The Very Tiny Edge of Evolution

_{November 5, 2010

Intelligent Design}

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There’s an item today at PhysOrg concerning an article in this week’s Science magazine. According to the study conducted on a bacterial population using a technique wherein mutations could be inserted anywhere along the length of the genome, each and every bacterial mutation had the same small effect on fitness of 0.5%, no matter if the mutation took place in a protein sequence or in a so-called non-coding section. I’m just bringing your attention to it. It would seem that for those who wish to use the RM + NS motif of Darwinian evolution, this study pretty much spells this motif’s deathknell. If the average mutation reduces fitness, how does any living organism improve? And, how can NS distinguish between mutations if they all look the same? Remember, per Dawkins, NS is what makes a random process no longer random. So, now, if one wants to posit that the accumulation of many such mutations can bring about improvement, then one has to maintain that the accumulation of bad stuff eventually makes good stuff—which, let us say, isn’t immediately obvious, and, one has to say this accumulation happened in a non-directed way.

Certainly, all of this is counter-intuitive. But, alas, that is exactly what Darwinism was from its beginning: the positing of the counter-intuitive in place of the intuitive. This study strongly suggests that the counter-intuitive remains counter-intuitive. And it becomes the other bookend to Michael Behe’s criticism of RM + NS in his The Edge of Evolution in undermining any remaining confidence one might have in the reigning neo-Darwinian motif. Isn’t it time to jettison the illogical? For me personally, “neo-Darwinism is dead” ( to quote Allen MacNeil). Now we can see why.

Comments

PaV (60):
As I begin, I want to note, Neil, your very respectful tone.
I do understand that this is an ID site. I might disagree with ID, but you still have a right to discuss your ideas, and I am not trying to disrupt that. I'm only commenting where I think I have something significant to contribute to the discussion.
There’s a simple way of testing your viewpoint. I’ve already mentioned it. Dogs!
Dogs are a rather atypical case, due to human involvement in their breeding. That doesn't make for a good test.
Again, let’s take this well-adapted bacteria and move it back ten evolutionary steps away from its peak-adaptivity.
I apparently didn't explain my position well enough. Firstly, I don't talk of "peak adaptivity". I mentioned only "highly adapted". Secondly, my point is that even if you move back 10 steps, then it is still highly adapted, though perhaps to a slightly different niche. If a species is not well enough adapted to maintain approximately the same population size, then it will decline exponentially, so will soon go extinct. If a species produces continuous increase in population size, it will grow exponentially and soon overwhelm its resources. So I would expect any stable species to be approximately maintaining the same population size, with some oscillation depending on whether the conditions are temporarily better or worse than average. I'll add that my use of "niche" is non-standard. I want to divide up niches rather more finely than is traditional. And what is usually considered competition, I want to think of as a different niche (one where food is harder to get). Oh, and yes, even the first biological organisms on earth (however they got here) would have to have been well adapted to what they found, or that exponential decay in numbers would have quickly eliminated them.Neil Rickert_{November 7, 2010
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Neil Rickert [46]: As I begin, I want to note, Neil, your very respectful tone. This is always appreciated here. I'd also like to acknowledge the sizable degree of openness you have to criticism of Darwinism. This, too, is also appreciated since most of us here at UD simply have scientific, and not religious, objections to the theory.
All evolutionists understand that niche change is involved in evolution. However, the traditional view emphasizes genetics, and pays only minor attention to niche change. My preference would be a theory that made niche change more central, and considered the genetics as an implementation detail in how a population manages niche change.
There's a simple way of testing your viewpoint. I've already mentioned it. Dogs! I don't think you would want to say that the difference between dog breeds is due to "niche changes"; thus you would be left having to say it is due to changes in genetics. So I don't see how this argument stacks up.
Yes, I expect that the bacteria are always highly adapted. As I see it, the only species that are not highly adapted are those on their way to extinction.
