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Recent papers confirm that genetic entropy decreases fitness

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entropy illustrated

Over at Creation-Evolution Headlines, Dave Coppedge reports that two recent journal article’s have confirmed Cornell’s John Sanford’s “genetic entropy”: An accumulation of mutations always decreases fitness (contrary to neo-Darwinists’ hopes):

For mutations under epistasis to produce innovation, there must be a way for them to work together (synergistic epistasis). This is often assumed but has not been observed. Most experiments have shown beneficial mutations working against each other (antagonistic epistasis; see 12/14/2006), or causing even less fitness than if they acted alone (decompensatory epistasis; see 10/19/2004). In a new paper in Science,3 Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.

Diminishing returns?

Like this, for example?: An increased number of spelling errors in a letter retyped in series by a number of different people does not add up to a new, better letter over time?

Coppedge also notes the way the science media handled the news, for example:

“The more mutations the researchers added, the more they interfered with each other,” was one of the “surprising” results.

Surprising to whom? Not to Dembski and other members of the No Free Lunch club.

Follow UD News for breaking news on the design controversy.

Comments
DrREC you state: 'So I’ve passed your test. Happy?' Actually no you haven't passed the test; When the sensitivity of the test is cranked up, genetic entropy holds!!! Testing the Biological Fitness of Antibiotic Resistant Bacteria – 2008 Initially, it was difficult to demonstrate differences between wild-type and clinical strains in a rich media (Nutrient or Typticase-soy agar). There were no differences in growth rate or colony size. However, after switching to minimal media and observing hourly, the differences were readily observed. http://www.answersingenesis.org/articles/aid/v2/n1/darwin-at-drugstore Also of interest DrREC, is that this 'law of diminishing returns with beneficial mutations due to negative epistasis' of Lenski's, is exactly the 'diminishing returns' we expect from a poly-functional constraint perspective!!! Poly-Functional Complexity equals Poly-Constrained Complexity http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjdoZmd2emZncQ “Whatever we may try to do within a given species, we soon reach limits which we cannot break through. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)-but no exit through that wall. Darwin’s gradualism is bounded by internal constraints, beyond which selection is useless.” R. Milner, Encyclopedia of Evolution (1990) Simplest Microbes More Complex than Thought - Dec. 2009 Excerpt: PhysOrg reported that a species of Mycoplasma,, “The bacteria appeared to be assembled in a far more complex way than had been thought.” Many molecules were found to have multiple functions: for instance, some enzymes could catalyze unrelated reactions, and some proteins were involved in multiple protein complexes." http://www.creationsafaris.com/crev200912.htm#20091229a DNA - Evolution Vs. Polyfuctionality - video http://www.metacafe.com/watch/4614519bornagain77
June 13, 2011
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diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation
and my previous answer to that was:
the question still stands…ever hear of Haldane’s dilemma? It takes a great many mutations to produce sight, for example, (although no one has any clue how many or what mutations produced sight) and with the rarity of beneficial mutations to begin with, coupled with the negative epistatic effect, how does anything evolve?
tsmith
June 13, 2011
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Science daily is not the scientific literature.
who cares? do you not understand a direct quote???tsmith
June 13, 2011
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DrRec wrote: "Again, fitness refers to fitness in the environment of selection. You are not naturally fit underwater. Fish are not fit on land. These are not arguments against evolution." Wouldn't we expect to find a really weak bacteria instead?oyer
June 13, 2011
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Science daily is not the scientific literature. From the Science papers: “These data support models in which negative epistasis contributes to declining rates of adaptation over time. ” “diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation.” declining rates of adaptation decelerating fitness gainsDrREC
June 13, 2011
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"(put more simply- alteration or ‘alternative splicing’ of a preexisting protein which allows the digestion of a ‘simple sugar’)," Bacteria are incapable of alternative splicing. Behe doesn't see a 'modification', he sees a novel binding site. ",,, DrREC if you think this actually added functional complexity/information over and above what was already present in the e-coli,,,, " That is Dr. Behe's conclusion. He calls it a gain-of-fct I agree with him. " that should read parent strain plus evolved ability is greater than parent strain alone, " In all cases, Behe is discussing gain-of-phenotype, where the parental has either no or very little function that is evolved by the progenitor. "Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video" Again, fitness refers to fitness in the environment of selection. You are not naturally fit underwater. Fish are not fit on land. These are not arguments against evolution. Some antibiotic resistant bacteria show no fitness cost in the absence of antibiotic. "we demonstrate that prolonged patient treatment can result in multidrug-resistant strains with no fitness defect and that strains with low- or no-cost resistance mutations are also the most frequent among clinical isolates." http://www.sciencemag.org/content/312/5782/1944.full So I've passed your test. Happy?DrREC
