.

The problem is that they are different things, and that there is a repeated shift from one to the other when we ask which of them is responsible for functional information in biology.

The traditional view, defended also by Matzke and by you, is that NS is responsible for that. In that case, neutral evolution is irrelevamt for biological function.

Others, like Moran and Nei, seem to suggest an important role for neutral evolution in generating function. Even if they do not exclude the importance of NS.

Shifting from one model to the other is a smart way to elude analysis. It’s certainly easier to analyze and falsify a well defined model, rather than a slipping one.

The simple truth is that neither can explain functional information, but for different reasons.

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74 Replies to “Commenter nails the problem with neutral theory of evolution

  1. 1
  2. 2
    Joe says:

    Natural selection does NOT act on mutations. Mutations are part of natural selection. And mutations are also part of drift.

    The difference is that natural selection is differential reproduction DUE TO heritable random mutations and drift is just heritable random muations.

  3. 3
    Piotr says:

    Oh, Joe, clueless as usual. I’ll leave it to Gpuccio to clarify things for you.

  4. 4
    gpuccio says:

    News:

    Thank you. I am honored! 🙂

  5. 5
    gpuccio says:

    Piotr:

    I have just won the prize of my life, and you instigate me against Joe? And I believed you were a friend! 🙂

    OK, now that’s what I will do. I will read your comment on the other thread, and will answer you here. After all, walking around (even randomly) is good for health.

  6. 6
    phoodoo says:

    Joe @2,

    I agree with you.

    I have to say, I can’t understand why there is even a discussion about the difference natural selection plays on evolution as opposed to some “neutral theory” . To me its sort of a pointless distinction, natural selection does nothing. Its not even a thing, and I think its intellectually of those who continue to speak of it as having some power of doing anything. Organisms become whatever they become, and NS has nothing to do with how they got that way.

    The neutral theory, or any other way one wants surmise why genes are conserved its a useless distraction towards understanding how complex features arose, which utilize multiple parts. Could a collarbone ever be neutral? Or an ear canal?

    I don’t know what I am missing, but it seems a dumb point to linger on by those who choose to do so, to me.

  7. 7
    phoodoo says:

    In fact why not just say, drift is the inheritance of useless mutations, and NS is the inheritance of (supposedly) somewhat useful mutations. Not that complicated of a distinction really.

    Neither has much explanatory power for building a complex structure that is novel and useful.

  8. 8
    gpuccio says:

    Piotr:

    No, they are not “different things”. They are two components of the same thing — the variable survival of alleles. Drift is the purely random component (accidental sampling error) and selection is the bias (in response to environmental and “internal” pressures).

    Well, how is it that as soon as we start discussing drift and NS, we have to fight about words’? Without reason, I would say.

    However, as fighting about words with linguists has recently become my favorite pastime, let’s say that:

    “They are two different components of the same thing”. Are you happy now?

    After all, two different components are two different things, aren’t they? “Thing” is a rather flexible word (one of my favorite, when I want to remain generic).

  9. 9
    Joe says:

    Piotr, Obviously it is YOU who is clueless as what I said is spot on. And it is very telling that all you can do is spew your nonsense as opposed to actually making a case.

  10. 10
    Piotr says:

    “They are two different components of the same thing”. Are you happy now?

    After all, two different components are two different things, aren’t they? “Thing” is a rather flexible word (one of my favorite, when I want to remain generic).

    If you want to point to a location somewhere on Earth, you can do so by specifying its geographical latitude and longitude. Latitude and longitude are also in some sense “two different things”.

  11. 11
    phoodoo says:

    Piotr,

    Aren’t you just trying to say that evolution happens but mutations that are either somewhat useful, or not useful at all-and we have no idea what percent each is.

    Is it a useful point?

  12. 12
    gpuccio says:

    Piotr:

    You are putting things in my mouth (and I suppose Nick’s, too). I don’t think anyone in the field seriously doubts that selection is the main engine of the spread and fixation of adaptations, which doesn’t mean that it’s the sole explanation of them (it certainly isn’t responsible for their origin), or that neutral evolution is irrelevant.
    Note that in real populations drift and selection always act in combination. For example, whether an innovation with a positive selection coefficient has a chance to spread depends on the relative strength of selection against drift. In nearly neutral evolution drift will often override selection, but still the probability of fixation is slightly influenced by the fact that the mutation is not entirely neutral. It isn’t a question of switching between one or the other mode. They are both present.

    Well, I think we agree that both drift and NS exist. That is not the point. The point is: what is their supposed role and relevance in trying to explain complex functional information, if you want to exclude design? Let’s suppose that we want to explain how some complex functional protein emerges for the first time at some point in natural history.

    There are two possible scenarios, if you don’t want to shift components ( 🙂 ).

    a) Drift has the most important role. RV generates the new sequence randomly, in some non coding non functional region, or in some duplicated inactivated gene. And drift expands it. Maybe in the end, when it becomes an ORF and becomes translated, NS can contribute to its expansion, and certainly can fix it by negative selection, so that it is conserved through time.

    The strongest argument against this scenario is probabilistic. It cannot empirically happen.

    b) NS has the most important role. RV generates small variations, in the range that is probabilistically possible, and each new state is a naturally selectable step towards the new functional sequence.
    So, each intermediate step is translated and confers a reproductive advantage. And, with a little luck (which is always necessary in life) it can be expanded and fixed by NS.

    Now, this scenario lowers very much the probabilistic walls (the random variations are relatively simple), but there are four big problems with it:

    1) To lower significantly the probabilistic walls, you need a lot of intermediate steps.

    2) Each step must confer a significant reproductive advantage (IOWs, it must not only be functional, but be naturally selectable). And have a little luck (which is always necessary in life).

    3) The individual variations which generate the naturally selectable steps must, for some reason, be exactly those that, when added, generate the sequence for the new, unexpected function. That borders with magic and miracles.

    That’s what I mean when I say that a complex function cannot be deconstructed into simpler, naturally selectable steps.

    4) There is no empirical trace of those selectable intermediate steps, indeed no evidence at all that they even exist.

    That’s what I mean when I say that RV + NS is an explanation which is neither logically consistent nor empirically supported.

    Even if you want to propose some intermediate scenario (a little more of this, a little less of that), things don’t become better:

    a) If you want to rely more on RV and drift, and you lower the number of hypothetical intermediate selectable steps in the model, the probabilistic walls immediately become insurmountable.

    b) It is difficult to rely more on NS, when there is no empirical example of its role in macroevolution (that is, in a complex functional molecular transition).

    So, as I said (speaking of drift and NS):

    “The simple truth is that neither can explain functional information, but for different reasons.”

  13. 13
    gpuccio says:

    Piotr:

    “Latitude and longitude are also in some sense “two different things”.”

    They are. But at least they are similar in nature (geographic coordinates for our planet).

    Instead, drift and NS are deeply different. One is a random process, the other is a process where function has a critical role.

    Moreover, RV is really a component of the whole process described as RV + NS. Drift instead is rather apart, a variation of RV. It happens, together with RV and the rare cases of NS. But RV and NS can happen even if there is no drift. And drift has no “interest” in NS. (Please, don’t attack me for the metaphor! 🙂 )

  14. 14
    gpuccio says:

    Piotr:

    I haven’t read Nei yet, but I agree with a lot of what Larry Moran says (not that my amateurish agreement carries much weight). Even if the non-random selection component is primarily responsible for the fixation of adaptive changes, its operation is constrained by mutations (which don’t happen just because they are needed) and may be helped along by neutral evolution (which prepares the scene for adaptive changes).

    I think I have already discussed that in my post #12.

  15. 15
    gpuccio says:

    Piotr:

    Your “slipping model” is a strawman. We can calculate the expected effects of drift and selection, depending on things like the size and structure of populations.

    Population genetics is one model taking into account both components (and much more).

    No. We can calculate the expected effects of drift. But I am not aware of models which take into account realistic parameters for NS, for the simple reason that those realistic parameters don’t exist, because we know of no case of NS leading to complex functions.

