“Competence” in the Field of Evolutionary Biology

_{Gil Dodgen

July 10, 2011

Intelligent Design}

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Thomas Cudworth in his post here referenced “…being competent in the field of evolutionary biology.”

My question is, What does it mean to be “competent” in the field of evolutionary biology?

It seems to me that it would mean providing hard empirical evidence that the mechanism of random variation/mutation and natural selection which is known to exist (e.g., bacterial antibiotic resistance) can be extrapolated to explain the highly functionally integrated information-processing machinery of the cell — at a very minimum! This empirical demonstration should be a prerequisite, before we even begin to entertain speculation about how this mechanism produced body plans and the human brain.

Yet, the theoretically most “highly competent” evolutionary biologists never even attempt to address this requirement. They just wave their hands, make up increasingly bizarre, mathematically absurd, unsubstantiated stories out of whole cloth (like co-option), declare that the solution has been found, and that anyone who questions them is a religious fanatic.

This is the antithesis of legitimate scientific investigation.

My definition of competence in the field of evolutionary biology is Michael Behe, who has actually empirically investigated the limitations of the creative powers of the Darwinian mechanism. The conclusion is clear: It can do some stuff, but not much of any ultimate significance, and cannot possibly be extrapolated to explain what Darwinists expect us to accept through blind faith, in defiance of all reason and evidence.

Comments

Ah yes, you are right. I always get cousins muddled! Yes, second cousin LCA would be great-grandmother. Thanks!Elizabeth Liddle_{July 12, 2011
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Elizabeth,
Take you and a hypothetical second cousin. Who is your LCA? (Last Common Ancestor). The answer is your grandmother.
2nd cousin LCA would be a great-grandmother, correct?lastyearon_{July 12, 2011
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Elizabeth: Anyway, nice to talk to you. It’s good when people return the ball Your serve. Me too! I enjoy talking to you, because you don't elude the arguments, understand them, and sincerely try to give your answers. That's very fine, and it's more than I usually can expect from many of my interlocutors here. Moreover, it's the first time that I can debate with a convinced neutralist, and it's fun. So, be sure that I respect you and your position, that I believe you entertain in full good faith. Unfortunately, I disagree with many of them and therefore, in a spirit of friendship, I will try to explain why. You raise many different points which deserve detailed discussion. Time is limited, so I will start in a brief way, and we can deepen any point that you find interesting, or simply don't agree with. I sincerely enjoy intellectual confrontation, provided that it conveys true reciprocal clarification, and not only stereotyped antagonism. So, let's start. First of all, the papers I quoted. The Durston paper is the one you have already found. Tha two Axe papers, instead, are the following: The Case Against a Darwinian Origin of Protein Folds http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.1/BIO-C.2010.1 and The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2011.1/BIO-C.2011.1 More in the next postgpuccio_{July 12, 2011
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Mung:
Hi Elizabeth, could you stick to one model please, lol. In addition to focusing on the cell, as in unicellular organisms, I also prefer to focus on a model that doesn’t depend on sexual reproduction.
OK, sure. But the evolutionary dynamics are very different.
Obviously the capacity for sexual reproduction itself had to evolve, and it had to do so based on some model other than sexual reproduction.
I don't expect it evolved "based on some model" at all. I expect it evolved because populations of organisms in which horizontal gene transfer regularly occurred went extinct less often than onse that didn't.
It just confuses things to be switching back and forth between the two. Apples and Oranges, and all that.
Sure, but drift dynamics will be totally different in a cloning population. In fact I don't even think people talk about "drift" with bacteria do they? It wouldn't really make much sense.
And the LUCA is the FUCA. Just think about it, please.
I might ask you to do the same :) Take you and a hypothetical second cousin. Who is your LCA? (Last Common Ancestor). The answer is your grandmother. What about her Mother? She is also a Common Ancestor (CA), but not the Last Common Ancestor (LCA) - she preceded the LCA. Yes?Elizabeth Liddle_{July 12, 2011
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Well, no, it’s more like shooting fish in a barrel With a pea shooter and using spitwads for ammo.Mung_{July 12, 2011
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Hi Elizabeth, could you stick to one model please, lol. In addition to focusing on the cell, as in unicellular organisms, I also prefer to focus on a model that doesn't depend on sexual reproduction. Obviously the capacity for sexual reproduction itself had to evolve, and it had to do so based on some model other than sexual reproduction. It just confuses things to be switching back and forth between the two. Apples and Oranges, and all that. And the LUCA is the FUCA. Just think about it, please.Mung_{July 12, 2011
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ScottAndrews:
I enjoyed your explanation of the irrelevancy of genetic drift. As I understood it, it takes the problem of specific improvements and seeks to make it smaller by spreading it out over the population.
huh?
