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First paragraph of Lenski paper contains an error

I started reading Lenski’s full paper myself to see what raw data was provided and I got no farther than the first paragraph beyond the abstract when I encountered a bias error that a chance worshipper would never notice. My emphasis:

At its core, evolution involves a profound tension between
random and deterministic processes. Natural selection
works systematically to adapt populations to their prevailing
environments. However, selection requires heritable variation
generated by random mutation
, and even beneficial mutations
may be lost by random drift. Moreover, random and deterministic
processes become intertwined over time such that future
alternatives may be contingent on the prior history of an evolving
population.

The bold portion is patently wrong. Selection operates on any heritable variation whether random or not. That the authors would use the language they did (random variation) and the peer reviewers didn’t notice it is testimony to the chance worshipper bias that pervades evolution
research.

I would refer Lenski et al to a Scripps Institute experiment with E. coli that Bill Dembski blogged here on Uncommon Descent over 3 years ago:

To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists

The Scripps researchers, in a nutshell, discovered that E. coli, when stressed (such as running out of food as in Lenski’s experiment or in the presence of antibiotics in the Scripps experiment) selectively increases the mutation rate on certain genes. Thus the mutations in this case are not random but rather directed at a certain area in an attempt to solve a certain problem. Lenski should have have been aware of this but even if he weren’t he should have known just by definition alone selection can operate on any heritable change no matter how the change happened.

Chance worshipping causes science to have blind spots like this. Perhaps if they’d read the book:

Science’s Blind Spot: The Unseen Religion of Scientific Naturalism

written by my friend Cornelius G. Hunter they wouldn’t make these kinds of simple, obvious mistakes. But NOOOOOOO… Hunter and Dembski are both knuckle-dragging ID creationists so what would they know about any of this?

I believe the peanut gallery, in their latest fashion in phraseology, would summarize this as:

Lenski FAIL.

But they won’t because they’re living in denial of their own failings.

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62 Responses to First paragraph of Lenski paper contains an error

  1. I thought there were 47 sources of variation. Larry Moran blasted “IDiots” for not crediting these other engines of evolution. Is Lenski saying that in his decade or so of e-coli evolution, none of these other sources of variation played a significant role? Mike Behe has been blasted for not giving these other sources of variation their due, but isn’t Lenski discounting them as well?

  2. Or, like Behe, Lenski could be using “random mutations” to encapsulate all non-foresighted sources of variation.

    In any case, there is a double standard at work.

  3. Hmm. Now, if I started throwing paper aeroplanes at Texas, in Might hit Dave. I’m sure I we would all agree that that would be random. Now, if I doubled the rate at which I threw paper aeroplanes, would hitting Dave now be non-random?

    The bacterium is doing the same thing: it increases the rate of mutation. It’s only non-random for a narrow definition of random that would exclude everything except rolled dice, tossed coins and possibly radioactive decay.

  4. Or like Moran and McNeill and all the other chance worshippers know very well that mutations of an ultimately random nature are all their dogmatic view of organic evolution allows them to consider. They’re lying through their teeth when they say that random mutations are not the ultimate source of all variation and casual mistakes like Lenski made that I spotted betray their belief system to attentive readers not indoctrinated in their pseudo-religious evolutionary narrative.

  5. Bob

    The mere fact that you’re throwing paper airplanes at Texas instead of New Jersey when it’s me you want to hit makes it something less than random throws. You are using foreknowledge of how to better your odds of hitting me. Is there something about that you don’t understand? If so I’ll see if I can find a kindergarten teacher to explain it to you as I have too little patience at explaining to adults what should be obvious even to a young child.

  6. Dave-
    Maybe that kindergarten teacher could help you with reading comprehension. Bob O’H said he was throwing paper airplanes at Texas, not that he was trying to hit you.
    Compare Bob O’H's original:

    Now, if I started throwing paper aeroplanes at Texas, in Might hit Dave.

    with your inadvertent misrepresentation:

    The mere fact that you’re throwing paper airplanes at Texas instead of New Jersey when it’s me you want to hit makes it something less than random throws.

  7. Congregate

    Bob mentioned me by name and associated me with Texas. That is foreknowledge.

    That’s beside the point in any case as I explained in the article. Even if Lenski wasn’t aware of the Scripps research he should know that selection can operate on mutations whether they are random or directed. Do you disagree with that?