    So, the models just assume some reproductive advantage, and just calculate how likely it is that such a reproductive advantage will be fixed. I am fine with that, but of what use is it?

    We know nothing of:

    a) How often some variation of defined complexity happens, and how often it realistically confers a reproductive advantage, and how great it can realistically be.

    b) If it is even possible that such variations can add up to give a complex function.

    So, population genetics is modeling its abstract assumptions, not reality.

  16. 16
    Dionisio says:

    gpuccio @ 4

    I think they realized that your friendly debating style does seem to attract quite a large number of visitors to the threads. Your latest OP brought in close to a thousand hits and almost 300 comments. Perhaps the announcement of a hypothetical live debate between you and Piotr could fill an auditorium pretty fast 😉

    Cool! 🙂

  17. 17
    gpuccio says:

    Joe:

    Natural selection does NOT act on mutations. Mutations are part of natural selection. And mutations are also part of drift.

    The difference is that natural selection is differential reproduction DUE TO heritable random mutations and drift is just heritable random mutations.

    I essentially agree with you. With some slight modifications:

    a) I am not interested in using or not using the verb “act”. We are describing processes. There is no need to reify the concepts, and I agree with you that they are often reified, and that is not good. But I believe that most serious interlocutors are well aware that we are discussing processes.

    b) “The difference is that natural selection is differential reproduction DUE TO heritable random mutations”

    That’s OK. IOWs, it is expansion due to heritable random mutations which confer a reproductive advantage.

    “and drift is just heritable random mutations.”

    Not exactly. That would be the definition for RV. All random mutations are heritable.

    Drift is rather the random expansion of heritable random mutations, independent from their function.

  18. 18
    Joe says:

    Hi gpuccio- News used the words “natural selection acting on random mutations”. That is what I was responding to- the OP.

    All random mutations are not heritable because some are fatal, cause sterility or some other malady that prevents reproduction.

  19. 19
    Piotr says:

    a) If you want to rely more on RV and drift, and you lower the number of hypothetical intermediate selectable steps in the model, the probabilistic walls immediately become insurmountable.

    I think you exaggerate the insurmountability of those “walls”. Let’s consider a simple example: a gene — let’s call it G — encodes for a protein with two important functions — let’s call them P and Q. Both are so important that losing one of them would be highly deleterious. But the protein is suboptimal: it could perform P or Q better, but neither function can be improved without sacrificing the other.

    G gets duplicated, producing two copies, G1 and G2. If there is no gain from maintaining a second copy, any inactivating mutation can damage it with impunity, so eventually only one copy will be left. If it’s beneficial to have both (the amplification of both P and Q is desirable), there will be purifying selection against anything that might damage eitehr function in either copy of the gene. However, if the gain is not great enough to override random drift, selection is relaxed: G1 or G2 may lose one of their functions, and still their “defective” alleles may be maintained in the population long enough for interesting things to happen. Let’s say that a mutation in G1 improves P but damages Q, and somewhat later a different mutation in G2 improves Q at the expense of P. This “division of labour” allows both G1 and G2 to evolve further: natural selection can now act on P and Q separately. Instead of one protein doing two jobs we have a small family of more specialised proteins doing the same jobs much better.

    b) It is difficult to rely more on NS, when there is no empirical example of its role in macroevolution (that is, in a complex functional molecular transition).

    I don’t quite understand this part. “Macroevolution” is normally used in a different sense. If you mean that selection can’t produce new functions — well, who says it can? Mutations and recombination are responsible for that part.

  20. 20
    gpuccio says:

    Piotr:

    Let’s clarify.

    Your example (which however is a little ad hoc) would anyway represent only the tweaking of an existing function, The sequence for the improved function (be it P or Q) is alredy in G. So, it is not a case of a new protein domain, or superfamily, emerging.

    I have already agreed that some cases of tweaking of function in a family could be explained in a darwinian context, provided the transition is very simple. The divergence of opsin L from opsin M could be an example: the difference is really of few AAs. We are borderline, here. Obviously, if we consider all the other changes which may be necessary to really exploit that change, the reasoning could be different.

    All depends on the functional complexity of the transition. That’s why the concept of functional information is so important.

    With “macroevolution” I mean the emergence of complex new functions at molecular level. The emergence of a new protein superfamily, or multiprotein system, and so on. Obviously, that would include the emergence of new regulatory networks, if we knew well their molecular basis.

    I never discuss morphology, or fossils, for a simple reason. We don’t know the molecular basis. If we don’t know the molecular basis, we cannot compute functional information, because genomic information, as far as we know, is digital (even regulatory information is probably digital).

    Therefore, we need to know what changes, how much the change if functionally constrained, what is the search space, and so on.

    As you have noticed, I don’t deal even with recombinations, exon shuffling, and similar, not because I don’t think that those events are designed (I believe that most of them, when they give functional results, are designed), but because at present I would not know how to analyze the problem.

    An interesting approach could be the transcriptome, because for the space of possible transcriptomes we can make some gross mathematical approximations, and many data are accumulating about that issue.

    Finally, when I say that:

    “It is difficult to rely more on NS, when there is no empirical example of its role in macroevolution (that is, in a complex functional molecular transition).”

    I don’t mean that “selection can’t produce new functions”. That is obvious: selection can only expand and fix, not produce anything.

    What I mean is that there is no example of selection taking place at many simple successive steps, each of them functional, each of them naturally selectable, which in the end for some strange magic produce a new functional sequence, with new structure and function: a new domain or superfamily.

    There is no selectable path to our famous 2000 superfamilies, and there is no trace of imtermediate functional states in the existing proteome, even if, for the scenario to be true, each of them should have been expanded and fixed at some time. That is completely unbelievable, as I have discussed for a long time at TSZ a lot of time ago (without, obviously, convincing anyone there).

    IOWs, there is no empirical example of my b) scenario in post 12, and my 4 objections remain completely valid.

  21. 21
    gpuccio says:

    Joe:

    OK. we agree.

    Just to be fastidious, 🙂 we usually speak of mutations which are in the parents, or at least in some of their gametes, which are by definition heritable. If the mutation is very deleterious, it will be indeed eliminated, but in the offspring that has inherited it.

    Well, there are mutations which happen in somatic cells, but usually they don’t give a new phenotype (sometimes a neoplasia). The only example of deleterious mutations which are not “inherited” but can interest the general phenotype would be mutations happening in the zygote, or after a few cell divisions (which would give a mosaic). Those cases are rare. If you are interested, you can find some discussion about these issues here:

    http://www.ncbi.nlm.nih.gov/pm.....MC3909954/

    I am afraid that I have been fastidious. I apologize.

  22. 22
    jerry says:

    In the past when we talked about the gene pool and allele frequency, it was about the coding section of the genome for proteins. We could point to the allele frequency as an indication of just what the gene pool was. After a generation of reproduction the frequency of the gene pool could change for various reasons.

    1. there could be a mutation to one of the alleles essentially creating a new allele. Hence the frequency has changed.

    2. there could be variable heredity of the alleles due to random reproduction processes. This too causes the frequency of the alleles to change. People call this result drift.

    3. there could be variable fecundity within the organisms of the gene pool due to environmental pressures. This too causes the frequency of the alleles to change. People call this result, natural selection.

    4. There could theoretically be a new coding section of the genome which essentially adds at least one allele to the gene pool. This too causes the frequency of the alleles to change since there is a brand new coding section.

    All of these cause evolution since evolution is defined as a change of the allele frequency over time. But for changes of 1, 2 and 3, the result is rarely of any interest since the phenotypes have not changed in any great way. Example 4 is of interest since the addition of a new coding section may affect the genome in unknown ways.

    What about the appearance of novel complexity?

    Can 1, 2 and 3 lead to this. Apparently reading Nick Matzke over the last few days, it can. But how? No new alleles are present. I believe the answer is that the combination of alleles that end up in the gene pool is what causes the morphological changes.