With all due respect, let me point out what I see as a logical inconsistency in this statement. Again, let's take this well-adapted bacteria and move it back ten evolutionary steps away from its peak-adaptivity. According to your statement, the bacteria ten steps away from peak adaptation is on its way to extinction. But, then, how did it come to have peak adaptation? By my assumption, it needed ten more steps to reach peak adaptation, so this means either (1) we don't know if something is coming or going, or, (2) bacteria came into the world already at peak adaptation. Do you see the problem? MathGirl: I just now remember what Allen MacNeil said. He said that the "Modern Synthesis" is dead. If you google that you'll find the thread where he said that. There really isn't any difference between Modern Synthesis and neo-Darwinism---they're basically the same thing.PaV_{November 7, 2010
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gpuccio (58):
why do you speak of “variation”, and not of “random variation”? Do you maintain that the variation in your theory is not random?
The learning theory does not require that it be random. It does require that it be a broadly distributed variation, rather than a narrowly focused variation. It happens that randomness is an effective way to achieve that, and what is observed does appear to be random.Neil Rickert_{November 7, 2010
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Neil: I am patient. I will wait. But allow me to consider your theory as non existent until I can know it. In the meantime, a couple of comments on what you did say: You could, of course, say that “differential survival” is another way of talking about natural selection, and that “engines of variation” is an alternative way of talking about random mutation. You bet. But there is a difference in emphasis here. Standard neo-Darwinism emphasizes the elimination of maladaptive variants, Not exactly. Standard darwinism emphasizes the negative selection of maladaptive variants and the positive selection, expansion and fixation of so called "positive mutations" (if they really exist). Positive selection is definitely the most important part to build new information. Negative selection could only preserve what already exists. while my view emphasizes maintaining as much variation as the population can bear as a way of allowing adaptation to niche change. Not very clear, indeed. But I will wait for further details. Maybe they will come, sometime. Just a question: why do you speak of "variation", and not of "random variation"? Do you maintain that the variation in your theory is not random? Just to know...gpuccio_{November 7, 2010
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gpuccio (54):
I am eager to know your theory, and to check what it can really explain at scientific level.
Then I suggest great patience, though I'll note that I am using my blog to discuss related issues. Philosophy asserts itself as the authority on questions of knowledge and learning. But philosophy is highly resistant to change.
you should be able to explain how “the population” achieves that.
The population maintains genetic variation within the population (that would be where "engines of variation" might fit in). And then the differential survival of different variants amounts to a kind of feedback, a way of measuring how well the population is adapted to its current niche. You could, of course, say that "differential survival" is another way of talking about natural selection, and that "engines of variation" is an alternative way of talking about random mutation. But there is a difference in emphasis here. Standard neo-Darwinism emphasizes the elimination of maladaptive variants, while my view emphasizes maintaining as much variation as the population can bear as a way of allowing adaptation to niche change. A shift toward a greater emphasis on variation was foreseen by Gould (or at least that is my reading of Gould). I'm not a biologist, so I don't try to keep up with all of the latest research papers. But it does seem to me that the biologists have been moving in the direction of placing increasing emphasis on variation.Neil Rickert_{November 7, 2010
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Errata corrige: the merit of the discovery is of BA (bornagain77), not "BS". I apologize, BA!gpuccio_{November 7, 2010
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In the meantime, I would really recommend to all here to read this new paper by Abel, brilliantly discovered by BS: http://www.bentham.org/open/tocsj/articles/V004/14TOCSJ.pdf I am still reading it. It's really a treasure, and it contains in a wonderful form all the basics of ID.gpuccio_{November 7, 2010
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Neil: I think I will go on with my broad generalizations, and take the risk. I am eager to know your theory, and to check what it can really explain at scientific level. In my world, an engine of variation must really be an explicatory model. And it must explain. So, when you say: "the population changes its own genetics in order to be able to fit into the new niche" you should be able to explain how "the population" achieves that. I am waiting.gpuccio_{November 7, 2010
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gpuccio (50):
The problem is that there is really no other quasi consistent theory than neo darwinism, if one wants to try to explain biological information in scientific terms without recurring to design.
I suggest you avoid those overly broad generalizations. The most you can say is that you are unaware of an alternative. I do have my own "theory". It is based on an unpublished theory of learning. I'll note that the idea of "engines of variation" that you mention in comment (51) would fit right in.
And what is your idea of how a niche change could implement detail at the genetic level?