  8. Dave,

    This post hits right at the center of the problem with most Science® and Reason™ zealots – this isn’t ‘A’ blind spot, it is ‘THE’ blind spot.

    The chance crowd is generally unaware of nor can elucidate the epistemological underpinnings of the arguments they make.

    It never ceases to amaze when chest thumpers bray about their devotion to the Truth© through Reason™ and Science® while displaying such fundamental ignorance of basic logic.

    That the question “What is Science?” cannot be answered scientifically is the first clue Science® is not an ultimate in understanding our experience in space & time. Ever try to get a Science® zealot to see their own philosophy?

    Looking at the first paragraph you quoted, Lenski writes “Natural selection works systematically to adapt populations to their prevailing environments.” I don’t want to be picky, but isn’t ‘selection’ something only performed by intelligent agency? Did the Colorado river ‘select’ its path which led the formation of the Grand Canyon? Even laying that aside, isn’t systematic work a product of teleology? The wording also seems backward – is it more correct to say populations adapt to environments?

  9. 9

    DaveScot said in the original post,

    The Scripps researchers, in a nutshell, discovered that E. coli, when stressed (such as running out of food as in Lenski’s experiment or in the presence of antibiotics in the Scripps experiment) selectively increases the mutation rate on certain genes. (emphasis added)

    How does running out of food increase the mutation rate on certain genes? I think that running out of food has the opposite effect. Errors in gene duplication during reproduction are a major source of mutations, and running out of food prevents reproduction.

    It appears to me that the glucose cycling (giving the bacteria insufficient glucose so that there are alternating periods of glucose feeding and glucose starvation) favored the evolution of citrate-eating bacteria in Lenski’s experiment in the following ways:

    (1) The glucose feeding period allows “silent” (unexpressed) mutations during reproduction in the bacteria that can eat only glucose, and

    (2) The glucose starvation period gives an advantage to Cit+ (citrate-eating) bacteria because they can continue to reproduce while the glucose-eating-only bacteria cannot.

    On Carl Zimmer’s “The Loom” blog, I asked Zachary Blount, the lead co-author of the paper, if a purpose of the glucose cycling was to favor Cit+ evolution, and he refused to answer. IMO when an author of a paper refuses to give straight answers to simple, basic questions about it, the paper has no credibility.

  10. I don’t understand the controversy.

    Is there something special about this mutation that contradicts Behe’s hypothesis regarding mutations rates and the need for multiple simultaneous mutations to reach novel beneficial functions?

    It certainly doesn’t appear so.

  11. I am sorry to tell you, DaveScot, that the error is yours.

    You misrepresented the work done in the Scripps Institute’s research. They did not find that E. coli was able to cause the mutation of a specific gene or even gene locus. What they found, was that E. coli can, when experiencing periods of stress, influence DNA repair machinery to increase the general mutation rate.

    The mutations are still random, but by allowing the rate (key word) of mutations to remain high, bacterial populations have more diversity so that, when in the presence of antibiotics (or other stresses) some of the individuals that happen to have evolved resistance can be selected for.

    It is a common mistake to associate evolution with the teleological. E. coli don’t choose to evolve any more than the earth chooses to revolve around the sun. The simple fact is that a behavior is beneficial to reproduction (and spreading of genes) than it can be selected for.

    If you have further comments or questions about your mistake (which I hope you will correct in the interest of academic integrity) please visit my blog and post a comment (I have recently made a post about this very entry)

    http://blogs.scienceforums.net/ecoli

  12. 12

    todd said (#8) –

    Looking at the first paragraph you quoted, Lenski writes “Natural selection works systematically to adapt populations to their prevailing environments.” I don’t want to be picky, but isn’t ’selection’ something only performed by intelligent agency?

    I think that you are being too “picky.” The term “natural selection” uses the word “selection” in a figurative sense.

    Also, I think that the statement “Natural selection works systematically to adapt populations to their prevailing environments” is wrong. Natural selection often does not “adapt populations to their prevailing environments” but often causes extinctions or decimations of populations because of those populations’ failure to adapt to their environments.

    Anyway, I am bothered much less by inaccurate statements in the paper than I am by principal author Zachary Blount’s failure to give straight answers to simple, basic questions about the research.