This ultimately accomplishes nothing because it still doesn’t explain why it constantly moves toward relatively small targets of improvement rather than behaving randomly.
What moves? Which targets?
The counterargument is that there are many possible targets, not just one, so we shouldn’t look at odds of just one outcome.
Yes indeed.
That’s a bit like saying that if you shoot a missile randomly into space, you’re bound to hit a star (gravity notwithstanding) because there are just so darn many of them.
Well, no, it's more like shooting fish in a barrel :)Elizabeth Liddle_{July 12, 2011
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gpuccio I enjoyed your explanation of the irrelevancy of genetic drift. As I understood it, it takes the problem of specific improvements and seeks to make it smaller by spreading it out over the population. This ultimately accomplishes nothing because it still doesn't explain why it constantly moves toward relatively small targets of improvement rather than behaving randomly. The counterargument is that there are many possible targets, not just one, so we shouldn't look at odds of just one outcome. That's a bit like saying that if you shoot a missile randomly into space, you're bound to hit a star (gravity notwithstanding) because there are just so darn many of them.ScottAndrews_{July 12, 2011
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gpuccio:
Elizabeth: I must say that you seem to understand well, and essentially agree, on my points, and I thank you for your correct interpretation of them.
No problem, and thank you :)
To your counterpoints, I answer the following: 1) “assuming an a priori “target””. That is the usual “argument” that any beneficial mutation will be selected, and that therefore the “target” is very big. That is false reasoning. First of all, it is not true at all that a lot of molecular variation can be beneficial. Please consider that: a) An existing system such as a living cell, with its structure and metabolism already extremely complex and fine tuned, canstrains highly possible variations. That should be obvious also to those who have some experience in programming. The more structure and complex a system already is, the more any useful variation will have to be complex and integrated just to work with waht is already there.
Absolutely. Once an organism is near-optimized for its environment, only a very small number of mutations are likely to offer net advantage over what is already there. In other words, in a population well-adapted ("fine tuned") to its environment, there are far more ways to make it worse than make it better. This is why we must assume of near-neutral mutations, more are likely to be very slightly deleterious than very slightly beneficial in that environment. But now change the environment - make it slightly cooler, or have the population migrate northwards. Now, the organisms are no longer "fine-tuned" for their environment, and what was very slightly beneficial may be very slightly deleterious and vice versa. So what we must think of, I submit, is that within any given population, there is a large amount of allelic variation, constantly, if slowly, being drip fed by new alleles, mostly near-neutral. The allele frequencies tend to stabilise at an optimum in a given environment. But change the environment, and these distributions will change, so that a different set of alleles have the highest frequencies and a different set have the lowest, and a different set have the mean. In the process, interactive combinations that are adventageous will tend to result in a boost in frequency to the alleles that work well in combo, so those combos will themselves tend to increase in frequency. But given a stable environment, of course you are absolutely right - if there is no-where to go but down, then "natural selection" will be a conservative force, or rather, the best reproducing individuals will be those that inherit the tried-and-true.
b) Going back to the problem of the structure of functional proteins, it can be reasonably calculated that the functional target is anyway small versu the search space, in spite of all the biased research which deperately tries to show the opposite, without succeeding. The Durston method, at present the only one which can evaluate functional information in protein families, gives very high values for most protein families, well beyond the reach of any random walk. And the recent papers by Axe show the improbabilities of any basci fold emerging by a random walk, and even of the following “evolution” of active sites in an already existing protein family. Nobody in ID has ever said that a single sequence is the target. We are well aware that the whole set of functional sequences is the target. And we take that into account in our calculations.
Well, I'd be grateful for a citation, and even better, a summary, of Durston's work. I've just read this paper: http://www.tbiomed.com/content/4/1/47/abstract What he seems to be saying is that for a known function, some proteins are more what I would term "brittle" (i.e. there are a smaller proportion of possible sequences are sequences that will perform the function) than others, and that the brittle ones won't readily evolve by random walk. In other words, that protein families are "irreducibly complex". Would you agree with that summary? I'll perhaps wait for you to comment before I comment further :)
2) “Secondly, but relatedly, the probability of propagation changes dynamically over time. The more individuals who bear an allele, the more probable it becomes that the mutation will eventually go to fixation.” This is nonsense. Your “allele” can exactly be the one which is not apt to receive the second mutation. There is no reason why drift should favor an allele which is compatible with the second, or any other, favourable mutation. Fixation by drift is random, and there is no reason why the fixed mutation should be better than any one that is lost or remains limited. In all cases. the random walk remains a random walk.