    To that end the examples used by Darwin and Matzke are instructive. They use artificial selection to show that dramatic changes in a phenotype can occur and the gene pool has not changed one iota in terms of coding sections. There is no need for mutations either. There is certainly a different allele frequency.

    So it is possible to get dramatic changes in phenotype by a new allele frequency in the genome. And this could affect fecundity. The new phenotype could be bigger and faster. (dog breeding is the best example of this.)

    Also there could be internal non visible changes to the organism that could affect fecundity, for example the amount of sperm produced or the number of neurons connections produced.

    When mutations just to the coding region are added then it may be possible to get even more possibilities.

    Then there is 4.

    This is the big difference and what Allen MacNeill, Brosius and apparently Nei are talking about. That what is needed is massive additions to the coding region through new variation.

    So we have two schools of evolution, the first thinks that most of the changes in life forms over time were due to changes in allele frequency and the second thinks that this is nonsense and there must be massive additions to the coding regions.

    This does not consider what is happening to the organism due to changes outside the coding regions.

  23. 23
    Axel says:

    Why don’t they call it ‘survival of the fittest’, instead of ‘natural selection’? ‘Selection’ predicates a mind and a will. Barmy.

  24. 24
    jerry says:

    Why don’t they call it ‘survival of the fittest’

    Natural Selection is too often used as a process. It is not. It is an outcome. So is genetic drift an outcome. Both are used nearly all the time in the active sense that they cause something. What causes the outcome is varied and generally creates a less fit gene pool since there is nearly always a reduction in alleles as a result.

    So “Survival of the Fittest” is not necessarily appropriate either.

  25. 25
    Axel says:

    Would it not be appropriate for the proximate outcomes, irrespective of the incrementally deleterious nature of the processes, particularly further down the pike?

  26. 26
    Axel says:

    Would it not still be ‘survival of the fittest’, despite the fittest not being half the man their gramps was?

  27. 27
    jerry says:

    Would it not still be ‘survival of the fittest’, despite the fittest not being half the man their gramps was?

    Theoretically, gramps was still in the gene pool before the processes that narrowed the gene pool did him in.

    One of the theories for extinction is this culling of the gene pool so that when a new environment comes along, the alleles necessary to survive in it are no longer there. We tend to look at it on a short term basis as opposed to the long term where the fittest do not necessarily survive.

    Of course the definition of fittest is usually circular.

  28. 28
    Piotr says:

    Your example (which however is a little ad hoc) would anyway represent only the tweaking of an existing function, The sequence for the improved function (be it P or Q) is alredy in G. So, it is not a case of a new protein domain, or superfamily, emerging.

    The sequence encodes for a protein, not for a function. You can’t calculate fitness from a DNA sequence, since selection acts indirectly, via the phenotype and its complex interactions with the environment. The same protein may have different functions and fitness values depending on the non-genetic context. So “function” is also something that changes and evolves, and is not given in advance.

    The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically, because it is not a simple function of something we can easily measure. This is no problem in science. The melting point of lead, the density of propanol at room temperature, or the drag coefficient of a rough-surface sphere travelling through the air (as a function of its Reynolds number) also have to be established experimentally if you want to know them with realistic accuracy.

    Once the different functions have been segregated and proteins begin to specialise, you already have the first step in the growth of a protein family. It’s normal for a protein to have many potential uses, so G1 and G2 may acquire new secondary functions (which may already have been present to a minor degree in the “universal protein” G, but could not be honed to perfection because P and Q were the main targets of positive selection). Then the whole cycle is repeated and the family grows.

    It’s like having a team of cooperating specialists (say, a blacksmith, a miller, a potter, a baker, a few shepherds, a dozen farmers etc.) in a village economy rather than a bunch of folk who in theory could do anything, but lack the skills to do any job well.

  29. 29
    Piotr says:

    Natural Selection is too often used as a process. It is not. It is an outcome. So is genetic drift an outcome.

    Nope. Both are “processes” in the dictionary meaning of the word (Oxfor Dictionaries online: process ‘a natural series of changes’). The outcome of selection is an adaptation. The outcome of drift is the fixation of alleles which do not confer an immediate advantage in terms of fitness.

  30. 30
    jerry says:

    Nope. Both are “processes”

    Nope, neither are processes. The outcomes are due to differential fecundity and differential heredity. These outcomes are caused by a myriad of different environmental pressures and internal cell division processes which is a very guided process that has a major random component.

    Oxford Dictionaries online: process ‘a natural series of changes’

    This is a very flawed definition if in fact it is one. Most of the processes I know about are not natural and are directed. For example, from

    http://dictionary.reference.com/browse/process

    process –

    1. a systematic series of actions directed to some end: to devise a process for homogenizing milk.

    2. a continuous action, operation, or series of changes taking place in a definite manner: the process of decay.

  31. 31
    Piotr says:

    jerry:

    You could use a reality check. There are lots of natural processes in the natural sciences. Google up any of the following:

    Adiabatic process
    Random/stochastic process
    Wiener process
    Thermodynamic process
    etc.

    Note that in the Wikipedia article on radioactive decay the word “process” is used 42 times, and radioactive decay itself (the very antithesis of anything systematic, guided or artificial) is defined as “the process by which a nucleus of an unstable atom loses energy by emitting particles of ionizing radiation.”

    You may try, like Humpty Dumpty, to order words to mean just what you choose them to mean — neither more nor less — but I’m afraid they won’t listen.

  32. 32

    Darwinists insist that some formulation of RM & NS **must** be the engine that creates FSCI, because they have nothing else in their ideologically predisposed toolbox to get the job done. Design – the most obvious candidate – is precluded from consideration.

    What we’re seeing here are Darwinists trying to come up with a palatable narrative of how the only resources they have – essentially, a tornado and a junkyard – can create a fully functioning, computerized, self-replicating 747. No matter how they try to put that theory together, it’s just not intellectually satisfying any more. You need blind faith to believe that fairy story.

  33. 33
    jerry says:

    You may try, like Humpty Dumpty, to order words to mean just what you choose them to mean — neither more nor less — but I’m afraid they won’t listen.

    You fell into my trap. I didn’t say that many processes were not natural and I purposely included a natural process in the definition I used. To see what some would say. And what was your response? You are not here to have an exchange of information. You are here to try and trip up people.

    I am aware of hundreds of natural processes but natural selection and genetic drift are not processes. They are outcomes of a lot of processes mainly due to environmental pressures. These pressures are sort of like boundary conditions within which reproduction takes place. And reproduction is a process.

    For your edification. Here is a comment from Allen MacNeill who teach evolutionary biology at Cornell and describes what the debate is really about. This is about the 6th time I posted it in the last few weeks so that shows most do not read comments in depth. Which I understand since there are a lot of comments. From Allen who is no friend of ID.

    This quote demonstrates a basic misunderstanding of the process of natural selection. According to Darwin (and virtually all evolutionary biologists), natural selection has three prerequisites:

    1) Variety (generated by the “engines of variation”

    2) Heredity (mediated by the transfer of genetic material, either vertically – from parents to offspring – or horizontally – via viral transduction, retrotranscription, etc.)

    3) Fecundity (reproduction, usually at a rate that exceeds replacement).

    Given these three prerequisites, the following outcome obtains:

    4) Demography: some individuals survive and reproduce more often than others. Ergo, the heritable variations of such individuals become more common over time in populations of those organisms.

    Natural selection is synonymous with #4; it is an outcome of the three processes listed first, not a “mechanism” in and of itself.

    Ergo, the real dispute here is not over natural selection per se, but rather the properties and capabilities of the “engines of variation”. I have written extensively about these here:

    http://evolutionlist.blogspot......ution.html

    and here:

    http://evolutionlist.blogspot......awman.html

    Yes, natural selection (i.e. #4, above) is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term “natural preservation” rather than “natural selection”.