  13. Good find Davy, I concur. Random mutation is a patently false umbrella to lump all mutations under. One of the main conceptual difficulties with using the word “random” to refer to beneficial mutations is the fact that under the Darwinian version of evolutionary theory, human beings are merely “evolved creatures” of and by natural selection and random mutation universally. The obvious problem here is that human beings do things “purposively” and hence are a contradictory example of Darwinian evolution “universally” acting in a “random” fashion on all life forms and things. The point is we can easily see, if from self phenomenological reflection alone, that oftentimes evolution is NOT heuristically random at all and hence the universal umbrella of random mutation thus becomes a question of “when is evolution acting purposively and when is it acting randomly?” Of course if we cannot explain a given event or structure via the virtue of a purely stochastic algorithm, then the word “random” as a descriptive designation for mutations must disappear from the gamut of possible explanatory tools. It just so happens that this is quite often the case.

    Human beings are not random- natural selection is not random- the mutations, as easily exemplified by the high ratio of negative to positive advantages passed onto living creature are not “random” either.

    Ergo, neither is the core driving force/s behind evolution.

    Here’s a not so random word of advice for all you Darwinists out there

    It’s about time you got another theory.

    I say, “The only thing random about life’s design is, perhaps, the theory of evolution itself.”

  14. Excellent observations, DaveScot. Chance worshipers is also funny.

    Chance is their God of the gaps.

    Have you guys seen the Lenski dialog at conservapedia?

  15. @10:

    Someone also made the point (in another thread) that flipping a coin is not random – that is just how we describe the probability. In reality the coin toss determined by the side it was flipped from, strength behind the flick, rotation, etc etc.

    Extrapolating, what ARE the actual mechanisms behind neo-darwinist evolution?

    They say ‘chance/random mutations’, but what are the supposed processes BEHIND the ‘chance’? Knowing that, we can work out what neo-Darwinism is capable of theoretically (I’m aware this is discussed heavily in EdgeoEvo, and elsewhere).

    Just from basic genetics, I can think of:
    -point mutations
    -deletions
    -insertions

    …what are the other Darwinistic processes that drive “chance/random mutation”?

  16. Ooooh. I also had a thought:

    At what point in our supposed ‘ancestors’ history did they (and all other animal species) develop a genetics system that actively INHIBITS random mutation? Because that makes it a whole lot harder to ‘evolve new species’.

    Is DNA/RNA transcription protection prevalent in bacteria/protzoa (similar to our DNA protection/correction mechanisms)?

    Sorry, I have no clue.

  17. Dave – my argument works no matter what I’m aiming at – I was just using hitting you as an example of something that might happen.

    The point is that the rate of mutation changes (so isn’t random), but what mutations actually occur, and where they occur in the region with the higher mutation rate, is random.

    BTW Dave, I was actually aiming at the clowns that keep on stalking you.

  18. Bob

    my argument works no matter what I’m aiming at

    Your argument doesn’t work if you’re aiming, period. Random mutations have no aim. In the case of E.coli‘s response to antibiotics the increased mutation rate is indeed aimed at something – finding a way to stop the antibiotic from killing it. It’s not a well targeted search but it is still targeted. If the increase in mutation rate occured randomly (for no particular reason) then your argument would work, but the increase in mutation rate is a response to a stimulus and that makes it not random.

    Let’s try a different example. Suppose some stalking clown throws, monkey-like, a handful of his own poop aimed directly at your pointy little head, Bob. You might respond by dodging to the left, dodging to the right, ducking down, or any combination thereof. The particular direction you move to avoid becoming a poopyhead might be random but the act of dodging itself is not random (unless you’re some kind of spastic that bobs and jinks around at random with no particular purpose).

    But this is still tangential to the point of my article which was to say that Lenski was flat out wrong to say that selection requires random mutations. I notice you haven’t disagreed with that. Good boy. You’re smarter than most of the peanut gallery which is why you continue to have a presence here. I note the peanut gallery is trying to say I’m pretending that this criticism of Lenski derails his whole paper. I made no such claim whatsoever. I merely pointed out that I didn’t get farther than the first paragraph before encountering an obvious error. I seriously doubt that this single brain fart of Lenski’s does much damage in an of itself to his methods or conclusions, it’s merely an early indicator of the kind of sloppy, biased thinking that went into it. Or maybe not. Maybe it’s an isolated error. Probably not, given the criticisms I’ve read and the basic sensationalist spin put on something that most bacteria are really good at – finding ways to eat things they normally don’t eat. This is hardly a surprising result. The most surprising thing is how LONG it took the bugs to find a way to digest citrate in an otherwise stress free environment. They only had one single challenge in their little lives and that was how to avoid starving after eating the low hanging fruit in the agar.