I'm sorry, but I'm not understanding your point. No, there is no reason why drift should favour one allele over another - that's why it is called drift! I'm just saying that the more copies of an allele there are in a population, the more likely it is that even more copies will by made. An allele that has drifted near fixation is much more likely to reach it, than one that hasn't! It's a simple point, but worth making nonetheless. Every organism bearing allele X represents an opportunity for allele X to be replicated. And once a large number of organisms have allele X, the probability that a new allele Y will end up in a genotype that also contains allele X, becomes quite high. But this is obvious, so I'm equally obviously missing your point :) Please advise.
3) “Thirdly, at any given time, a population hosts a large number of polymorphisms, most of which are probably selectively neutral, in the current environment.” The point of polymorphism does not help in explaining how new folds and superfamilies emerge, which was my question.
If some new alleles are selectively neutral (for example Valine-methionine substitutions are fairly neutral, then you will get protein families arising because mutations that result in a functional protein won't be deleterious, and some of them will propagate by drift. The ones that result in a degradation of the protein will tend not to. So over time, swilling around the population will be many polymorphisms, some of which will be more prevalent than others. However, in a sexually reproducing population, as well as Single Nucleotide Polymorphisms (SNPs) recombination processes will mean that from time to time, during recombination, part of one allele will be spliced with part of another - so the offspring ends up with part of her grandmother's allele and part of her grandfather's. And again, if these recombined alleles are selectively neutral they will drift around the population, sometimes dropping right out, sometimes propagating extensively, sometimes in between. And they, in turn will be subject to recombination events. So new alleles are not only being produced all the time by substitution and repetition and deletion events they are also being recombined, so that we can think of the gene as consisting of sub-genes that can move independently through the population. Which, in turn, means that from time to time a combination of parts will show up that has some advantageous characteristic - a new fold pattern perhaps. Then, with a bit of luck, that allele will propagate, by Darwinian means, through the population. My point being that mutations with a potential advantage when found in combination don't have to arise simultaneously in the same individual. They can arise at widely spaced time points, as long as they can drift independently through the population, which, in a sexually reproducing population, they can.
The emergence of a new protein fold from an existing one require the change of a lot of aminoacids, a coordinated change which is utterly unlikely by any random walk.
Why is it? Any one fold may be unlikely, but we are back to the Texas Sharpshooter. The appearance of new fold of some kind may have a perfectly good non-zero frequency over time. In fact I'd expect the pdf to have a Poisson distribution!
Funtional and selectable intermediate steps have never been shown for any such theorical transitions, for the simple reason that they don’t exist and there is no reason that they should exist.
But, as I keep saying, selectable intermediate steps aren't required. That's one of several huge problems with the concept of Irreducible Complexity, which is what we are, in fact, talking about here. Sure, a couple of selectable (i.e. advantageous in some environment in which the population finds itself at some point) will give the probabilities a healthy kick, but stuff drifts. Some of that stuff comes in useful, sometimes singly, sometimes only in combination. But given enough independence of the drifting process, useful combos are bound to happen. What we can't then do is turn round and say "hey, look! isn't it awesome that this protein, which won't perform this amazing function unless it's just the way it is, just happened to arise!" Because that really is just like dealing hand after hand of cards and then expressing astonishment when one day you get a really good hand. Moreover, back to biology, if that lucky hand does something like confer immunity to some environmental pathogen, then those individuals bearing the lucky hand may speciate - move into environments where the pathogen hitherto prevented them from moving, and interbreed, and adapt in other ways to that new environment. Whereas the rest of the population doesn't, and the lucky hand actually drops out of that population. Then a biologist comes along, eons later, and says: "how come this population just happened to get this necessary allele?" when she should simply be noting "this allele enabled this population to evolve in this environment, which would otherwise have been inimicable to its continuation">
4) “And our LUCA was almost certainly more complex than its predecessors, so asking why “1000 superfamilies were already present in LUCA” is a bit like asking why a runner half way round the track has “already” completed half a lap!” What a pity that there is no evidence of such predecessors, and no reasonable theory about what they were, and no example of any independent living thing in the universe which is simpler than bacteria or archea. So, your “half a lap” is what we in ID call a “just so story”.
What do you mean "there is no evidence of such predecessors?" Absence of evidence is not evidence of absence. Why should we assume that our LUCA was also our FUCA? And if our LUCA was very much more efficient than than other descendents of the then LUCA, why would we not expect that they would have eventually have gone extinct? Indeed the argument is circular! The LUCA is defined as the ancestral population to all currently living things, so if our LUCA's cousins hadn't gone extinct, that LUCA wouldn't be our LUCA!