June 13, 2011
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are you just dispensing with the words “the rate of”? How can you conclude fitness is decreasing given the context of the news article, and the original publications?
apparently Dr. Cooper the author of those papers is too...tsmith
June 13, 2011
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DrREC, falsely states: 'It is perhaps ambiguous, but if you are interpreting that overall fitness is declining, you are wrong.' Slowly but surely Lenski's 'cuddled' e-coli, which Lenski dare not let compete with wild parent strain for they would be eliminated, are getting less and less fit than the parent strain. Even more crushing evidence can be gleaned from Lenski's long term evolution experiment on E-coli. Upon even closer inspection, it seems Lenski's 'cuddled' E. coli are actually headed for genetic meltdown instead of evolving into something, anything, better. New Work by Richard Lenski: Excerpt: Interestingly, in this paper they report that the E. coli strain became a “mutator.” That means it lost at least some of its ability to repair its DNA, so mutations are accumulating now at a rate about seventy times faster than normal. http://www.evolutionnews.org/2009/10/new_work_by_richard_lenski.htmlbornagain77
June 13, 2011
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tsmith-are you just dispensing with the words "the rate of"? How can you conclude fitness is decreasing given the context of the news article, and the original publications? Maybe you can't get the publications free, but at least read the abstracts, or at the very least, the quotes I've provided you!DrREC
June 13, 2011
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DrRec wrote: "No kidding, animals living on land have lost the ability to breathe underwater, too" Soooo....if a pop of bacteria keeps losing functional elements the"ll gain the ability to walk like us?oyer
June 13, 2011
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of course Cooper's statement of the fitness declining over time fits in well with the following from the article I posted earlier...
Threshold robustness is inherently epistatic— once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.
tsmith
June 13, 2011
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"These results point us toward expecting to see the rate of a population's fitness declining over time even with the continual addition of new beneficial mutations," he said. "As we sometimes see in sports, a group of individual stars doesn't necessarily make a great team."
notice the quotes...and HE SAID...tsmith
June 13, 2011
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The original papers, not Science Daily are the authority on this. The wording and context in them is 100% unambiguous.
oh please...this is a direct quote from cooper.
the transcriber missed it
again its not transcribed...its a direct quote from cooper himself.tsmith
June 13, 2011
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DrREC, if you honestly think that this variation (which is questionable as to its 'randomness),,,
“An interesting variation on this pattern is reported in Chapter 5 by Lin and Wu (1984). Mutants of E. coli and S. typhimurium (S. enterica var Typhimurium) gain the ability to metabolize the unusual substrate d-arabinose by altering the specificity of a regulatory protein. …because the protein has apparently gained an additional binding site for the novel substrate, the mutation is classed as gain-of-FCT.”
(put more simply- alteration or 'alternative splicing' of a preexisting protein which allows the digestion of a 'simple sugar'), ,,, DrREC if you think this actually added functional complexity/information over and above what was already present in the e-coli,,,, then in order to validate your claim that this is the type of proof that you need in order to make your case for neo-Darwinian evolution, then what you are claiming is happening should look something like this: ,,,parent e-coli plus evolved ability to digest a novel 'simple sugar' is greater than the ability that was originally present in parent e-coli alone,,, Is this or is this not what you are claiming for neo-Darwinian abilities??? If you agree that you are claiming that simple should 'evolve' into more complex, then DrREC, why is it whenever we test any of these 'beneficial adaptations', that should read parent strain plus evolved ability is greater than parent strain alone, according to your neo-Darwinian reasoning, why do we find, after literally millions upon millions of tests, that parent strain plus evolved ability is LESS THAN parent strain alone???,,, thus completely contradicting neo-Darwinian reasoning!!! Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video http://www.metacafe.com/watch/3995248 Testing the Biological Fitness of Antibiotic Resistant Bacteria - 2008 http://www.answersingenesis.org/articles/aid/v2/n1/darwin-at-drugstore Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology Excerpt: it (an antibiotic resistant bacterium) reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution. http://www.evolutionnews.org/2010/03/thank_goodness_the_ncse_is_wro.html List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria: http://www.trueorigin.org/bacteria01.asp further note as to the severe limit of neo-Darwinian processes ever generating protein-protein binding sites; 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). http://creation.com/review-michael-behe-edge-of-evolution Dr. Behe states in The Edge of Evolution on page 135: "Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would actually explain the generation of the complex molecular machinery we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite." That order of difficulty is put at 10^20 replications of the malarial parasite by Dr. Behe. This number comes from direct empirical observation. 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. http://www.evolutionnews.org/2009/10/richard_dawkins_the_greatest_s.html An Atheist Interviews Michael Behe About "The Edge Of Evolution" - video http://www.in.com/videos/watchvideo-bloggingheads-interview-with-michael-behe-4734623.html 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 for explaining the diversification of all life on earth, of Genetic Entropy, a rule which draws 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."bornagain77