    On the matter of no one rushing in to independently duplicate or validate Lenski’s experiment I’ll concede that not much time has passed but I’ll still stand by the prediction that no one will bother no matter how much time passes. It’s just not important and not surprising. There’s nothing new or exciting about it. It’s like announcing that after 20 years of observation he found dirt and water make mud. The Cold Fusion annoucement I contrasted this with had teams all over the world on it like flies on garbage the day after it was announced. THAT claim WAS important and surprising if valid.

  19. Random mutations have no aim.

    Yes, that’s my point.

    In the case of E.coli’s response to antibiotics the increased mutation rate is indeed aimed at something

    Note what you wrote. it’s the rate of mutation that is increased. But the actual mutations are still random: the only difference is that there are more of them.

    But this is still tangential to the point of my article which was to say that Lenski was flat out wrong to say that selection requires random mutations.

    Well, where would the genetic variation come from if not through random mutation?

  20. ecoli

    Sorry, but the mistake is yours not mine.

    http://lib.bioinfo.pl/pmid:9192894/pmid/cit

    We have recently shown that the evolution of resistance to ciprofloxacin in vivo and in vitro requires the induction of a mutation that is mediated by the cleavage of the SOS repressor LexA and the associated derepression of three specialized DNA polymerases (polymerase II [Pol II], Pol IV, and Pol V).

    These are specialized polymerases. The mutation rate of the entire genome doesn’t increase, just the subsets of it that these particular polymerases work with.

    Nice try though. I suppose I can forgive you because the original Scripps paper made no mention of specificity in the mutation rate increase. I merely assumed by the mechanism they identified that it wasn’t going to be a genome-wide mutation increase. That would be rather stupid of the designer to do it that way. For instance, it wouldn’t be a good idea to start mutating the crap out of rDNA in response to stress. Some bits of DNA are far less tolerant of mutations than other bits.

    See, this is another example of science’s blind spot. From a design theoretic view I wouldn’t expect a designer to start mutating DNA that had no relation to the problem of toxins in the environment. Ribosomal DNA would be one example. Mutating that will almost certainly kill the organism and not solve the problem with the toxin. So we want to somehow protect that DNA from the increased mutation rate. As it turns out the assumption was correct and that was quickly discovered by Scripps about a year later. Pol III deals with rDNA and you’ll note from the referenced article Pol III is not in the list of specialized polymerases found to part of the LexA cascade.

    Take off the blinders, man. Life was designed. It’s a fruitful heuristic as I just demonstrated.

  21. Bob

    No, the mutations are not randomly increased over the entire genome. They’re targeted at where they are more likely to solve the problem versus making a bigger problem. See the comment to ecoli above. Is is even possible for you to admit when you’re wrong?

  22. Dave Scot

    ecoli is right and you are wrong. Obviously you are confusing DNA polymerase with RNA polymerase.

    DNA(!) Pol II, Pol IV, and Pol V are polymerases used by bacteria to replicate a damaged region of DNA and hence survive under adverse conditions.
    DNA polymerase III is part of the primary enzyme complex involved in bacterial DNA replication.

    “Pol III deals with rDNA…”

    Not really. That would be right for eucaryotic RNA (!) polymerase III which is required to synthesizes tRNAs, rRNA 5S and other small RNAs in eucaryotes.

  23. imsds

    I’ll concede the point that Pol III and rDNA exclusion was my mistake in the SOS response but you’re all still wrong that hypermutation in respones to stress is genome-wide.

    Hypermutation in bacteria and other cellular systems.

    B A Bridges
    MRC Cell Mutation Unit, University of Sussex, Brighton, UK. [email protected]

    In bacteria there are numerous examples of transient mutator states, often occurring as a consequence of stress. They may be targeted to certain regions of the DNA, for example by transcription or by recombination.