5) “The “mean functional unit” now may well be 100-150 AAs long (and may have been in our LUCA, though I don’t know), and I agree it seems unlikely that the required sequence would have emerged through “random walk”, but that doesn’t mean that its predecessors didn’t, or that nothing simpler conferred reproductive advantage.” Again, we must reason on what we know, not on just so stories. In the whole known proteome, the “mean functional unit” is 100-150 AAs long. This is a fact, and I reason on facts.
Yes, indeed, but it is surely unsound to assume that what is true of living organisms must have been true of long dead ones. Unless you can supply a good argument that our LUCA was not only our LUCA but the FUCA. Without that argument, we simply cannot extrapolate as you suggest, because by definition, our LUCA is going to have characteristics all living things share, whereas the FUCA (unless it is the same as the LUCA) won't.
6) “But this is a very different question.” No, it isn’t. And anyway, please would you answer it?
Well, I've had a go :) Anyway, nice to talk to you. It's good when people return the ball :) Your serve.Elizabeth Liddle_{July 12, 2011
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Sorry, that last sentence should read.. What if the initial mutation drastically increases the functional target be simplifying the protein?lastyearon_{July 12, 2011
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Going back to the problem of the structure of functional proteins, it can be reasonably calculated that the functional target is anyway small versu the search space, in spite of all the biased research which deperately tries to show the opposite, without succeeding.
How is it possible to calculate the functional target? The only measure of success for any genetic mutation is that it makes the host organism better able to reproduce. Aren't there many examples of proteins that once did one thing and now perform a completely different function? Also, what if the initial mutation drastically reduces the functional target be simplifying the protein?lastyearon_{July 12, 2011
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LYO: Pardon, but that's nonsense. Parts have to work with other parts that are matched to them in any reasonably precise system. Actually, that starts with building a chair or a bookshelf. Yes adaptability is key to a robust design, but that is not as opposed to being properly matched together to work. GEM of TKIkairosfocus_{July 12, 2011
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gpuccio,
The more structure and complex a system already is, the more any useful variation will have to be complex and integrated just to work with waht is already there.
That is a hallmark of poor design. Well designed systems are scalable. Good designers understand that current system may need to adapt, that parts or functions may need to be added later. As much as possible, they plan for the future in their designs.lastyearon_{July 12, 2011
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Elizabeth: I must say that you seem to understand well, and essentially agree, on my points, and I thank you for your correct interpretation of them. To your counterpoints, I answer the following: 1) "assuming an a priori “target”". That is the usual "argument" that any beneficial mutation will be selected, and that therefore the "target" is very big. That is false reasoning. First of all, it is not true at all that a lot of molecular variation can be beneficial. Please consider that: a) An existing system such as a living cell, with its structure and metabolism already extremely complex and fine tuned, canstrains highly possible variations. That should be obvious also to those who have some experience in programming. The more structure and complex a system already is, the more any useful variation will have to be complex and integrated just to work with waht is already there. b) Going back to the problem of the structure of functional proteins, it can be reasonably calculated that the functional target is anyway small versu the search space, in spite of all the biased research which deperately tries to show the opposite, without succeeding. The Durston method, at present the only one which can evaluate functional information in protein families, gives very high values for most protein families, well beyond the reach of any random walk. And the recent papers by Axe show the improbabilities of any basci fold emerging by a random walk, and even of the following "evolution" of active sites in an already existing protein family. Nobody in ID has ever said that a single sequence is the target. We are well aware that the whole set of functional sequences is the target. And we take that into account in our calculations. 2) "Secondly, but relatedly, the probability of propagation changes dynamically over time. The more individuals who bear an allele, the more probable it becomes that the mutation will eventually go to fixation." This is nonsense. Your "allele" can exactly be the one which is not apt to receive the second mutation. There is no reason why drift should favor an allele which is compatible with the second, or any other, favourable mutation. Fixation by drift is random, and there is no reason why the fixed mutation should be better than any one that is lost or remains limited. In all cases. the random walk remains a random walk. 3) "Thirdly, at any given time, a population hosts a large number of polymorphisms, most of which are probably selectively neutral, in the current environment." The point of polymorphism does not help in explaining how new folds and superfamilies emerge, which was my question. The emergence of a new protein fold from an existing one require the change of a lot of aminoacids, a coordinated change which is utterly unlikely by any random walk. Funtional and selectable intermediate steps have never been shown for any such theorical transitions, for the simple reason that they don't exist and there is no reason that they should exist. 4) "And our LUCA was almost certainly more complex than its predecessors, so asking why “1000 superfamilies were already present in LUCA” is a bit like asking why a runner half way round the track has “already” completed half a lap!" What a pity that there is no evidence of such predecessors, and no reasonable theory about what they were, and no example of any independent living thing in the universe which is simpler than bacteria or archea. So, your "half a lap" is what we in ID call a "just so story". 5) "The “mean functional unit” now may well be 100-150 AAs long (and may have been in our LUCA, though I don’t know), and I agree it seems unlikely that the required sequence would have emerged through “random walk”, but that doesn’t mean that its predecessors didn’t, or that nothing simpler conferred reproductive advantage." Again, we must reason on what we know, not on just so stories. In the whole known proteome, the “mean functional unit” is 100-150 AAs long. This is a fact, and I reason on facts. 6) "But this is a very different question." No, it isn't. And anyway, please would you answer it?gpuccio_{July 12, 2011
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GP: on the ball as usual.kairosfocus_{July 12, 2011
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Gpuccio:
Elizabeth: I am well aware of the concept of genetic drift, and I have always found it completely useless for evolutionary theory. I will try to explain myself better. OK, genetic drift, if and when it happens (you certainly know that some essential conditions must be satisfied) can expand a neutral or quasi neutral mutation without the need of a positive selection due to survival benefit. OK. And so? The problem, apparently overlooked by neutralists (and by you) is that any neutral mutation can randomly expand, and any neutral mutation can randomly be lost. And most neutral mutations will simply remain there, in a minority of the population.
