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Darwinists are Always Surprised

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Here’s a study on E. Coli. They force the bacteria to “mutate” to process glycerol. After six days, sure enough, a kinase shows up to handle the glycerol. But what is a “surprise” is that RNA polymerase shows up besides. It seems that two simultaneous mutations took place. But, of course, this is ONLY a surprise if you think RM+NS brought it about.

The authors say:

Mutations also appeared in a second, unrelated gene for an enzyme called RNA polymerase. “That was a surprise to almost everybody because RNA polymerase is involved in one of the core processes of any cell,” said Palsson. “You wouldn’t expect that gene to change because a wide variety of cellular process would be affected; it’s like replacing the wiring system in a building when a light bulb burns out. But we repeated the experiment more than 50 times and mutations in the RNA polymerase gene appeared again and again.”

I also enjoy the hesitation you almost hear as the reporter has to backtrack somewhat from RM+NS (listen for the word “presumably”):

All the mutants arose in the experiments presumably as the result of naturally occurring errors in copying DNA into daughter cells during cell division.

We here at UD have a better idea about what’s going on.

Here’s the link to the article.

By the way, some time back, in a heated debate over bacterial mutation and point mutations, I calculated that the amount of bacteria needed to provide TWO simultaneous point mutations simply through random chance would be so large that the known universe couldn’t contain it. I’m sure my calculation was off somewhere, but I think you get the picture: two genes being affected simultaneously is something that cannot happen by chance alone.