    However, it is also abundantly clear that the “engines of variation” – that is, the processes the produce phenotypic variation among the members of populations of living organisms – are both extraordinarily creative and extraordinarily fecund. The real problem in biology is not producing new variation, but rather limiting the production of new variation to the point that the “engines of variation” do not cause the rapid disintegration of living systems.

    As just one example of this problem, the genetic elements known as transposons generate a huge amount of new genetic variation, much of which is either phenotypically neutral or deleterious to the organism. There are biochemical mechanisms by which cells can monitor the incidence of transposition in themselves, and limit its consequences (up to and including the active self-destruction of the cell via apoptosis).

    At the same time, there is very good evidence in the genomes of many organisms that retrotransposition events mediated by transposons have produced genetic changes that have resulted in increased survival and reproduction of the organisms in which such events have taken place. There is a large and growing literature on this phenomenon, all of which points to the inference that retrotransposition via transposons both creates new genetic and phenotypic variation, and that in some cases such variation can provide the raw material for evolutionary adaptations, which are preserved via natural selection.

    So, if you really want to find out where the “intelligent designer” might create new variations, you should follow the lead of Darwin’s good friend, Asa Gray, and look for the telltale evidence for such intervention in the “engines of variation”. Of course, you will have to show pretty conclusively, using empirical investigations and statistical analysis, that such “creation events” are not the result of purely natural, unguided processes. If you can do this, you will undoubtedly win a Nobel Prize and a Crafoord Prize (plus a MacArthur or two).

    Notice that this will involve looking carefully into the mechanisms by which new variations are produced, rather than pointing to the outcomes of such processes (i.e. natural selection) and simply asserting that “you can’t get here from there”. Simply asserting (without empirical evidence) that something can’t happen isn’t “doing science” at all. In fact, it’s doing just the opposite…

  34. 34
    Piotr says:

    Allen McNeill does not say, in so many words, that “natural selection is not a process”. He actually calls it a process in the very first sentence of your quotation. Calling natural selection “the outcome” of the processes he lists is confusing: he conflates selection (change extended in time) with its result (adaptation). Anyway, McNeill is entitled to his views, but if you want to play the Authority game, here’s Douglas J. Futuyma, author of Evolutionary Biology and former President of the Society for the Study of Evolution:

    Natural selection is the process by which species adapt to their environment.

    Concise, precise, and correct.

  35. 35
    gpuccio says:

    Piotr at #28:

    I am sorry for you, but your argument is meaningless. Please, give real examples, and not only words.

    Some of the problems:

    a) Proteins must be biochemically functional to be of use, in most cases. Again, what use is ATP synthase if it does not sinthesizes ATP?

    b) “The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically, because it is not a simple function of something we can easily measure.” That is pure philosophy. Again, proteins are wonderful molecular machines. They do incredible things, or they do nothing. In many serious genetic diseases (the Mendelian diseases) a single mutation in the sequence inactivates the protein completely, wit tragic consequences.

    An enzyme is a wonderful machine, which achieves what can never be achieved by “natural” biochemical reactions. The activity of an enzyme can be measured in the lab. Maybe selection for an enzymatic activity can depend by environmental changes, but if the activity is not there, there is nothing to be selected.

    And please, give real examples of how the “selection coefficient” is measured in real cases.

    c) “Once the different functions have been segregated and proteins begin to specialise, you already have the first step in the growth of a protein family. It’s normal for a protein to have many potential uses, so G1 and G2 may acquire new secondary functions (which may already have been present to a minor degree in the “universal protein” G, but could not be honed to perfection because P and Q were the main targets of positive selection). Then the whole cycle is repeated and the family grows.”

    With all respect, these are pure fairy tales. Please, give empirical examples.

    I have tried, up to now, to debate facts and give facts. Please, do the same.

  36. 36
    Axel says:

    It doesn’t really matter that my alernative definition is not always appropriate, Jerry. You ‘hit the nail on the head’ (my tunnel-visioned, nailicidal hammer is feeling very angry…) with these words, didn’t you?

    ‘Natural Selection is too often used as a process. It is not. It is an outcome. So is genetic drift an outcome. Both are used nearly all the time in the active sense that they cause something. What causes the outcome is varied and generally creates a less fit gene pool since there is nearly always a reduction in alleles as a result.’

    To atheists, such phantasmagorical contortions of language are perfectly normal. They twist language with the same airy insouciance as they reject the ineluctable logic of valid assertions they find inconvenient to their world-view.

    I sometimes wonder whether we might be more successful in making the dirt-worshippers see elementary reason, if we wheedled and cajoled them like my mother used to do to me when, as a toddler, I wouldn’t eat my greens: ‘Your hair won’t grow curly…! Don’t you want your hair to grow curly?’

    I suspect some such an infantile ploy might work with them (though it didn’t with me). But, then, trying to second-guess the infantile predilections of such fonts of lunacy would be as futile as randomosity trying to build and sustain a universe.

  37. 37
    Axel says:

    GP, I do believe you are beginning to lose your patience with Piotr!

    It’s always funny, I’m afraid (to my sick sense of humour, admittedly), when a thoroughly reasonable and engaging person finally cracks under the strain of arguing with ‘loony-toons’.

    I look forward eagerly, when watching the video-clips of NDEers, for the moment when they are told they have to go back to their battered bodies and earthly lives again, and they start wailing and protesting bitterly, the heavenly honey-moon temporarily over. My ‘banana-skin sense of humour’, my wife used to call it.

    Go get him, GP!!! Well, you already have. Now Piotr has to produce some empirical evidence!!! That’ a dirty trick to play on any dirt-worshipper, you know.

  38. 38
    Mung says:

    Walter ReMine exposed the evolutionist shell-game years ago.

    If you haven’t read it, it’s not to late!

    The Biotic Message

  39. 39
    Mung says:

    I will say again though, folks, please stop conflating neutral theory with random genetic drift. They are not the same thing!

  40. 40
    Mung says:

    gpuccio, I am with Sherlock Homes here, when you have eliminated the impossible, whatever remains, however improbable, must be the truth.

    If natural selection is impossible, then it must be drift!

  41. 41
    Mung says:

    gpuccio:

    But RV and NS can happen even if there is no drift.

    Drift always happens, because real populations are always finite. It’s the infinite population sizes assumed by population genetics models for natural selection that Nei questions in his book.

  42. 42
    Querius says:

    I would also question the assumption that members of this infinite population has unrestricted and immediate mobility to mate with any other member.

    It’s all “massless elephants on frictionless ice” to me.

    -Q

  43. 43
    Querius says:

    has => have. 😛

  44. 44
    Mung says:

    Piotr:

    The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically

    If that were the case neo-Darwinism would never have gotten off the ground.

    The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically, because it is not a simple function of something we can easily measure. This is no problem in science.

    It is if your science is evolutionary biology and you want your science to be empirical.

    The melting point of lead, the density of propanol at room temperature, or the drag coefficient of a rough-surface sphere travelling through the air (as a function of its Reynolds number) also have to be established experimentally if you want to know them with realistic accuracy.

    Those depend upon a realistic means of physical measurement and are hardly analogous to the mystical selection coefficient of population genetics.

    gpuccio:

    And please, give real examples of how the “selection coefficient” is measured in real cases.

    spot on

  45. 45
    Joe says:

    Natural selection is the process by which species adapt to their environment.

    Propaganda. If Douggie had some evidence he would present it in his book. But all he sez is “Natural selection is the only process known to produce adaptations- here are some adaptations” (paraphrasing).

  46. 46
    Mung says:

    Piotr:

    The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically…

    What happens in the various mathematical models of population genetics if the selection coefficient is not constant?

    e.g.,

    “We predict that the A2 allele will decrease in frequency over time if there is a fixed relationship between phenotype and fitness (constant selection coefficient).”

    How does that work with “seasonal variations” in fitness?

  47. 47
    Upright BiPed says:

    #40

    lol

  48. 48
    Piotr says:

    What happens in the various mathematical models of population genetics if the selection coefficient is not constant?