June 13, 2011
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I’m not sure what the other references are for. I’m not denying epistasis.
just more support to genetic entropy... I find the one from nature interesting because it seems there is a certain amount of mutations that are tolerated...until a certain point is crossed. the other one is interesting because of the following:
Synthetic lethals represented 50% of the latter. In a second set of experiments, 15 genotypes carrying pairs of beneficial mutations were also created. In this case, all significant interactions were antagonistic
these are just pairs of beneficial mutations...and such poor results...tsmith
June 13, 2011
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interview=interviewee. oops.Elizabeth Liddle
June 13, 2011
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It's a direct quote from an interview apparently: "These results point us toward expecting to see the rate of a population's fitness declining over time even with the continual addition of new beneficial mutations," he said. "As we sometimes see in sports, a group of individual stars doesn't necessarily make a great team." But either interview missed out a word (easily done), or the transcriber missed it. "rate..of fitness" doesn't make sense. Fitness is a scalar, it doesn't have a rate. It must be a rate of change of fitness, and in the context, only rate of increase makes sense.Elizabeth Liddle
June 13, 2011
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It is perhaps ambiguous, but if you are interpreting that overall fitness is declining, you are wrong. The original papers, not Science Daily are the authority on this. The wording and context in them is 100% unambiguous. “These data support models in which negative epistasis contributes to declining rates of adaptation over time. ” “diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation.”DrREC
June 13, 2011
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I don’t know where that quote came from. It is not in the papers.
its from: http://www.sciencedaily.com/releases/2011/06/110602143202.htm I think it means just what it says...tsmith
June 13, 2011
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tsmith, I don't know where that quote came from. It is not in the papers. There, it is abundantly clear the authors would mean: ...the rate at which a population’s fitness increases declining over time even with the continual addition of new beneficial mutations. As the papers say: "These data support models in which negative epistasis contributes to declining rates of adaptation over time. " "diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation." I'm not sure what the other references are for. I'm not denying epistasis.DrREC
June 13, 2011
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BA77: I think you could be a little more polite (1 Peter 3:15)... "Elizabeth, ignoring your blatant ‘excuse mongering’ in the main of your post, let’s just look at your cited claim for a beneficial mutation:" Such flamboyant language actually detracts from your argument -- imo at least...NZer
June 13, 2011
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I assume that means: "...the rate of a population's fitness increase declining over time..." Or conceivably "decrease". But it doesn't parse as written, so there must be a word missing. But if a rate-of-increase declines, that doesn't mean it decreases, unless the rate goes negative. In fact a decline in rate-of-increase makes sense; at some point a ceiling must be reached, certainly if resources are finite.Elizabeth Liddle
June 13, 2011
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The rate, not overall fitness. Fitness is improving, that rate just slows over time.
I do think you missed this part of the quote... “These results point us toward expecting to see the rate of a population’s fitness declining over time even with the continual addition of new beneficial mutations,”tsmith
June 13, 2011
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Subjecting TEM-1 to random mutational drift and purifying selection (to purge deleterious mutations) produced changes in its fitness landscape indicative of negative epistasis; that is, the combined deleterious effects of mutations were, on average, larger than expected from the multiplication of their individual effects. As observed in computational systems, negative epistasis was tightly associated with higher tolerance to mutations (robustness). Thus, under a low selection pressure, a large fraction of mutations was initially tolerated (high robustness), but as mutations accumulated, their fitness toll increased, resulting in the observed negative epistasis. These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness. Threshold robustness is inherently epistatic—once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.
rshtein et al, “Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein,” Nature 444, 929-932 (14 December 2006) | doi:10.1038/nature05385.tsmith
June 13, 2011