The niche does not change the genetics. Rather, the population changes its own genetics in order to be able to fit into the new niche. That's part of how I use my learning theory. While this learning could be said to be purposeful, it is only so in terms of a very weak non-cognitive sense of "purpose" that is fully explainable on a natural basis. I do see involvement of the homeostatic processes that are abundant in biological systems.Neil Rickert_{November 7, 2010
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MathGrrl (49):
Your predictive powers are as strong as my Google-Fu.
It wasn't much of a prediction, given that the empirical evidence does not support ID. The title of the linked page was "The Modern Synthesis is Dead - Long Live the Evolving Synthesis!" That's a good way of putting it. The reason ID criticisms of the modern synthesis don't stick, is that biology has moved on. It is still using the name "modern synthesis", but what they mean by that term has evolved considerably from the original meaning.Neil Rickert_{November 7, 2010
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MathGrrl: Allen McNeill's ideas about a "whole new world of theoretical and practical empirical research" in evolution which would be substantially different form neo darwinism are at best poetical, and in no way explicatory. I have remarked many times that his famous list of "engines of variation" is in no way explicatory. One thing is to make philosophy, another thing is to make science. Science has to explain data. Neo darwinisn at least tries to explain data, even if it does not succeed. But I have the strong impression that the fashionable new forms of "neo neo darwinism" don't even try. They just try to entertain, but rarely to explain. They are more philosophy (not a good one, IMO) than science. So, I will be clear. Neo darwinism invests all its explanatory hopes in RV + NS. It is a wrong model, it is never detailed, but at least an explanatory mechanism based on chance and necessity is proposed. What other non design model do we know that can take its place? What "engine of variation" do we know that is neither RV not NS, and that can begin to explain what we observe?gpuccio_{November 7, 2010
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Neil: I’ll add that if neo-Darwinism were to be replaced by a better theory, I doubt that ID proponents would find the replacement theory any more congenial. Unless it is ID theory, I suppose. The problem is that there is really no other quasi consistent theory than neo darwinism, if one wants to try to explain biological information in scientific terms without recurring to design. IOWs, neo darwinism is the best that non design theorists have, and the best is not much. All evolutionists understand that niche change is involved in evolution. However, the traditional view emphasizes genetics, and pays only minor attention to niche change. My preference would be a theory that made niche change more central, and considered the genetics as an implementation detail in how a population manages niche change. I don't understand. Are you invoking neo Lamarckism? And what is your idea of how a niche change could implement detail at the genetic level? Because I suppose that is the real scientific question. All the rest is philosophy.gpuccio_{November 7, 2010
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Neil Rickert, Out of my own curiosity, I did a quick Google on "allen macneill neo-darwinism dead" and found this post on his blog from last year. Your predictive powers are as strong as my Google-Fu. You said:
I’ll add that if neo-Darwinism were to be replaced by a better theory, I doubt that ID proponents would find the replacement theory any more congenial.
Allen MacNeill wrote:
Some ID supporters have also suggested that Dr. Koonin might be taking a “big career risk” in stating the obvious. I don't think so. On the contrary, what Dr. Koonin has pointed out is that evolutionary biology today is broader, more generally applicable, and less narrowly focused than at any time since the publication of the Origin of Species 150 years ago. Being an evolutionary biologist today is like being a physicist in 1905 — a whole new world of theoretical and practical empirical research is opening up, with new discoveries being made every day.
Do you have any lottery numbers or horse names you'd like to share?MathGrrl_{November 7, 2010
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Pedant: #42: Your argument is correct, but I would say that 4% is not a small sample. Rather, the argument about testing only ribosomal proteins is IMO a greater limitation of the study. But there is no doubt that this kind of research must be expanded. #43: I think your point here is weaker. Remember what the abstract says: "We used a bacterial system in which the fitness effects of a large number of defined single mutations in two ribosomal proteins were measured with high sensitivity." (emphasis mine). So, the "potentially neutral" mutations are probably really neutral. Or anyway, they could be either negative or positive mutations, but whose effect on fitness is so small that the "highly sensitive system" could not detect the difference. It would be interesting to know how many of the mutations were synonymous or non synonymous in the two groups (slightly negative or potentially neutral). Has anybody here access to the full paper?gpuccio_{November 7, 2010
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Neil Rickert,
I did not read that, and I will not dispute what I have not read. He may have been writing metaphorically.