    It’s still mathematically tractable (if not analytically, then at least with the help of numerical simulations). If the selection coefficient varies in time, the changes are either seasonal (i.e. periodic) and can be averaged out over long spans of time, or follow environmental change (which is usually so slow that changes of s can be considered linear (I think we can leave aside extremely rare chance events like asteroid impacts). You can even model cases when selection coefficients vary randomly around certain mean values over generations. There are also mathematical models in which selection coefficients vary geographically (as a result, you get allele frequency clines between subpopulations inhabiting different environments). You can find basic references to relevant literature in Joseph Felsenstein’s Theoretical Evolutionary Genetics (which even Sal Cordova agrees is a great book ;-)). See also this article:

    Uecker & Hermisson 2011, On the Fixation Process of a Beneficial Mutation in a Variable Environment

    and references therein.

    e.g.,

    “We predict that the A2 allele will decrease in frequency over time if there is a fixed relationship between phenotype and fitness (constant selection coefficient).”

    How does that work with “seasonal variations” in fitness

    Come on, this is a problem for students in a four-credit honours course. They have to consider a problem using simplifying assumptions.

  49. 49
    Piotr says:

    And please, give real examples of how the “selection coefficient” is measured in real cases.

    Try this, for example: Mathieson & McVean 2013, Estimating selection coefficients in spatially structured populations
    from time series data of allele frequencies

  50. 50
    gpuccio says:

    Piotr:

    Real case?

    We do this by considering evolution in a simple lattice model of spatial population structure

    What about real data of real populations?

    I quote myself:

    “No. We can calculate the expected effects of drift. But I am not aware of models which take into account realistic parameters for NS, for the simple reason that those realistic parameters don’t exist, because we know of no case of NS leading to complex functions.

    So, the models just assume some reproductive advantage, and just calculate how likely it is that such a reproductive advantage will be fixed. I am fine with that, but of what use is it?

    We know nothing of:

    a) How often some variation of defined complexity happens, and how often it realistically confers a reproductive advantage, and how great it can realistically be.

    b) If it is even possible that such variations can add up to give a complex function.

    So, population genetics is modeling its abstract assumptions, not reality.”

  51. 51
    gpuccio says:

    Axel:

    I love to be the bad guy. It’s my favorite role! 🙂

  52. 52
    Piotr says:

    Gpuccio:

    Yes, it’s a real case. Did you read beyond the abstract? See the section “Real data” (pp. 19-20) and the discussion that follows. You wanted an example of selection coefficients being estimated from empirical data and I provided one. Now you are shifting the goalposts.

    Selection coefficients can also be estimated for macroevolutionary changes using phylogenetic data, but of course the margin of error is wide and what you get is a distribution rather than an exact value. Population genetics makes no predictions as to how often “complex functions” arise (the rate of a given mutation is a parameter of the model), but, of course, once they do appear, a selection coefficient can be computed for them.

    You can take any species in which newly evolved proteins (or, say, recently duplicated gene families) are still getting fixed under positive selection (various species of Drosophila are strongly polymorphic in this respect), collect some data on the distribution of the competing alleles and do the calculations. Needless to say, it’s being done too.

    While we are at it: how about a formal mathematical model of guided evolution by quantum-level manipulations conducted by an unobservable designer? Does it yield any quantifiable predictions? Can you please refer me to any literature on the subject, containing real-life case-studies? Or does it all boil down to the contemplation of wonderful molecular machines doing incredible things?

  53. 53
    gpuccio says:

    Piotr:

    a) It is true that I don’t always read the whole article that is proposed (although generally I read more than the abstract), but it’s only for lack of time. It is in the interest of those who suggest a reference to point to the relevant aspects, if possible.

    b) OK, they developed a simulated model and then they tested it against some datasets of the frequency of moth alleles, and similar. This is an example, if not of the measure of a coefficient, at least of an empirical validation of an assumed one in certain circumstances. OK, thank you for providing that. So, we know that NS probably works for those moth alleles. Which was never a point of controversy.

    c) About shifting posts, who is doing that? Which were the points of controversy?

    In my posts 4 and 12 I made many points to which you have not answered. In particular, in #12 I say:

    “Well, I think we agree that both drift and NS exist. That is not the point. The point is: what is their supposed role and relevance in trying to explain complex functional information, if you want to exclude design? Let’s suppose that we want to explain how some complex functional protein emerges for the first time at some point in natural history.”

    Emphasis added. And I go on detailing the problem.

    In #15, I explain why population genetics cannot help solve those problems. I quote myself again:

    “No. We can calculate the expected effects of drift. But I am not aware of models which take into account realistic parameters for NS, for the simple reason that those realistic parameters don’t exist, because we know of no case of NS leading to complex functions.

    So, the models just assume some reproductive advantage, and just calculate how likely it is that such a reproductive advantage will be fixed. I am fine with that, but of what use is it?

    We know nothing of:

    a) How often some variation of defined complexity happens, and how often it realistically confers a reproductive advantage, and how great it can realistically be.

    b) If it is even possible that such variations can add up to give a complex function.

    So, population genetics is modeling its abstract assumptions, not reality.”

    It is rather clear that the problem is not if NS can expand an existing tract which is functional (which I have always admitted), but of how it can contribute to its generation by expanding its precursors and creating new complex functional information.

    You have not answered any of that.

    Your only answer, in #19, has been to propose a fairy tale model, completely disconnected from any real data, about some imaginary G protein. I have detailed my objections to that in #20. You have “answered” in #28 with other vague reasoning, none of which was pertinent to my arguments, stating among other things that:

    “The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically, because it is not a simple function of something we can easily measure. This is no problem in science.”

    That was still about you example of the G gene, of its functions and of how protein families can evolve, as shown by the following paragraph:

    “Once the different functions have been segregated and proteins begin to specialise, you already have the first step in the growth of a protein family. It’s normal for a protein to have many potential uses, so G1 and G2 may acquire new secondary functions (which may already have been present to a minor degree in the “universal protein” G, but could not be honed to perfection because P and Q were the main targets of positive selection). Then the whole cycle is repeated and the family grows.”

    In #35, I detail my objections to what you are saying. I quote myself again:

    “I am sorry for you, but your argument is meaningless. Please, give real examples, and not only words.

    Some of the problems:

    a) Proteins must be biochemically functional to be of use, in most cases. Again, what use is ATP synthase if it does not sinthesizes ATP?

    b) “The selection coefficient may be variable (e.g. seasonally or regionally) and has to be determined empirically, because it is not a simple function of something we can easily measure.” That is pure philosophy. Again, proteins are wonderful molecular machines. They do incredible things, or they do nothing. In many serious genetic diseases (the Mendelian diseases) a single mutation in the sequence inactivates the protein completely, wit tragic consequences.

    An enzyme is a wonderful machine, which achieves what can never be achieved by “natural” biochemical reactions. The activity of an enzyme can be measured in the lab. Maybe selection for an enzymatic activity can depend by environmental changes, but if the activity is not there, there is nothing to be selected.

    And please, give real examples of how the “selection coefficient” is measured in real cases.

    c) “Once the different functions have been segregated and proteins begin to specialise, you already have the first step in the growth of a protein family. It’s normal for a protein to have many potential uses, so G1 and G2 may acquire new secondary functions (which may already have been present to a minor degree in the “universal protein” G, but could not be honed to perfection because P and Q were the main targets of positive selection). Then the whole cycle is repeated and the family grows.”

    With all respect, these are pure fairy tales. Please, give empirical examples.

    I have tried, up to now, to debate facts and give facts. Please, do the same.”

    Of all that, you only answer in #49 to the single phrase:

    “And please, give real examples of how the “selection coefficient” is measured in real cases.”

    And you give me a reference where a model of selection is tested against data of existing alleles frequencies in moth. Which was never the object of the discussion.

    So, who is “shifting the goalposts”?