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a few earlier studies produced rather interesting results...
The tendency for genetic architectures to exhibit epistasis among mutations plays a central role in the modern synthesis of evolutionary biology and in theoretical descriptions of many evolutionary processes. Nevertheless, few studies unquestionably show whether, and how, mutations typically interact. Beneficial mutations are especially difficult to identify because of their scarcity. Consequently, epistasis among pairs of this important class of mutations has, to our knowledge, never before been explored. Interactions among genome components should be of special relevance in compacted genomes such as those of RNA viruses. To tackle these issues, we first generated 47 genotypes of vesicular stomatitis virus carrying pairs of nucleotide substitution mutations whose separated and combined deleterious effects on fitness were determined. Several pairs exhibited significant interactions for fitness, including antagonistic and synergistic epistasis. Synthetic lethals represented 50% of the latter. In a second set of experiments, 15 genotypes carrying pairs of beneficial mutations were also created. In this case, all significant interactions were antagonistic. Our results show that the architecture of the fitness depends on complex interactions among genome components.
http://www.pnas.org/content/101/43/15376.abstracttsmith
June 13, 2011
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The rate, not overall fitness. Fitness is improving, that rate just slows over time.
the question still stands...ever hear of Haldane's dilemma? It takes a great many mutations to produce sight, for example, (although no one has any clue how many or what mutations produced sight) and with the rarity of beneficial mutations to begin with, coupled with the negative epistatic effect, how does anything evolve?tsmith
June 13, 2011
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bornagain77 @22 Citing Behe's review without reading it might not be the best idea. Where you claim "you ain’t got ANY evidence for mutations that build functional complexity/information" Behe lists a number of 'gain-of-FCT' mutations. "An interesting variation on this pattern is reported in Chapter 5 by Lin and Wu (1984). Mutants of E. coli and S. typhimurium (S. enterica var Typhimurium) gain the ability to metabolize the unusual substrate d-arabinose by altering the specificity of a regulatory protein. ...because the protein has apparently gained an additional binding site for the novel substrate, the mutation is classed as gain-of-FCT." "Both the 6-nucleotide deletion and the 14-nucleotide duplication are gain-of-FCT mutations since they both produced new coded molecular features in the virus that did not exist in the immediate precursor...." So, even Behe (with his odd definition, where what look like totally novel functions still get lumped in as 'modifications of function') has to acknowledge the direct observation of gain-of-FCT mutations that increase fitness! Several of Lenski's have the potential to fall in this class as well-that appeared as unknowns in Behe's review. Now, this is a pretty tough definition, with Behe selecting very carefully. But even he can't deny the novel functional information emerging from these evolution experiments.DrREC
June 13, 2011
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DrREC, your whole problem is that you have to show a GAIN in functional complexity/information over what is already present yet,,, Michael Behe’s Quarterly Review of Biology Paper Critiques Richard Lenski’s E. Coli Evolution Experiments – December 2010 Excerpt: After reviewing the results of Lenski’s research, Behe concludes that the observed adaptive mutations all entail either loss or modification–but not gain–of Functional Coding ElemenTs (FCTs) ,,, you ain't got ANY evidence for mutations that build functional complexity/information!!! So, even though you make lame excuses as to why we ALWAYS observe loss of function/information mutations, and how that consistent loss is compatible with neo-Darwinian evolution, the plain fact is that you are blatantly ignoring the fact that you DON"T have the types of complexity building 'beneficial' mutations that you absolutely need to make evolution work!!!bornagain77
June 13, 2011
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tsmith @ 18: The key phrase is : "the rate of a population’s fitness declining over time" The rate, not overall fitness. Fitness is improving, that rate just slows over time.DrREC
June 13, 2011
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"Mutants of E. coli obtained after 20,000 generations at 37°C were less “fit” than the wild-type strain when cultivated at either 20°C or 42°C. Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates. .... Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment." So, E. coli grown at 37 lose ability to grow at cold or hot temperatures. E. coli grown on glucose lose other pathways. No kidding. Animals living on land have lost the ability to breath underwater, too. Natural selection selects for fitness only in the environment that the selection occurred in. Organisms growing in a yellowstone hot spring are poorly adapted to your refrigerator. Fish are poorly adapted to life on land. Now, if that environment changes frequently, the organism might appear robust and adaptable. If it is constant, that organism will lose adaptability to other environments. This is likely why wild organisms deal with differing conditions better than ones grown in a lab under a single condition. You're actually making an interesting anti-design argument. 'Front-loading' would fail, because the 'front-loaded' information would be lost if not used and selected for.DrREC
June 13, 2011
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