I read it, it wasn't a metaphor.Clive Hayden_{November 7, 2010
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PaV (41):
Allen MacNeil has written–right here at UD–that neo-Darwinism is dead. Are you disputing him?
I did not read that, and I will not dispute what I have not read. He may have been writing metaphorically. To be clear about my own position, I do not much like neo-Darwinism. I think it a poor account of evolution, and better accounts are possible. That neo-Darwinism is under constant attack is evidence that it fails in one of the roles of a scientific theory, that of adequately explaining the science to a lay audience. However, it is well known that scientists will continue to use an imperfect theory, as long as it serves them well enough for their ongoing research. So I don't expect neo-Darwinism to be replaced in the near future. I'll add that if neo-Darwinism were to be replaced by a better theory, I doubt that ID proponents would find the replacement theory any more congenial.
Did you notice that all of the mutations—ALL—not only were mildly deleterious, they were all of the same negative effect.
My reading was that most were mildly deleterious, but "most" is not "all". I'll also note that I was careful to use "ToE" rather than "Darwinism", since I consider myself an evolutionist but not a Darwinist.
The only logical conclusion is that all parts of the genome are equivalent in terms of fitness.
Most traits depend on many genes, and most genes affect many traits. And that is part of why the reported results are unsurprising. It is also part of why I am not a fan of neo-Darwinism.
To spell it out more clearly, let’s examine your statement that it is because of the bacteria’s extreme degree of adaptation that all mutations are deleterious.
Well, that is not what I stated. You expressed that as a statement of causation. However, I merely made a comment about what we should expect. And again, both the reported research and my comments were about "most mutations" rather than "all mutations."
Let’s, then, start with this condition and go back in time—unless, of course, you want to state that the bacteria has always been highly-adapted.
Yes, I expect that the bacteria are always highly adapted. As I see it, the only species that are not highly adapted are those on their way to extinction. My preferred view of evolution is in terms of niche change, with a population gaining the ability to move into a new niche, while remaining highly adapted during that change of niche.
Neil, eveyone knows that fitness is relative to environmental niches. I’m sure the authors know this. Isn’t it very likely that the authors ‘tested’ all of these developed strains of bacteria against the same environment?
I agree with that. I must have communicated poorly, if you thought that had to do with what I was saying. I often hear neo-Darwinists talking of adaptation as solving an optimization problem (optimizing a population to its current niche). I think that a rather poor explanation of evolution. Since that is what you are arguing against, I see your argument as missing the point at least with respect to how I think about evolution. All evolutionists understand that niche change is involved in evolution. However, the traditional view emphasizes genetics, and pays only minor attention to niche change. My preference would be a theory that made niche change more central, and considered the genetics as an implementation detail in how a population manages niche change.Neil Rickert_{November 7, 2010
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Pedant:
One or more of those “potentially neutral” mutations might have been weakly beneficial, but that would have been beyond the scope of the study.