Yes indeed (I have not overlooked it!)
Now, from the point of view of probabilities, that does not give any advantage versus a purely random walk. If I need, for a selectable trait to emerge, the coordinated mutation of two aminoacids, and if the forst mutation happens in one individual, the propbability of that specific mutation to expand by genetic drift is extremely low, because any new mutation can expand by drift, but only a few will do that, while a few will be lost. So, the probability that the second necessary mutation may happen in the subclone with the first mutation is extremely low if no drift happens (probabilities here obviously multiply), but the probability that the first mutation be expanded by drift and then the second mutation may happen in the expanded clone is similarly low, due to the low probability of the first event (expansion by drift) for that particular mutation.
I think metaphors is tripping you up here. Let me try to rephrase (without change in meaning, I hope, but trying to avoid metaphors where possible) what you just wrote, above: "Now, purely random walk will not result in an advantageous trait. If an advantageous trait requires two changed aminoacids in a protein, neither of which, singly, confer any advantageous phenotypic effect, and if the mutation that produces the first change happens in one individual, the probability that it will propagate solely through genetic drift is low, because only a few will do that, to any great extent, and a few will be lost completely. So the probability that the second mutation will occur in a bearer of the first will be extremely low. And if it does not, the probability that it will propagate by drift will be as low as the probability of the first propagating by drift. And because probabilities here obviously multiply, probability of the two mutation ever meeting up in the same individual are even more extremely low. I think this is what you are saying (I've kept in the random walk metaphor as we both seem clear about what it signifies). If so, my response to your summary here:
In brief, genetic drift in no way adds to the probability of having a complex functional new trait by purely random mechanisms (and genetic drift, like mutation, is a purely random mechanism).
is threefold. Firstly, you are assuming an a priori “target” – a specific trait, that involves two independent amino acid changes, and that will confer a reproductive advantage. However, this would be the Texas Sharp Shooter fallacy! There may be many many proteins that would confer the same or similar advantageous trait, and, indeed, there may be (and are) many advantageous traits. So computing the probability of any one, by the method you give, is the equivalent of computing the probability of a single hand of cards, instead of the probability of a good hand, or even more appositely, the probability of a hand that may become a good hand after some subsequent draw. Which is obviously much higher. Secondly, but relatedly, the probability of propagation changes dynamically over time. The more individuals who bear an allele, the more probable it becomes that the mutation will eventually go to fixation. Thirdly, at any given time, a population hosts a large number of polymorphisms, most of which are probably selectively neutral, in the current environment. They may have propagated because at some previous time they were advantageous, or they may simply have drifted into substantial prevalence. It’s quite salutary to write a program of the kind I just recommended to Mung, and to how true the Central Limit Theorem really is. You always end up with a Gaussian, in which a few alleles are very rare, a few are very common, and a very large number are borne by about half the population. So even if we assume (probably a fair assumption) that many advantageous traits arise from gene-gene interactions (you need a specific combo to get the advantage), the opportunities for those combinations to occur is actually quite substantial. Of course the probability of any one specific combination, out of all the alleles, occurring, may be very low, but that is not the relevant probability. The relevant probability is the probability of some advantageous combination occurring in some individual at some point. And if that individual has lots of offspring (or if it occurs in several individuals, and they all tend to have more offspring), then individuals with the combination will become more prevalent in the population. It’s fairly easy to model, and I may do it later if I have a moment. Start off with no selection at all, then modify the model so that a minority of combinations are advantageous, and see how often an advantageous combination emerges and propagates through the population.