  54. 54
    gpuccio says:

    Piotr:

    While we are at it: how about a formal mathematical model of guided evolution by quantum-level manipulations conducted by an unobservable designer? Does it yield any quantifiable predictions? Can you please refer me to any literature on the subject, containing real-life case-studies? Or does it all boil down to the contemplation of wonderful molecular machines doing incredible things?

    Some brief clarifications (which should already be clear, after our long exchanges):

    a) A design origin is inferred by observing:

    – Functional information which

    – Is vastly beyond the probabilistic resources of the system and

    – Cannot be explained algorithmically.

    The design inference is an inference, not a model.

    b) Once design is inferred, we can try to model the details of the implementation, as far as the data allow it. That has different aspects:

    – The modality of the interaction between the designer and biological matter is at present mainly the object of speculation. As you have asked my ideas about that, I have offered them. But I have no specific model beyond what I have already said.

    – On the contrary, it is certainly possible to model different aspects of how and when functional information appears in biological beings. For example, the observations about non coding regions which gradually become ORFs suggests gradual guided mutation. Another possibility is RV + IS, but at present I don’t think that empirical observations support that model.

    The observations about the appearance of new superfamilies in natural history suggests a pattern with sudden increase of information at focal points, like OOL and the appearance of eukaryotes and of metazoa.

    Another aspect that can be studied is the role of NS in expanding the designed information, after it appears. And another one is the possible role of designed adaptation algorithms.

  55. 55
    Piotr says:

    The modality of the interaction between the designer and biological matter is at present mainly the object of speculation. As you have asked my ideas about that, I have offered them. But I have no specific model beyond what I have already said.

    OK. I will comment on that later.

    The observations about the appearance of new superfamilies in natural history suggests a pattern with sudden increase of information at focal points, like OOL and the appearance of eukaryotes and of metazoa.

    You don’t know how sudden they were. You are taking advantage of gaps in the fossil record. The origin of Eukaryota and Metazoa can be dated only within a margin of error of the order +/- a few hundred million years. In the case of “focal points” which are well documented by fossils, e.g. the origin of birds, there is no real discontinuity and no “sudden increase” of anything. You can’t even tell where “non-avian dinosaurs” end and “real birds” begin.

  56. 56
    Joe says:

    Piotr,

    No one even knows if the transformations required for a dinosaur to become a bird are even possible via genetic changes. Not only that but unguided evolution can’t even account for the origin of Eukaryota, never mind Metazoa.

  57. 57
    Piotr says:

    Gpuccio:

    Now I could go on showing how the selection coefficient of de numerous novo genes is determined in real populations of fruit flies, but it’s obvious that it isn’t population genetics, its models and their parameters that really bother you, but the origin of new genes and functions (as opposed to their spread and fixation).

    It isn’t quite fair to dismiss my abstract scenario as a fairy tale (especially if your alternative is spooky action by otherworldly mental powers). It is abstract, but it can easily be illustrated with actual examples of known gene families. I’ll try to do that, but I’ll need a little time to prepare my case. I can’t hope to convince you, I suppose, but what the hell, It’s a nice discussion.

  58. 58
    Jehu says:

    Piotr

    Start with an Orphan gene.

  59. 59
    gpuccio says:

    Piotr:

    Give your models with references to real proteins, and I will try to analyze them from my point of view (the emergence of functional information).

    And you are right, it isn’t population genetics, its models and their parameters that really bother me, but the origin of new genes and functions (as opposed to their spread and fixation).

    And you are right, it’s a nice discussion. 🙂

    Take all the time you need.

  60. 60
    Mung says:

    Section 2.3 of Nei’s book Mutation-Driven Evolution is Difficulties of Defining and Estimating Selection Coefficients

    It opens as follows:

    Although it is easy to develop mathematical theories of natural selection, it is very difficult to estimate genotype fitnesses or selection coefficients in natural populations.

    Subsections:
    Estimates of Selection Coefficients and their Reliability
    Fluctuation of Selection Coefficients
    General Considerations

    For those who are interested it’s worth a read.

  61. 61
    gpuccio says:

    Piotr and all:

    In the meantime, I want to profit of this quiet moment to clarify some important differences between drift and NS.

    To avoid confusion, let’s calrify in the beginning that the term “fixation” is usually used in population genetics in the sense of “spread”. I often use the term “expansion”. However, “fixation” means “complete expansion”.

    From Wikipedia:

    In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) to a situation where only one of the alleles remains.[1] The term can refer to a gene in general or particular nucleotide position in the DNA chain (locus).

    In the process of substitution, a previously non-existent allele arises by mutation and undergoes fixation by spreading through the population by random genetic drift and/or positive selection. Once the frequency of the allele is at 100%, i.e. being the only gene variant present in any member, it is said to be “fixed” in the population.[1]

    Now, we have already clarified that the spread/expansion of an allele is random in the case of drift: of all the possible mutations that happen, some are fixed, and many are lost. Which are fixed does not depend on the properties of the mutation itself, least of all on its function.

    That is the first and most important difference between drift and NS.

    The second difference is that, as most mutations are neutral or slightly deleterious, most mutations can be involved in drift, while only a tiny subset of mutations (those which can confer a reproductive advantage) can be involved in NS. That’s why, even if in theory a functional mutation could be fixed by drift, if we observe a functional mutation that is fixed we can safely assume that it was fixed by NS.

    But there is a third, important difference between drift and NS that we must remember.

    I would sum it up as follows:

    Drift can only expand (fix) a mutation. NS not only expands (fixes), but also conserves.

    IOWs, drift is a single process, while NS is a double process:

    a) Positive selection: a mutation is expanded (fixed) because it confers reproductive advantage (IOWs, though selective elimination of the old form).

    b) Negative (purifying) selection: The expanded (fixed) mutation is conserved, because new mutations are selective eliminated because of the loss of function (reproductive disadvantage).

    So, in NS the new state (allele) is fixed and it is is then conserved.

    In drift, only the first thing happens. The new state is as subject to new changes as any other neutral sequence.

    A final note is that expansion/spread/fixation need not be complete: at each moment, a trait can be present in different percentages of the population (polymorphism). However, as the origin of each mutation happens in one copy only, any gene which is polymorphic, that is present in significant percentages of the population, must have undergone some important expansion, either through drift or NS.

    A last reflection: is expansion/spread/fixation important to understand the mechanism of generation of new complex information?

    The answer is: it depends.

    The only possible role of expansion/spread/fixation is to lower the probabilistic barriers.

    I will try to explain how.

    Let’s say that mutation A is a step to some function F, but is not enough to achieve the function.

    Let’s say that mutation B, added to A, achieves the function.

    Let’s say that pA and pB are the probabilities of getting each of the two mutations in time t in a population of N numerosity.

    The probability of having both A and B in the same individual in time T is therefore pA X pB, which is much lower than either pA or pB.

    But, if A happens in one individual, and then in a short time is fixed, the probability of getting B together with A in one individual is now pB, and not pA x pB. IOWs, the probability of getting F in time t has become much higher.

    That means, in few words, that is A (a step to F) has a special reason to be expanded preferentially (vs other possible mutations that can be expanded), than the probability of getting F increases significantly.

    Fixation by drift cannot do that. Why? Because all mutations have the same probability of being expanded/fixed by drift. Therefore, A can get no preferential expansion versus all other mutations. And all other mutations are not a step to F, and their expansion will prevent the walk towards F, or at least not help it. IOWs, drift does not change the probabilities of getting F.

    What about NS? The situation is not very different. Why?

    Because, for NS to work as a facilitator in getting F, two things must be true at the same time:

    a) A must confer a reproductive advantage, so that it can be fixed by NS.

    b) A must be a step which, at sequence level, takes us nearer to F (A + B).

    Now, there is absolutely no reason why a) and b) should be connected, and therefore be true at the same time.

    If A is functional for reasons different from those for which F is functional, why should it also be a step towards the sequence of F? For sheer luck? But again, invoking sheer luck does not improve probabilities.