So you think that the rate for "weakly beneficial' mutations may be within 1% to 1/2% of all mutations? Well let's kick a few more numbers around: "I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998). Therefore, I cannot ...accurately represent how rare such beneficial mutations really are." (J.C. Sanford; Genetic Entropy page 24) - 2005 "Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.” Sanford: Genetic Entropy Inside the Human Genome: A Case for Non-Intelligent Design - Pg. 57 By John C. Avise Excerpt: "Another compilation of gene lesions responsible for inherited diseases is the web-based Human Gene Mutation Database (HGMD). Recent versions of HGMD describe more than 75,000 different disease causing mutations identified to date in Homo-sapiens." http://books.google.com/books?id=M1PRvkPBKfQC&pg=PA57&lpg=PA57&dq=human+75,000+different+disease-causing+mutations&source=bl&ots=gkjosjq030&sig=gAU5AfzMehArJYinSxb2EMaDL94&hl=en&ei=kbDqS_SQLYS8lQfLpJ2cBA&sa=X&oi=book_result&ct=result&resnum=6&ved=0CCMQ6AEwBQ#v=onepage&q=human%2075%2C000%20different%20disease-causing%20mutations&f=false I went to the mutation database website and found: HGMD®: Now celebrating our 100,000 mutation milestone! http://www.biobase-international.com/pages/index.php?id=hgmddatabase I really question their use of the word "celebrating". A review of The Edge of Evolution: The Search for the Limits of Darwinism The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have "invented" little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155). "The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable." Michael J. Behe PhD. (from page 146 of his book "Edge of Evolution") Richard Dawkins’ The Greatest Show on Earth Shies Away from Intelligent Design but Unwittingly Vindicates Michael Behe - Oct. 2009 Excerpt: The rarity of chloroquine resistance is not in question. In fact, Behe’s statistic that it occurs only once in every 10^20 cases was derived from public health statistical data, published by an authority in the Journal of Clinical Investigation. The extreme rareness of chloroquine resistance is not a negotiable data point; it is an observed fact. Thus, the actual rate for 'truly' beneficial mutations, which would account for the staggering machine-like complexity we see in life, is far in excess of one-hundred-billion-billion mutational events. So this one in a thousand, to one in a million, number for 'truly' beneficial mutations is actually far, far, too generous for an estimate for evolutionists to use as an estimate for beneficial mutations. In fact, from consistent findings such as these, it is increasingly apparent the principle of Genetic Entropy is the overriding foundational rule for all of biology, with no exceptions at all, and belief in 'truly' beneficial mutations is nothing more than wishful speculation on the materialist part which has no foundation in empirical science whatsoever. Evolution vs. Genetic Entropy - video http://www.metacafe.com/watch/4028086 The foundational rule of Genetic Entropy for biology, which can draw its foundation in science from the twin pillars of the Second Law of Thermodynamics and from the Law of Conservation of Information (Dembski, Marks, Abel), can be stated something like this: "All beneficial adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of the optimal functional information that was originally created in the parent species genome." further notes: Distribution of fitness effects caused by random insertion mutations in Escherichia coli Excerpt: At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect. http://www.springerlink.com/content/r37w1hrq5l0q3832/ Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon) Abstract......It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate. http://www.nature.com/hdy/journal/v84/n5/full/6887270a.html This following study confirmed the "detrimental" mutation rate for humans, of 100 to 300, estimated by John Sanford in his book "Genetic Entropy" in 2005: Human mutation rate revealed: August 2009 Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. (Of note: this number is derived after "compensatory mutations") http://www.nature.com/news/2009/090827/full/news.2009.864.html This mutation rate of 100 to 200 is far greater than even what evolutionists agree is an acceptable mutation rate for an organism: Beyond A 'Speed Limit' On Mutations, Species Risk Extinction Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material. http://www.sciencedaily.com/releases/2007/10/071001172753.htm Experimental Evolution in Fruit Flies - October 2010 Excerpt: "This research really upends the dominant paradigm about how species evolve".,,, as stated in regards to the 35 year experimental failure to fixate a single beneficial mutation within fruit flies. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_fliesbornagain77_{November 7, 2010
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Pedant: We're left, really, with neutral drift a la Kimura. But, of course, in Kimura's book on neutral drift, he clearly calls into question the neo-Darwinian model. Genome wide studies now make the problems of evolution per neutral drift unimaginably difficult to surmount. Neo-Darwinism is dead. That's just how things are. Further--and I'm quite alone on this even here at UD---I predict that NS will be shown not to be any kind of effective seletive mechanism at all. That's how wrong all of this is. It will take time---years---for this to become clear, but it will. [That is, what we call RM + NS is simply a mechanism that genomes use to adapt to their environment. You might reply that this is of course what Darwinists claim; however, this mechanism is a property of the genome, integral to it, and part of its survival package. It is not a means of becoming what it is not. The parallel is artificial selection, wherein wolves become dogs, and some dogs become different kinds of dogs. And, so, dogs never become anything else than dogs. This is perhaps only a matter of perspective, but it demonstrates the "tiny edge of evolution".]PaV_{November 7, 2010
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PaV:
Did you notice that all of the mutations—ALL—not only were mildly deleterious, they were all of the same negative effect.