Only positive natural selection, if and when it happens, adds a necessity component to the algorithm, and therefore can in principle increase the probabilities of complex new functional traits. That’s why the whole darwinian mechanism is useless, if complex traits are not deconstructable into simple selectable variations. Which is exactly the case.
Except that it isn’t :)
Moreover, you insist on allele shuffling, but I can’t see how you can even begin to try to explain the emergence of new protein superfamilies by that mechanism. Please, try to explain how about 1000 superfamilies were already present in LUCA, and how 1000 more were generated in the course of evolution, keeping in mind that the mean functional unit (the protein domain) is usually 100 – 150 AAs long, with a functional complexity well beyond the reach of any random walk, with or without drift. Good luck.
Well, “allele shuffling” isn’t the only mechanism of mutation, and indeed, wouldn’t have been relevant to our LUCA which can’t have been a sexually-reproducing organism. And our LUCA was almost certainly more complex than its predecessors, so asking why “1000 superfamilies were already present in LUCA” is a bit like asking why a runner half way round the track has “already” completed half a lap! Because he started earlier than the time you are asking about! The “mean functional unit” now may well be 100-150 AAs long (and may have been in our LUCA, though I don’t know), and I agree it seems unlikely that the required sequence would have emerged through “random walk”, but that doesn’t mean that its predecessors didn’t, or that nothing simpler conferred reproductive advantage. But this is a very different question.Elizabeth Liddle_{July 12, 2011
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Elizabeth: I am well aware of the concept of genetic drift, and I have always found it completely useless for evolutionary theory. I will try to explain myself better. OK, genetic drift, if and when it happens (you certainly know that some essential conditions must be satisfied) can expand a neutral or quasi neutral mutation without the need of a positive selection due to survival benefit. OK. And so? The problem, apparently overlooked by neutralists (and by you) is that any neutral mutation can randomly expand, and any neutral mutation can randomly be lost. And most neutral mutations will simply remain there, in a minority of the population. Now, from the point of view of probabilities, that does not give any advantage versus a purely random walk. If I need, for a selectable trait to emerge, the coordinated mutation of two aminoacids, and if the forst mutation happens in one individual, the propbability of that specific mutation to expand by genetic drift is extremely low, because any new mutation can expand by drift, but only a few will do that, while a few will be lost. So, the probability that the second necessary mutation may happen in the subclone with the first mutation is extremely low if no drift happens (probabilities here obviously multiply), but the probability that the first mutation be expanded by drift and then the second mutation may happen in the expanded clone is similarly low, due to the low probability of the first event (expansion by drift) for that particular mutation. In brief, genetic drift in no way adds to the probability of having a complex functional new trait by purely random mechanisms (and genetic drift, like mutation, is a purely random mechanism). Only positive natural selection, if and when it happens, adds a necessity component to the algorithm, and therefore can in principle increase the probabilities of complex new functional traits. That's why the whole darwinian mechanism is useless, if complex traits are not deconstructable into simple selectable variations. Which is exactly the case. Moreover, you insist on allele shuffling, but I can't see how you can even begin to try to explain the emergence of new protein superfamilies by that mechanism. Please, try to explain how about 1000 superfamilies were already present in LUCA, and how 1000 more were generated in the course of evolution, keeping in mind that the mean functional unit (the protein domain) is usually 100 - 150 AAs long, with a functional complexity well beyond the reach of any random walk, with or without drift. Good luck.gpuccio_{July 12, 2011
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Mung:
But then, assuming that other organisms in the population which do not carry that mutation are reproducing at at least the same rate (it’s neutral, after all), then that mutation is not increasing in frequency in the population, is it.
You are a programmer - program a simple drift model and see what happens :) In other words, make reproduction entirely orthogonal to genotype, and see what happens to allele frequencies in each generation. You can keep the population constant, or let it fluctuate, as you like. I might even post one later - race you :)Elizabeth Liddle_{July 12, 2011
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oops yet again messed up the quote tags! Sorry!Elizabeth Liddle_{July 12, 2011
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gpuccio:
The point you seem not to understand is that a mutation has to be “selected”, that is to “expand” in the population, and not only to “survive”, if that mutation has to have any advantage versus a random search.