  24. imsds

    [even better] (everything below quoted, don’t want to waste time formatting)

    Starvation-associated mutation in Escherichia coli: a spontaneous lesion hypothesis for “directed” mutation.Bridges BA.
    MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.

    When stationary phase E. coli WU3610, carrying an ochre mutation in the tyrA gene, were incubated on plates lacking tyrosine, tyrosine-independent (Tyr+) mutants appeared from day 7 onwards in a time-dependent manner. These starvation-associated mutants did not contain either identifiable tRNA suppressors or reversions at the ochre site and are thus quite distinct from the mutants commonly found to arise during active growth. When an appropriate fluctuation assay protocol was employed slow growing Tyr+ mutants were also found to arise in growing cells, and their distribution was more characteristic of a replication-dependent than a time-dependent process. The rate of appearance of starvation-associated mutants at 37 degrees C was somewhat less than at 27 degrees C and this was attributed to a reduction in viability at the higher temperature. There was no evidence for the accumulation on the plates of mutations in other genes. Tyr+ mutants were, however, shown to arise during incubation of stationary phase cells under conditions where there was no selection for tyrosine independence, provided outgrowth was subsequently permitted on plates lacking tyrosine. This distinguishes the present system from those systems exhibiting genuine “directed” or “adaptive” mutation, should they exist. To explain the specificity which occurs, it is proposed that the appearance of stationary mutants in ochre strains reflects the time-dependent accumulation in the transcribed strand of a DNA lesion that has a high probability of miscoding during transcription and replication. A mutant RNA transcript permits protein synthesis which in turn triggers DNA replication. The mutation is then fixed in the DNA as a permanent heritable change. The apparent “directedness” of the process is, on this model, determined solely by the particular miscoding DNA lesion occurring in a transcribed strand at a site where a change in phenotype permits DNA replication to occur.

  25. and more

    Mechanisms of directed mutation.Foster PL, Cairns J.
    Department of Environmental Health, Boston University School of Public Health, Boston University School of Medicine, Massachusetts 02118.

    Spontaneous mutants arise among nondividing populations of Escherichia coli in apparent response to selective conditions. In this report we investigate several hypotheses to account for the role of selection in the production of these “directed” or “adaptive” mutations. We found that the Lac+ phenotypes of some mutants that arise late after lactose selection are due to suppressor mutations that are unlinked to the mutant lacZ allele; thus the production of these Lac+ mutants does not require an information flow from successful proteins back to the DNA that encodes them. Transcriptional induction of the lac operon, even in the presence of another, utilizable carbon source, did not stimulate the occurrence of Lac+ mutants in the absence of lactose, indicating that the role of the selective agent is not merely to induce transcription. The absence of two DNA repair pathways-methyl-directed mismatch repair and alkylation repair-also did not result in an accumulation of Lac+ mutants in the absence of lactose, suggesting that these repair pathways are not normally responsible for correcting transient variants that might arise in the absence of selection. However, in one case the Lac+ mutation is likely to be due to a miscoding lesion occurring on the nontranscribed DNA strand, indicating that, at least in this instance, DNA replication is required before directed mutations can arise.

  26. Oh my. I stumbled onto a huge controversy from decades past. Google Lenski and “directed mutation”. It seems Lenski, 15 years ago, was arguing that directed mutation didn’t exist. It’s pretty much accepted now. Evidently he still can’t bring himself to admit it and that’s why he wrote that selection requires *random* mutations. It wasn’t an innocent slip of tongue!

    This is why it was such a hot controversy:

    Directed Mutation
    Dear reader, things have a way of working out serially. For several months, we have had in our possession a paper from Nature, by J. Cairns, of Harvard, plus some passionate correspondence stimulated by the paper. Now that the circle-forming sheep have provided a good introduction, we will jump into the fray, too.

    Basically Cairns (in Nature) and B. H. Hall (in Genetics) say that organisms can respond to environmental stresses by reorganizing their genes in a purposeful way. Such “directed mutation” shifts the course of evolution in a nonrandom way.

    Such a conclusion was like waving a red flag in front of the evolutionists. R. May, at the University of Oxford, complained, “The work is so flawed, I am reluctant to comment.” On the other side, a University of Maryland geneticust, S. Benson, comments, “Many people have had such observations, but they have problems getting them published.”