This is incorrect. As gpuccio quoted in post #10:
The obtained DFE appears to be unimodal, where most mutations (120 out of 126) are weakly deleterious and the remaining ones are potentially neutral.
One or more of those "potentially neutral" mutations might have been weakly beneficial, but that would have been beyond the scope of the study.Pedant_{November 7, 2010
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In the study by Lind et al., the authors created 126 random base-pair substitutions in two bacterial genes, ribosomal S20 (87 amino acids) and L1 (234 amino acids). This is a total of 321 amino acids, each of which is specified by a 3-base codon. Since there are three (out of four) possible base changes at any given site, the authors changed 126 out of 321*3*3 = 2889 bases, or 4% of all possible changes. Any speculations about the applicability of their data to other issues in biology should bear in mind that limitation.Pedant_{November 7, 2010
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Neil Rickert:
UD is repeatedly ringing the death knell of evolution. Yet, somehow it never dies.
Allen MacNeil has written--right here at UD--that neo-Darwinism is dead. Are you disputing him? Besides, this is just one study of many that have rung the deathknell of neo-Darwinism. It only lives because there are professors in universities who would be out of jobs if neo-Darwinism were declared officially dead. It is only unofficially dead. But official notice will be shortly coming---which, per University/educational establishment time, would be about 15-20 years.
I don’t see this study as posing any particular problem for ToE. If an organism is well adapted, then it is to be expected that most changes would be deleterious.
With all due respect, Neil, this is exactly the problem with Darwinists: you loop yourself around reality using made-up, ill-defined, question-begging categories. Did you notice that all of the mutations---ALL---not only were mildly deleterious, they were all of the same negative effect. The only logical conclusion is that all parts of the genome are equivalent in terms of fitness. But, if all parts of the genome are equivalent in terms of fitness, then on what basis does NS 'choose' anything? This study is basically saying that SNP's are nothing more than white noise. To spell it out more clearly, let's examine your statement that it is because of the bacteria's extreme degree of adaptation that all mutations are deleterious. Let's, then, start with this condition and go back in time---unless, of course, you want to state that the bacteria has always been highly-adapted. So, going back in time, let's say that starting from some other bacteria, ten changes have occurred. So, let's go back ten steps, if you will. We know that anytime bacteria replicate, mutational errors occur. So, that makes EACH replicated bacteria inferior to the highly-adapted one. Now, according to my hypothetical, the bacteria has to take ten steps, and at each of these steps NS has to make a choice, and at each of these steps a series of mutations is added because of replication, and, according to this study, as far as NS is concerned, ALL of these mutations move the bacteria BACKWARDS an equal amount. So, again, which mutation does NS select, and why? I think in the face of this it is hard to just hand-wave and say that you see no problem here. There's a problem.
The question seems to come from a misunderstanding. Fitness is relative to the environmental niche.
Neil, eveyone knows that fitness is relative to environmental niches. I'm sure the authors know this. Isn't it very likely that the authors 'tested' all of these developed strains of bacteria against the same environment? Otherwise, how could they make the claim that they do. If they were using different environments willy-nilly, or even just a few different environments, then they wouldn't be in a position to compare results. So, assuming that all of these bacteria are being 'tested' in the same "environmental niche", then why are they equally less fit no matter the place at which the mutation takes place? Again, that means that any step back away from its present genomic configuration is equal in its loss of fitness, and the implication is that any steps that have to be taken from less fit to more fit, are basically random. Or, shall we say, of equiprobability as far as NS is concerned. This, then, makes NS something that operates at random. And, NS operating at random, leaves Darwinism naked---it has no way of getting from point A to point B. Or, shall we say, it has no chance of 'climbing Mt. Improbable'. You can run, but you can't hide from the logical implications here.PaV_{November 7, 2010
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Neil: Maybe I have misunderstood your words. You said: "The bacterial mutation that gives a bacterium antibiotic resistance may actually be deleterious in an environment where there is little antibiotic. But it is beneficial in an environment where significant antibiotic is present.". That seems to refer to spacially separated environments as "niches". That is locality. The populations available for evolution are reduced. Another possibility is that a "niche" is a temporally isolated environment. That is locality too. The time available for each population's evolution is reduced. If you mean as "niches" different characteristics of the same environment, that is another concept, but then all the replicators in the environment have the same chances. Even in that case, if an initial mutation in a direction "separates" part of the population functionally, and the "evolution" of that trend of functionality can go on only in that part of the population, you have a functional "niche": but the result is the same, you have functional locality, and the population available for future useful events is hugely reduced. So, I believe that all my observations about the limiting role of locality for evolution remain completely valid.gpuccio_{November 6, 2010
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Just a quick reminder: even a beneficial mutation can have a negative fitness cost. I don't see how anyone can deny that this study presents a challenge to evolution. Sure, evolution is possible; it just keeps getting less and less likely.Collin_{November 6, 2010
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gpuccio (35):
Locality is not a good answer for events which are already completely unlikely in the whole span of existence of our whole planet.