Forget the language of "select" and "search" for now - they are just metaphors. Think of what actually happens. If a mutation is truly neutral (confers a phenotypic effect but that effect makes no difference at all to the chances of survival), then it may die out within a generation, if its owner happens to be eaten by a predator before reproducing, or it may be passed on. And you read my post about the drunkard's walk,you will see that even a truly neutral mutation (an absolutely flat street - no bias in the drunk towards staggering one way or the other) have a non-zero chance of ending up at the North end of the street, and the further up they get, the better there chances of making it to the other end. This is what we call drift.
The whole necessity algorithm of neo-darwinian theory relies on positive selection, even if darwinists often seem to forget that.
Ultimately, yes. But propagation of potentially useful mutations does not necessarily depend on "positive selection" at the time when they first appear. Indeed, my hunch is that most ultimately useful traits i.e those that really do increase the probability of survival are combinations of alleles that have already been swimming around neutrally in the gene pool for some time. My guess is that mutations that are useful at their time of first appearance are probably the exception rather than the rule.
Without expansion of the selected trait in the population, the chances of a coordinated double or multiple mutation are not essentially different from a random search: IOWs, no even slightly complex functional trait can ever be generated by random mutations alone.
Except that I think your premise is wrong, as I explain above. If most advantageous traits (in a particular environment) are polygeneic traits that have been drifting around for many generations until they proved advantageous, then there isn't a problem, is there? A criticism often leveled at the extrapolation from "micro" to "macro" evolution is that "micro" evolution doesn't involve new alleles. This is probably false, in fact - new alleles are appearing all the time, and there's no good reason to think they don't contribute to microevolution. But I would agree that most evolution (including microevolution) occurs by means of differential reproduction, from generation to generation, arising from the interaction between genotype and environment, those with the best allele "cocktails" for the current environment preferentially passing on those "cocktails" to the next generation. So alleles that tend to appear most often in the most successful cocktails become more prevalent, and those that appear less commonly, less Then the environment changes, and the best-performing cocktail changes. Some alleles may be common to both optima, some may not. But I do think it's important to get away from the idea that single genes/alleles are what matter in evolution. It's simply wrong, not least because gene-gene and gene-environment interactions matter too.
Elizabeth Liddle_{July 12, 2011
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Mung:
As in leaving 1.022 offspring rather than 1.020 offspring?
Averaged across a population, yes.Elizabeth Liddle_{July 12, 2011
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But then, assuming that other organisms in the population which do not carry that mutation are reproducing at at least the same rate (it's neutral, after all), then that mutation is not increasing in frequency in the population, is it.Mung_{July 12, 2011
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The point you seem not to understand is that a mutation has to be “selected”, that is to “expand” in the population, and not only to “survive”, if that mutation has to have any advantage versus a random search.
The near neutral mutation doesn't need to be selected for, the organism that carries it just needs to survive and reproduce, thus reproducing the neutral mutation. Take this (overly simplistic for the point of pedagogy) example: If the organism has four offspring that carry the mutation, and two of them have another four offspring each, of which two reproduce, after four generations you should have 16 individuals who carry that mutation, and 32 in the next generation. The mutation is not selected 'for' it just isn't selected against and the natural process of reproduction spreads the mutation.DrBot_{July 12, 2011
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Elizabeth: So we can say that half of all near-neutral mutations have a chance of surviving several generations, and of those that do, quite a number of them will propagate quite widely. The point you seem not to understand is that a mutation has to be "selected", that is to "expand" in the population, and not only to "survive", if that mutation has to have any advantage versus a random search. The whole necessity algorithm of neo-darwinian theory relies on positive selection, even if darwinists often seem to forget that. Without expansion of the selected trait in the population, the chances of a coordinated double or multiple mutation are not essentially different from a random search: IOWs, no even slightly complex functional trait can ever be generated by random mutations alone.gpuccio_{July 12, 2011
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What is probably more true is that in general, those effects are likely to have only a small effect on successful reproduction.
As in leaving 1.022 offspring rather than 1.020 offspring?Mung_{July 11, 2011
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Strange that there isn’t a Nobel Prize for “evolutionary biology”. Nor has anyone in evolutionary biology made any discovery worth one.
Not really strange - the Nobel prizes were instituted over 100 years ago, before evolutionary biology was its own discipline. But even then the 1973 prize was awarded to Karl von Frisch, Konrad Lorenz and Nikolaas Tinbergen for their work in animal behaviour, using an evolutionary framework:
The way out of this dilemma [between vitalists and reflexologists] was indicated by investigators who focused on the survival value of various behaviour patterns in their studies of species differences. Behaviour patterns become explicable when interpreted as the result of natural selection, analogous with anatomical and physiological characteristics. This year's prize winners hold a unique position in this field.