Comments
I'm also hesitant to claim this change wasn't due to NDE without knowing all the details involved. Many here have jumped straight to the assumption that CSI is involved without first using the EF. Changes, however striking, that appear by natural necessity and are therefore highly probable don't end up at the filter's design node. This find may be in the same category as that nylon-eating enzyme discussed a while back.Patrick
November 7, 2006
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Joseph- re: "I don’t have access to the paper so could you please tell me if the the two genes were the same but the mutations to those genes different?" There are two different genes involved, both found mutated in survivors. In different E. coli survivors, the genes have distinct(different) mutations.RobertC
November 7, 2006
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Robert C- I am partial to design solutions exemplified by the Feb 2003 SciAm article "Evolving Inventions". That would explain why the solutions differ and why some don't find the solution in time. However the goal in this experiment would be the survival of the population. And sometimes that occurs at the expense of a few or even many individuals. I don't have access to the paper so could you please tell me if the the two genes were the same but the mutations to those genes different?Joseph
November 7, 2006
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@RobertC: I don't know the specifics of this search problem's combinatorial complexity, so I'm speaking generally. When we see a chance event occuring that shouldn't have enough replicational resources to get "lucky" enough, (the odds are stacked against us enough to not expect random success), and when this occurs over and over again, then we have evidence of non-random processes taking place. In this specific situation, maybe there were enough bacteria to randomly get one error needed to make the first enzyme, but when you also have the second one occuring, it makes the combined probablility out of the expectation of random chance guessing. (According to PaV.) It is then legitimate to look for non-chance processes, such as guided genome engineering.Atom
November 7, 2006
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The article also makes a point about how we can witness change occuring in these bacteria in real time, "evolution" as the scientists interviewed referred to it. (Making a polemical point agianst those who don't accept NDE). Anyway, as another author once brought up, NDE advocates often say that evolution occurs much too slowly to witness directly, yet too fast to be preserved faithfully in the fossil record. (A convienient position, I'm sure.) But why should that be the case? With organisms like fruit flies and bacteria, that reproduce in large numbers quickly, why shouldn't we be able to view large scale change? What first principles of biology would make that a logical impossibility? The fact that we've yet to witness novel cell types, tissue types, organs and body plans develop is telling. If directional, CSI-rich change is really due to DNA copying errors, then the more copies, the more expected change, right? Why then don't we ever witness large-scale changes (cell types, tissue types, organs, body plans)? (Sorry mods if this is off topic, but it is a question that seems related to issues of telic vs. random change.)Atom
November 7, 2006
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I suppose this proposed system would be sort of like the immune system, which has to adequately respond to all sorts of combinations in order to be effective. As such, a "solution set" might include multiple approaches that would end in the same or similar result.Patrick
November 7, 2006
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Atom, Re: "if solutions are found much faster than we’d expect from random guessing" What would you expect from random guessing. How fast is evidence of design? This study lasted 44 days (660 generations), where 10^7 bacteria were passaged daily. From the few 'winners,' the authors conclude 1.8x10^-11 beneficial mutations are fixed per genome per generation. Is this quick? (I'm not being sarcastic, I honestly want a number placed on what would be a detection of non-random sampling.RobertC
November 7, 2006
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@Robert, in regards to #1: Since we basically have a search problem, if solutions are found much faster than we'd expect from random guessing, we know that something non-random is occuring. When searching large spaces and finding very small targets within those spaces, consistently and quickly, we then have even greater suspicion to suspect the use of heuristics, rather than random sampling. And heuristic mechanisms are signs of design. (See Dembski's displacement argument to see why randomly finding a suitable heuristic is harder than simply finding your original target.)Atom
November 7, 2006
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DaveScot, RE: "If the product is substantially different every time then the toolkit hypothesis isn’t supported" From the sequencing of the E. coli that grows fast on glycerol, the authors conclude "We identified 13 different de novo mutations in five different E. coli strains and monitored their fixation over a 44-d period of adaptation." Not all confer the same level of fitness-and most affect different amino acids in the kinase or the polymerase. It also reads that some of the mutations happen first, followed by the second-not simultaneously. Lastly, very few of the E. coli are surviors. I wonder if Eukaryotes are a better place to look for such a toolkit-multi-domain proteins, with recobination between them?RobertC
November 7, 2006
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RobertC I don't have a subscription to Nature. If the product is substantially different every time then the toolkit hypothesis isn't supported. The hypothetical toolkit is something of a holy grail where biologically useful proteins are constructed from a finite subset of building blocks larger than individual amino acids but smaller than typical whole proteins. Since we don't know how to predict protein folding building blocks that produce the same major and minor biologically active sites needn't have remarkably similar sequences but still be components that produce the same topography in the final product. We might not be able to recognize it until we learn how to predict protein folding. Or it may not exist at all. I believe IBM has done more work than anyone else in looking for repeating patterns that could be a set of building blocks for genes. IIRC they haven't found anything significant in that regard.DaveScot
November 7, 2006
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I'm fascinated by the idea of a "enzyme design toolkit," but I have a few questions. 1) If the mechanism of the "toolkit" is mutation at the DNA level, how is it distinguished from random mutation? 2) I read the Nature genetics paper. The commenters here seem to suggest the SAME modification happens each time. Acutally, there are an array of different mutations/modifications that make a 'faster' glycerol kinase, and more polymerase. Is this variety 'random' or a predicted by frontloading? 3) It seems like the solutions are not universal-as the mutant/modified outcompete the others. Why does the 'toolkit' fail to fire in some clones, but succeeds in others?RobertC
November 7, 2006
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"It seems that two simultaneous mutations took place." Im curious as to what you mean by simultaneous, because if it means two mutations occuring simultaneously in the same organism I can't see any evidence for that here.Chris Hyland