You are confusing niche with location. Both humans and honey bees exist in many parts of the world, but they occupy very different niches. A niche can be thought of as a way of life, a way of eking out an existence. The division of the world into a large variety of niches is complex. The biological complexity echos that complexity of the division into niches.Neil Rickert_{November 6, 2010
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Mung: It was an analogy. What makes it the “best” analogy? --- You need to chill mung...I was speaking for myself...aka my personal opinion of how well that analogy summed up the false belief that mutations could build up the genome over time.Blue_Savannah_{November 6, 2010
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gpuccio, to echo your comment that antibiotic resistance has 'always been there',, the following video is interesting in that he speaks of bacteria that had been gathered from 'pre-antibiotic times' that showed the same resistance that modern strains have though never being exposed to antibiotics: Evolution Tested and Falsified - Dr. Don Patton - video http://www.metacafe.com/watch/4036803/ The following site lists the degraded molecular ability of many of the different strains of antibiotic resistant bacteria: List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria: http://www.trueorigin.org/bacteria01.asp Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video http://www.metacafe.com/watch/3995248bornagain77_{November 6, 2010
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Neil: The question seems to come from a misunderstanding. Fitness is relative to the environmental niche. The bacterial mutation that gives a bacterium antibiotic resistance may actually be deleterious in an environment where there is little antibiotic. But it is beneficial in an environment where significant antibiotic is present. ToE should be seen as a theory of niche change, and of adaptation to new niches. I disagree. That is a common simplification made by darwinian thought, and one really misleading. I would say that this kind of resoning too comes from the main "empirical model" of darwinism, antibiotic resistance. The problems with that way of reasoning are many: a) Most complex functions cannot have arisen simply because of a new "niche". Most complex functions are about basic vital organization. I don't undesratnd how a "niche" could explain the transition from prokaryotes ot eukaryotes, for instance, or the transition from single celled organisms to multicellular organisms. Or the simultaneous emergence of complex body plans at the cambrian explosion, all of them in the same environment. Basic organization of life is not the result of a "niche". b) Antibiotic resistance is an extreme scenario, characterized by two properties: - a specific biochemical aggression (the antibiotic) conditions survival more than any other factor. - a simple mutation, usually of one aminoacid, in a target structure can help "evade" the threat in a short time. Nothing of that kind applies to the emergence of complex functions. Even antibiotic resistance through a complex molecule, like penicillinase, is due to HGT, and never to the emergence of a new complex molecule. Penicillinases have always been there, and nobody knows how they emerged. c) The "niche" scenario is at best an adaptation scenario. It is fine for some simple microevolutionary events, or for neo Lamarkian events, if they exist. But in no way it can explain the emergence of complexity. Indeed, nor even the general scenario can explain that, but the "niche" scenario is even more inappropriate, because of its severe limitation both of space and time. A "niche" is by all means a "smaller place" than the general life environment: it implies smaller populations, and shorter times. Locality is not a good answer for events which are already completely unlikely in the whole span of existence of our whole planet.gpuccio_{November 6, 2010
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It would seem that for those who wish to use the RM + NS motif of Darwinian evolution, this study pretty much spells this motif’s deathknell.