Heinrich_{July 11, 2011
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So we can say that half of all near-neutral mutations have a chance of surviving several generations, and of those that do, quite a number of them will propagate quite widely. Even if they confer no benefit at all, alone, and even, interestingly, if the confer a slightly disadvantage. So the chances of several near-neutral mutations “meeting up” is no stranger than finding several drunks near the north end of the street, if rather more of them started off near the lamppost.
Mutation and selection of beneficial genes is an insufficient explanation for most any feature of living things. It enables the hope that very best of many tiny modifications add up to something. How is mutation and selection of just about anything, beneficial, neutral, or disadvantageous, a better explanation? That's akin to using those wandering drunks to explain an orchestrated cheerleading routine or a successful corporation. So much is set about what might be hypothetically possible and how genes propagate, but there's no actual explanation buried in there.ScottAndrews_{July 11, 2011
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Both questions really apply. No organism is guaranteed survival to reproduction or the survival of its offspring due to a single potentially beneficial gene. The difference would be marginal, perhaps undetectable. And yet the explanation is built upon those changes being selected. And, at the same time, the concept of things competing for survival and to reproduce doesn't take into account that multiple beneficial mutations (generously allowing that such things occur as often as raindrops) must also compete against each other. Why are so many smart people still chasing after this?ScottAndrews_{July 11, 2011
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ScottAndrews:
Population geneticists even have equations for it. In my example I used tiny changes because those are the only sort that individual mutations can account for.
Actually, that's not quite true. Mutations that affect developmental trajectory can have quite marked phenotypic effects (limb length, for example). But generally, of course, you are correct. What is probably more true is that in general, those effects are likely to have only a small effect on successful reproduction.
But the implication is that such tiny changes, each originating in a single organism, add up to staggering, varied works of art, marvels of engineering, and ingenuous behaviors.
Yes, when accumulated over many generations.
And supposedly each mutation must survive and propagate, despite conferring at best mininal benefit, until it meets up with several more and finally accomplishes something. (Wow, that sounds an awful lot like foresight and planning.)
No, not really, because neutral, or near neutral mutations do in fact propagate, in the manner of the drunkard's walk. The usual picture is: imagine a drunk at a lamp post. Every step he takes will take him either North or South, with equal probability. After a couple of hours, the chances that he will be at the lamp-post is very small, and the chances he will be quite a long way from the lamp post are quite high. The chances that be a quite long way North of the lamp post are half that. So we can say that half of all near-neutral mutations have a chance of surviving several generations, and of those that do, quite a number of them will propagate quite widely. Even if they confer no benefit at all, alone, and even, interestingly, if the confer a slightly disadvantage. So the chances of several near-neutral mutations "meeting up" is no stranger than finding several drunks near the north end of the street, if rather more of them started off near the lamppost.
I hope no one reads the cited comment and gets the mistaken impression that there are verifiable formulas for such things or even specific hypotheses to explain them. I wonder how many times people read that ‘x happens and then y happens and then z happens’ and because of the confident wording they never realize that no one has ever seen x, y, or z.
You are right that population genetics is a very theoretical field (which is why their pronouncements and dilemmas should be taken with a large pinch of salt!) But asexual populations have been extensively studied (obviously in an asexually reproducing population, you won't get coincident mutations at all, but you can measure the relative fitness of a mutated population with its ancestral population), and genetic accumulations can be traced statistically. For instance, in the human genome, gene-gene interactions are the subject of important investigation, and that is precisely about what happens "when x happens and then y happens then z happens" and the result is an individual with x, y and z. But I do think that the Selfish Gene concept has been a misleading one (though Dawkins had an important, if minor, point). Genes aren't selected, phenotypes are, and phenotypes bear vast cocktails of genes many of which have large numbers of polymorphisms. That's why we are all unique, genetically. So if a certain range of allele cocktails are beneficial in a certain environment, by conferring a certain range of a certain trait, those alleles will tend to become more prevalent in the population, and any new alleles that contribute extend the range of that trait in the same direction will tend to join the favoured cocktail. Then, when the environment changes, the optimal cocktail will shift, and again, any new alleles that contribute to that shift will tend to join the crowd. A bit like fashion and celebrity, really :) And the interesting thing is that because most traits that are polygeneic, the contributor genes will tend to be preserved in a population, even when the environment changes, precisely because no one gene is responsible for the trait, leaving the gene pool rich enough to respond to new changes. As you say, a kind of "foresight", or perhaps "memory" - but one that is perfectly explicable by means of fairly simple naturalistic stochastic models.
Elizabeth Liddle_{July 11, 2011
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Strange that there isn't a Nobel Prize for "evolutionary biology". Nor has anyone in evolutionary biology made any discovery worth one. Perhaps that answers Thomas' question about competence...Joseph_{July 11, 2011
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