    Our template in this discussion is an article by A.S. Moffat in American Scientist. She says, “The stakes in this dispute are high, indeed. If directed mutations are real, the explanations of evolutionary biology that depend on random events must be thrown out. This would have broad implications. For example, directed mutation would shatter the belief that organisms are related to some ancestor if they share traits. Instead, they may simply share exposure to the same environmental cues. Also, different organisms may have different mutation rates based on their ability to respond to the environment. And the discipline of molecular taxonomy, where an organism’s position on the evolutionary tree is fixed by comparing its genome to those of others, would need extreme revision.”

    What sort of experiment did Cairns do to cause such a ruckus? In particular, he studied E. Coli bacteria. Normally, these bacteria cannot metabolize the sugar lactose. Cairns exposed the E. Coli to a sudden dose of lactose, demonstrating that if the bacteria must have lactose to survive, they quickly cast off the two genes that inhibit their metabolizing of lactose. Of course, the experiments were more complicated than this, but the fundamental finding was that the bacteria mutated so that they could use lactose much, much faster than chance mutation would permit, stastically speaking.

    The battle lines are forming. A sup-porter of directed mutation, J. Shapiro, of the University of Chicago, is quoted as follows in Moffat’s article:

    “The genome is smart. It can respond to selective conditions. The signifi cance of the Cairns paper is not in the presentation of new data but in the framing of the questions and in changing the psychology of the situation. He has taken the question ‘Are mutations directed?’ which was taboo, and made it an issue that people will now do experiments on.”
    (Moffat, Anne Simon; “A Challenge to Evolutionary Biology,” American Scientist, 77:224, 1989.)

    It seems I’ve reopened a big can of worms that I wasn’t aware even existed. Fascinating.

  27. Directed vs. random mutation.

    There’s no controversy in evolution. Move along people, nothing to see here.

    ROFLMAO!

  28. For example, directed mutation would shatter the belief that organisms are related to some ancestor if they share traits. Instead, they may simply share exposure to the same environmental cues.

    Cool. It certainly doesn’t shatter my front-loaded ID hypothesis which requires trigger events for saltations into new (pre-planned) species.

    Nothing in evolution makes sense except in light of front loading.

  29. DaveScot –

    I apologise and stand corrected on the point of the gene specific directed mutation. I didn’t read subsequent papers, because the original news stories on the ‘Scripps study’ only referenced the one.

    However, this still does not point to the teleological: that E. coli are somehow deciding which gene locus to induce mutations.

    It is altogether possible that random mutation(s) produced a protein that, when under stress from a particular antibiotic, caused an increase in mutation rate in a gene specific region. Such random mutations would be selected for if the environmental pressures are present.

    The point being, if the source of proteins that can direct mutations are themselves produced by random mutations, then they can be understood by evolutionary theory.

    You’re assumption that E. coli are purposefully directing this mutation has NOT been demonstrated by any of the studies you have brought up so far. Nor can I imagine how one could prove that E. coli are self-directing mutations… where did this unique inhibitory proteins come from? If the answer is intelligent design, then there’s no way to prove that scientifically anyway, and I think you’ll have a hard time proving that the ultimate source was not evolution.

    At any rate, it is of little consequence that Lenski was arguing against the notion of directed mutations 15 years ago. Our knowledge of science is expanding exponentially, but not every new discovery requires us to draft a completely new model to study it. I’m sure given new research, Lenski would revise his opinion of (it appears) proximate directed mutation.

  30. ecoli

    there’s no way to prove that [intelligent design] scientifically anyway

    I don’t share your limited vision of what science can and cannot demonstrate. It appears I have more faith in science than you do.

    I tell you what. Describe an observation which, in principle, could NOT be understood by chance & necessity. Keep in mind a theory that explains everything explains nothing. In other words, it’s not a theory unless it can, in principle, be falsified (Karl Popper – Philosopy of Science 101).

    To be fair, I’ll offer you a falsifiable ID hypothesis.

    “Symbolic coding systems can be found in nature in two places. Incorporated in things invented by humans (example: morse code) and incorporated into all living cells (the genetic code). In all cases where the origin of symbolic coding systems can be determined with surety it was via intelligent agency. It is hypothesized that no unintelligent mechanism can produce a symbolic code because symbols are abstract and only an intelligence can create abstractions.”