UD is repeatedly ringing the death knell of evolution. Yet, somehow it never dies. I don't see this study as posing any particular problem for ToE. If an organism is well adapted, then it is to be expected that most changes would be deleterious.
If the average mutation reduces fitness, how does any living organism improve?
The question seems to come from a misunderstanding. Fitness is relative to the environmental niche. The bacterial mutation that gives a bacterium antibiotic resistance may actually be deleterious in an environment where there is little antibiotic. But it is beneficial in an environment where significant antibiotic is present. ToE should be seen as a theory of niche change, and of adaptation to new niches.Neil Rickert_{November 6, 2010
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Mung:
The problem with the OP is that it claims that Darwinism is counter-intuitive and then fails to explain it’s near universal acceptance.
How can it have near universal acceptance when the vast majority of people don't accept it? Mung:
What is the primary claim of Darwinism?
That all o life's diversity owes it collective common ancetry to some unknown population(s) of single-celled organisms via an accumulation of genetic mistakes. Mung:
Why is that claim counter-intuitive?
Because we have neve observed mistakes/ errors/ accidents accumulate in suc a way as to produce complex functional systems.Joseph_{November 6, 2010
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Pedant (and others): OK, let's say that it is the first step in analyzing fitness effects with this approach :) One of the problems with the traditional approach of analyzing genomes and proteomes is that the interpretation of what we observe depends heavily on our basic assumptions. It's not a mystery that in the last decades the only allowed assumptions have been those of the neo darwinian model. So, you will understand if we in ID, who disagree with many of those assumptions, are specially happy that new lines of enquiry, more direct and less subject to cognitive bias, are pursued. Now, leaving aside ideological polemics, I would like to reason a little on this paper and what it could mean. Obviously, I have access only to the abstract, so I will try to stick to what can reasonably be understood from that. First of all, I agree with you on one important point: the work was done on two ribosomal proteins, and that can certainly condition the results, as they are part of a much more complex functional unit, the ribosome. I would like to see the same approach with individually functional proteins, like enzymes, and possibly with many different ones. That said, here are some comments n the results: a) The first point is that no "positive" mutation was found. Well, that is not so surprising after all. They tried only 126 mutations. But it is, however, a fact. b) The second point is that no really "negative" mutation was found. The negative effect on fitness was small, and the same for almost all the cases. That is more interesting. Frankly, I would have expected more substantial negative mutations. I suppose that the model (ribosomal proteins) could be in part responsible for that result. The whole ribosome could be a rather robust machine, relatively "resistant" to small changes in some of its components. c) The most interesting point, however, is the similar result with synonymous and non synonymous mutations. That is, I believe, really unexpected. And it could have important consequences on many common assumptions. Well, we certainly knew that sometimes synonymous mutations can cause phenotypic differences, probably through modifications of the mRNA structure. But who would have said that practically all of them have a slightly negative effect? Comparable with that observed in non synonymous mutations? I wonder if that could cause some review in the theories about molecular clocks, for instance. Anther possible consequence is: the functional information in the protein coding gene could definitely be higher than in the final protein. I will explain that better. We have usually assumed that reasoning about the protein was grossly equivalent to reasoning about the protein coding gene, at least in terms of final function. But if synonymous mutations consistently influence the final function, then the functional space of the gene is definitely smaller than we could think, and therefore the dFSCI in the gene is higher than the dFSCI in the protein, because it is constrained not only by the final sequence of aminoacids to be obtained, but also by the necessity to correctly control the mRNA phase of translation and its regulation. That could be an important concept for ID. Finally, I have a question which is probably of some importance. Given that most mutations explored here are "slightly negative", have we any idea of how much they could be "seen" by negative NS? IOWs, would the mutated strains be eliminated in a lab system with a mixed population? And in the wild? I think this are important questions, and objective answers are needed to understand what really happens in this "most common" case. Again, the problem is the difference between artificial selection (measuring fitness) and NS (just observing if a fitness difference is tolerated, eliminated or even expanded in a natural, or quasi natural, setting). I somebody has access to the full article, he could maybe check how fitness was measured, and if any information about "natural" fitness behaviour is given.gpuccio_{November 6, 2010
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