November 7, 2006
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Can anyone explain to me how this experiment proves evolution ?...Sladjo
November 7, 2006
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Atom, I'm trying to figure out an ID research plan here, rather than simply making pronunciations of design. Perhaps the next time the Templeton Foundation comes around offering money, ID scientists will have be able to put forth some concrete ideas. We also don't know whether the mutations were the same in the replications of the experiment (though someone with full access to the paper could tell us). We only know that mutations occurred in two different genes, and often in conjunction.
But we repeated the experiment more than 50 times and mutations in the RNA polymerase gene appeared again and again." The researchers report that mutations in both genes appeared together in several cases after six to eight days in the glycerol-based cultures, and E. coli cells containing both mutated genes grew 150 percent faster than the starting strain of E. coli.
HodorH
November 7, 2006
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HodorH, RM is just that: Random. This is statistically NOT random, since the same solution appears with the same side effect mutation. In other words, engineering on the cellular level, not random mutation, is what is responsible. Bacteria apparently have the ability to actively change their genomes to meet pressures, rather for waiting around passively for "random mutations" to occur (or not occur). Darwinists are surprised, because RM+NS (the bedrock of NDE) is not responsible for directed change. Something more telic apparently is.Atom
November 7, 2006
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DS- If the solution is passed to the other cells then it would have to be on some form of mobile DNA. I don't have access to the paper, but it sounds like the changes were chromosomal. The passing on of the solution to others is readily testable, though. Just generate some "improved" bacteria and mark an unrelated gene so that its decendents are traceable, then drop it in a culture with regular bacteria under selection (high glycerol) conditions. Wait a couple days, test a bunch of clones for the traceable marker (as well as the presumably selectable mutations). If the information is passed, then most clones should NOT have the marker, whereas if it is strictly inherited, they will. Aside from that, except for extensive use of telic language, I don't really see how your scenario is distinguishable from normal mutation and selection scenarios.HodorH
November 7, 2006
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Hodor If the cells are frontloaded, then all or most should experience the mutation upon replication. No. The cells are probably front-loaded with some sort of enzyme design toolkit. Under stress they all start working to build a new enzyme and when one of them succeeds it passes the solution along to the others. If the toolkits are all the same and the solution is something that can be built with it then it's just a matter of time before the solution emerges (or they all die before the first one of them has time to discover it). If there's only one solution possible and the order in which trial balloons are constructed is the same then the observed result should be the same enyzme emerging over and over again in approximately the same length of time.DaveScot
November 7, 2006
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rrf The designer isn't intervening. Obviously since the same enzyme keeps "evolving" over and over again in a matter of days (the experiment was repeated 50 times) it isn't appearing de novo but exists in some form where its emergence is inevitable. That's not evolution. Evolution isn't supposed to be repeatable like that. If you didn't know that you really shouldn't be commenting here.DaveScot
November 7, 2006
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It’s a “pre-programmed response” on the part of the organism.
Well, then this would represent an opportunity for some real ID/frontloading research. If the cells are frontloaded, then all or most should experience the mutation upon replication. Conversely, RM/NS would predict that the population of new and improved bacteria arose from a single mutant (or one mutant followed by another, since there are apparently 2 mutations). I think this is a doable experiment -- I'll think about how it would be done.HodorH
November 7, 2006
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Benjy_Compson: "Would you please spell it out? " It's a "pre-programmed response" on the part of the organism.PaV
November 7, 2006
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JFD: No, it seems the RNA polymerase is used to speed up the production of the glycerol kinase. The bacteria would die without the presence of some RNA polymerase. These two mutations worked in tandem to simultaneously produce the kinase and "extra" production of RNA polymerase. That's how I read the resume of the article.PaV
November 7, 2006
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A guestion, When the bacteria was forced to mutate was the second mutation a response by the bacteria so the first mutation would not be destructive? Was the second mutation a way to preserve itself?JFD
November 7, 2006
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When you said that UD has a better explanation for what is going on, I assume you mean that the RNA polymerase mutation was the result of Intelligent Design. Interesting! Do you have any thoughts why the Designer is intervening in what seems a routine experiment on E. Coli? This could be a really fruitful avenue of scientific research for the ID community.rrf
November 7, 2006
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PaV: "I calculated that the amount of bacteria needed to provide TWO simultaneous point mutations simply through random chance would be so large that the known universe couldn’t contain it. " Perhaps you are already aware of this but there is experimental evidence to confirm your suspicions - see the link below and click onto 'What Can Evolution Really Do?' http://www2.uwsuper.edu/rseelke/index.htm Bottom line: under the RM&NS paradigm, evolution can only plausibly plod on one little step at a time.antg
November 7, 2006
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We here at UD have a better idea about what’s going on.
Would you please spell it out?Benjy_Compson
November 7, 2006
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It’s just a matter of time till this is spun and heralded as “proof” of evolution. Everything is proof of evolution – everything but the actual evidence. That’s just an inconvenience though.shaner74
November 6, 2006
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Atom, "Self-genetic engineering." In light of the repeatability of this experiment, that does seem to be Ockham's explanation.bFast
November 6, 2006
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Did anyone read the article on epigenetic effects in mice defied the paradigm of genetic mutation. I think in the latest or last months edition of Discover. It was a very interesting surprise that contradicted a deleterious mutation as the culprit of certain deleterious & heritable trait.JGuy
November 6, 2006
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Given how repeatable this experiment apparently is, i'll be interested to see what is going on when they pick apart what is going on in more detail.jwrennie
November 6, 2006
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Self-genetic engineering.Atom
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