    That’s another way of saying what I often say: complex functions cannot be deconstructed into simpler steps, each of them functional and naturally selectable.

    That is logic and reasonable, but there is further proof: those intermediate steps to a complex function, each of them functional and naturally selectable, have never been observed in biology.

    And yet, if the theory were true, each of them would have been fixed in its population at some time. So, why isn’t there any trace of them in the proteome?

  62. 62
    Piotr says:

    Gpuccio:

    Sorry, I’m teaching today and have little time for pleasures. I agree with much of what you say in the last post, but some caveats are in order:

    So, in NS the new state (allele) is fixed and it is is then conserved.

    Only as long as the selective pressure continues. It may continue almost indefinitely (as in the case of some really fundamental vital functions), but if, say, environmental pressures change, selection may be relaxed or even change its sign.

    a) A must confer a reproductive advantage, so that it can be fixed by NS.

    b) A must be a step which, at sequence level, takes us nearer to F (A + B).

    Only of you think change is teleological (we are searching for a combination that allows us to achieve F. But an “intermediate” step is not really intermediate except with hindsight.

    A camera obscura eye is fine if you can’t build anything more sophisticated with the tools available. It isn’t an unsuccessful attempt to build an eye with a lens. Evolution doesn’t predict or anticipate its future solutions. But if a small improvement becomes possible, it outcompetes the old version which then and only then begins to look “primitive”. There is no “nearer F” until F appears (and F may itself be far from perfect — as is the human eye, notwithstanding its complexity).

    Sorry for using an example from morphology — it’s only for illustration.

    That is logic and reasonable, but there is further proof: those intermediate steps to a complex function, each of them functional and naturally selectable, have never been observed in biology.

    As soon as a more functional version appears, the old one is outcompeted and no longer protected by conservative selection. We probably won’t see it in the same species (unless it manages to survive by acquiring a new function), but it may be still present as a simpler homologue in the genomes of more distant relatives.

  63. 63
    gpuccio says:

    Piotr:

    Only as long as the selective pressure continues. It may continue almost indefinitely (as in the case of some really fundamental vital functions), but if, say, environmental pressures change, selection may be relaxed or even change its sign.

    OK. I tend to think more in terms of fundamental functions, but what you say is correct, and we see it happening in antibiotic resistance, for example.

    But I think that darwinist interpretations tend to overemphasize the role of environmental pressure, and completely forget the importance of basic needs. For example, the adaptive immune system appears in jawed fish, and it can be explained as a result of the necessity of better defense of the new complex animals from their “simpler” competitors. Complexity makes biological beings frailer, and they need to defend themselves more and better, in order to be able to express new functions. That has not changed after that because of any environmental fluctuation, because it is a basic need.

    I have argued many times that, if mere survival and reproduction were really the driving engines of evolution, the process should have simply stopped at the first, remarkable achievement of prokaryotes.

  64. 64
    gpuccio says:

    Piotr:

    Only of you think change is teleological (we are searching for a combination that allows us to achieve F. But an “intermediate” step is not really intermediate except with hindsight.

    A camera obscura eye is fine if you can’t build anything more sophisticated with the tools available. It isn’t an unsuccessful attempt to build an eye with a lens. Evolution doesn’t predict or anticipate its future solutions. But if a small improvement becomes possible, it outcompetes the old version which then and only then begins to look “primitive”. There is no “nearer F” until F appears (and F may itself be far from perfect — as is the human eye, notwithstanding its complexity).

    Sorry for using an example from morphology — it’s only for illustration.

    You have to use an example from morphology, because the reasoning would not work if we pass at the level of molecular sequence.

    I will try to be more clear.

    Let’s say that we observe the appearance of a new protein (domain, superfamily, as you like) at some time in natural history, for example in jawed fish. That’s what we have to explain, and it’s not important if we think it is teleological or not: it’s what we observe. Also, it is not important if it happened in one day, one million years or 100 million years. We have a window of time in which it must have happened. Speaking of jawed fish, 4 billion years are certainly too many, so let’s say we have a window of 100 million years.

    Now, let’s say that we model what we observe as a transition form A to B to C.

    What is C? It is the new protein we observe in jawed fish. By definition, it is a new protein of a new superfamily.

    What is A? It is the original sequence, present in the immdediate ancestors, from which we believe that the transition towards C starts. It can be another protein gene, more or less duplicated or inactivated, or a non coding sequence, more or less functional. It does not matter.

    The important point is: A and C are unrelated at sequence level. Why? Because C is a new protein of a new superfamily, and therefore by definition it is unrelated at sequence level to all the other existing proteins. The sequence relation between superfamilies is lower than 10% identity, in the range of random identity. Even if A is a non coding sequence, there is absolutely no reason to assume that it has some relation with the future protein coding sequence C. Unless you are assuming design or, again, sheer luck.

    So we say that, if C is long enough and functionally complex, the transition from A to C is practically impossible by mere RV, because of the probabilistic barriers which I have discussed in detail. It is a random walk which will never happen.

    That’s where B should help.

    More in next post.

  65. 65
    gpuccio says:

    Piotr:

    So, what is B? It is supposed to be a functional, naturally selectable intermediate step.

    To work as that, B must have two different properties:

    a) It must be related, at sequence level, both to A and to C. IOWs, in the sequence space it must be somehwere “in the middle” between A and C.

    b) It must be functional and naturally selectable (confer a reproductive advantage), so that it may be expanded/fixed by NS.

    The second point is fundamental. If B is not fixed by NS, the following variations that have to take place to get C must happen in the same individual in which the transition from A to B has taken place (or its individual clone). There is no multiplication of the probabilistic resources, and the probabilities of getting to C remain the same.

    Only the expansion of B multiplies the probabilistic resources of the system, and lowers the probabilistic barriers.

    But the first point is fundamental too. B must be related to A, and it must be related to C, at sequence level. Otherwise, it is of no help.

    If B is “near” A, but is unrelated to C, the transition from B to C is as improbable as the transition from A to C, even after B expands.

    If B is “near” C, but unrelated to A, the transition from A to B will simply never happen, because it has the same probabilities as the transition from A to C.

    So, B must be “in the middle” to be of some help.

    Please, remember that we are discussing the sequences here. That has nothing to do with structures and functions. RV happens at the sequence level. It knows nothing of structure and function. The random walk is a walk in the sequence space. All unrelated states have the same probability to be reached. Only related states at sequence level have higher probabilities.

    So, for B to be useful, it has to be a “step” from A to C at sequence level. And it has to be functional and selectable, and it must expand / be fixed.

    Otherwise, it is of no utility in the process.

  66. 66
    gpuccio says:

    Piotr:

    As soon as a more functional version appears, the old one is outcompeted and no longer protected by conservative selection. We probably won’t see it in the same species (unless it manages to survive by acquiring a new function), but it may be still present as a simpler homologue in the genomes of more distant relatives.

    That is the old answer: “They were eaten!”.

    But it is not possible.

    Remember, B is a functional protein which was expanded to the whole population at some time. And you need many Bs for each complex transition (we can discuss that later). And you need them for each transition which generated (at least) each of the 2000 superfamilies which we observe in the proteome.

    Can you really believe that we can find no trace of all that in the existing proteome? You yourself say that “it may be still present as a simpler homologue in the genomes of more distant relatives”. But not even that happens.

    No, to believe that new functional sequences arise through a long chain of functional expanded intermediate proteins of which no trace remains in the proteome is really beyond any credibility. Only a dogmatic attitude can justify that kind of faith in so many self professed “skeptics”.

  67. 67
    Piotr says:

    I have argued many times that, if mere survival and reproduction were really the driving engines of evolution, the process should have simply stopped at the first, remarkable achievement of prokaryotes.

    It did stop there for at least two billion years; and two billion years later most life on Earth is still bacterial and archaeal (and, well, viral). The eukaryotic “revolution” succeeded only once (perhaps there were other false starts, but we can’t know for sure). I don’t intend to deny that the rise of Eukaryota was extremely unlikely, given that they had to compete against extremely well-adapted and efficient life forms. Prokaryotes have vast effective population, so even very slight selective pressures force them to adapt. “Junk DNA? No, thank you, sir; I have to keep fit.”

    So, what is B? It is supposed to be a functional, naturally selectable intermediate step.

    Intermediate with hindsight, as I said. B is not a step towards anything. It’s a derivative of A, full stop. It doesn’t know where it’s going (figuratively speaking). If selection fixes and conserves B, the further course of evolution is constrained by the structure and functionality of B, not the other way round. Constrained, but not strictly determined. B may in due course become C, or possibly D, or E, or simply remain B. There is no unique target.

    To work as that, B must have two different properties:

    a) It must be related, at sequence level, both to A and to C. IOWs, in the sequence space it must be somehwere “in the middle” between A and C.

    Please let me do my homework and I’ll be back with concrete examples. When I speak in abstract terms like A, B and C, you accuse me of telling fairy tales.

  68. 68
    Piotr says:

    Can you really believe that we can find no trace of all that in the existing proteome?

    Nah, I’m sure we can find such traces if we know what to look for.

    You yourself say that “it may be still present as a simpler homologue in the genomes of more distant relatives”. But not even that happens.

    Doesn’t it? We shall see. Please don’t be impatient, I need to do a little reading.

  69. 69
    gpuccio says:

    Piotr:

    Do your work. I am not impatient. I just wanted to make more arguments more explicit.

    B needs to be an intermediate at sequence level, if we want to explain what we observe with that model. There is no hindsight, we are only truing to build a model that works to explain something we observe.

    And My A, B and C are not abstract. C is any new observed protein in the course of natural history. And A and B are necessary actors in the context of a darwinist explanation based on RV + NS. Indeed, I believe that B simply does not exist, and A can be any unrelated sequence which is modeled by design. For example, the non coding regions which become ORFs, ad observed in many cases.

  70. 70
    Jehu says:

    Most of us are familiar with the mutations in the PfCRT gene of P. falciparum that confer chloroquine resistance. As I recall, two mutations are required at the 76 and 163 position in order for there to be chloroquine resistance and a selective advantage where chloroquine is in use. The mutations can happen in any sequence but the first would be an example of a neutral mutation and the second a mutation that would be selected.

  71. 71
    Jehu says:

    Of course, I guess mutant PfCRT does not qualify as “C,” a new protein.

  72. 72
    gpuccio says:

    Jehu:

    Everything can qualify as “C”, but only transitions that generate new complex functional information would be considered for design inference.

    A transition of two AAs which generates a new function (in this case chloroquine resistance) is in the range of RV. It is much rarer of the more common 1 AA transitions which generate some other types of antibiotic resistance, even in palsmodium (see Behe), but it can happen by RV. The functional complexity of this transition would be 2 AAs, that is 8.64 bits. Behe considers that as the observed hedge of evolution. Axe considers 4-5 AAS (let’s say 22 bits) as a computed “hedge” based on different observations about protein functionality.

    I have suggested 150 bits (35 AAs) as a very safe threshold to infer design in any biological system on our planet.

    So, let’s say that is the transition from A to C implies more than 150 bits of functional information, we can be rather safe in inferring design for that transition, provided there is no evidence of an explicit path through some well demonstrated “B” (and there is no evidence, for all known basic protein superfamilies).

    All the scenarios we know of imply one aminoacid, maybe two. Classic simple antibiotic resistance, the expansion of Hemoglobin S in populations exposed to malaria, nylonase. These are good examples of molecular “microevolution”: single or double mutations which, for particular environmental conditions, confer some remarkable advantage under strong selective pressure. That is all that pure RV can accomplish.

    As for the natural selection of intermediates as a step to complex function, I am aware of no observed example of such a mechanism. Let’s see what Piotr can dig up.

    If two connected AAs is the best RV can do in decades of strong selection (see Behe), I suppose that a 35 AAs transition (my threshold) should be deconstructed at least into 17-18 two AAs transitions, each of then naturally selectable, to explain the complete process. Who can really believe that’s the way 2000 protein superfamilies, most of them well beyond that threshold, were found?

    (In his paper, Durston computes the functional complexity for 35 protein families. 28 of them are beyond my threshold of 150 bits, with a range of 156 – 2,416 bits. The remain 7 families are short proteins, less than 100 AA long, and have functional complexity of 46 – 123 bits, well beyond Axe’s threshold of 5 AAs – 22 bits. We could probably infer design for them too, considering carefully the context of their emergence, but let’s say that they are not our priority).

  73. 73
    Jehu says:

    Thanks gpuccio,

    I am not familiar with Axe.

    With respect to Behe, I think it should be further elaborated that he places the edge at different places depending on the reproductive capacity of the system where the protein in evolving. For example, 2 AAs may be the edge with respect to p falciparum but not HIV.

    I am interested to see what Piotr comes up with.

    So far, the experiments that I am aware of that attempt to refute Behe are shockingly weak. I would think they could do better. It makes me wonder if I am still giving too much credit to the power of RM+NS.

  74. 74
    gpuccio says:

    Jehu:

    That paper about cortisol receptor “evolution” is not only “weak”. It is no refutation of anything at all, least of all of Behe’s irreducible complexity concept.

    It is indeed a very good example of a good research paper which says interesting things, which are then inflated, in the conclusions, to the level of simple propaganda, completely unjustified by the facts in the paper.

    First of all, it has nothing to do with Behe’s irreducible complexity. Behe’s concept is about complex machines whose function is determined by the interaction of different complex parts, different molecules, different proteins, which are not in themselves functional out of the “meta-machine” of which they are part.

    Nothing of that is investigated in the paper. The paper is about the supposed derivation of GRs form an ancestor which was mainly sensitive to aldosterone (or rather to DOC or some other similar molecule, because aldosterone did not exist yet). The reasoning is fine, and the paper is well made.

    But it has nothing to do with Behe’s irreducible complexity. Here we only have a protein which changes its ligand affinity (but always in the same group of ligands) by mutations at the active site.

    So, is it an example of a complex functional transition?

    Not at all. The transition is certainly functional (GRs are certainly used in specific pathways), but it is not complex.

    Guess how many mutations are necessary to transform the ancestor receptor into the GR?

    Two mutations. Two AAs.

    One combination—replacement of Ser106 with Pro (S106P) and Leu111 with Gln (L111Q) (numbered by position in AncCR-LBD)—conferred a GR-like phenotype: The receptor_s median effective concentration (EC50) for aldosterone increased by three orders of magnitude, but moderate cortisol and DOC sensitivity were retained (Fig. 4C). None of the other mutants showed this pattern (table S4). Structural studies of the human GR have shown that these two residues change the architecture of the ligand-binding pocket and alter contacts with steroid in ways that exclude aldosterone and facilitate cortisol activation (18, 25). Our data thus indicate that the aldosterone specificity of MR has a simple and conserved mechanistic basis—two crucial replacements in the GRs that wiped out ancestral sensitivity to aldosterone.

    Like chloroquine resistance. Like nylonase.

    With an important difference.

    While in the case of chloroquine resistance, and probably of nylonase, the mutation itself is enough to give a new function, in the case of GRs the scenario is not so simple.

    It is true that we have a new receptor, which has a different, specific affinity with a specific ligand (cortisol). But that means only that we have a possible new messenger for cell to cell interactions.

    What this new messenger does, what kind of new adaptations and cellular pathways are elicited by this particular interaction, is in no way explained by the existence of a new affinity for a ligand.

    That meta-function, which uses the new local biochemical function, is in no way simple like the mutation of two AAs, and in no way it is explained by it.

    That’s where Behe’s concept of irreducible complexity would be pertinent. But, obviously, the paper which was conceived to refute Behe says nothing about that.

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