    This can be falsified by a single observation of an unintelligent process creating a symbolic code.

  31. 31

    Avonwatches said (#15) –

    Someone also made the point (in another thread) that flipping a coin is not random – that is just how we describe the probability. In reality the coin toss determined by the side it was flipped from, strength behind the flick, rotation, etc etc.

    But those factors — the side it was flipped from, etc.. — are themselves random, and there are other random factors, e.g., wind gusts and unevenness of the landing surface. If there is any bias in the results of the coin toss, the bias would show up in a very large number of tosses — e.g., the result might be heads 55 percent of the time. The mathematics of probability and statistics is well understood — for example, see this long list of topics on the subject –
    http://en.wikipedia.org/wiki/L.....ity_topics

    DaveScot said (#18) –

    The most surprising thing is how LONG it took the bugs to find a way to digest citrate in an otherwise stress free environment.

    I suspect that one of the reasons why it took so long is that probably many mutations were lost because (1) only one percent of the old populations were transferred to start the next populations and (2) there was an average of only six generations per population. IMO much more of the old populations — maybe half — should have been transferred to start the next populations.

    Bob O’H said (#19) –

    Well, where would the genetic variation come from if not through random mutation?

    The recombination of genes in sexual reproduction causes genetic variation without changes in the genes themselves (of course, this is just a general statement that does not apply to E. coli).

    BTW, Dave, my comment always show the message, “Your comment is awaiting moderation.” Why, if I may ask? My comments are almost never censored here. Do all other commenters get that message? Does the message mean that my comment is not visible to other readers until the message disappears?

    Your history warrants screening your comments for foul and/or abusive language. -ds

  32. Dave, I haven’t read through all the replies, but I believe you are wrong here. In order for selection to be the creative element in evolution, it must select from a pool of RANDOM variants. If variants are not random (that is, they arise nonrandomly in response to some cue) then these nonrandom variants are in themselves adaptive, and thus, selection becomes redundant as an adaptor.

  33. van

    You’re presuming that all directed mutations would be fitter than the unmutated version which isn’t true at all.

    The best laid plans of mice, men, and bacteria often go awry. -Robert Burns

    Selection still has to choose the fittest (if any) of the mutations. Consider that many times there is no solution found and the population, despite its best effort, still dies. Selection never stops working unless mutation ceases completely.

  34. dave: “You’re presuming that all directed mutations would be fitter than the unmutated version which isn’t true at all.”

    Gould: “The essence of Darwinism lies in its claim that natural selection creates the fit. Variation is ubiquitous and random in direction. It supplies the raw material only. Natural selection directs the course of evolutionary change.” (Gould 1977, p. 44)

    So in essense, what Gould is saying is that evolution/adaptation via darwinism is a two-step process: random variation and selection, as opposed to a one-step process: adaptive variation only…(which would require some sort of intelligence within the organism, which darwinists/materialists are trying to avoid.) A one-step process of adaptation would eliminate selection as an adaptor and would require some sort of scientific explanation as to how it happened.

    This is not to say, as you are suggesting, that I believe all mutation that arises in response to an environmental challenge is beneficial. Case in point: sickle cell mutation, which produces an often-fatal disease in exchange for malaria resistance. Both outcomes are bad.

  35. by the way, if selection is acting upon nonrandom variation, as you suggest, then it is only acting as a population stablizer, not as a population adaptor, which is what Lenski and other darwinists are trying to make NS be.

  36. 36

    You’re presuming that all directed mutations would be fitter than the unmutated version which isn’t true at all.

    I have what is probably a dumb question. Why exactly would the intelligent designer direct a mutation that was less fit?

  37. Describe an observation which, in principle, could NOT be understood by chance & necessity.

    In all fairness to ecoli, is there an observation which, in principle, could NOT be understood by design?

  38. “I have what is probably a dumb question. Why exactly would the intelligent designer direct a mutation that was less fit?”

    I would have to agree with you; that is a dumb question, as no informed creationist would suggest that God Himself is directing mutations or any other molecular event. Mutations are internal consequences of internal and external events…they are often last-ditch efforts to achieve stability.

  39. Van you wrote

    I would have to agree with you; that is a dumb question, as no informed creationist would suggest that God Himself is directing mutations or any other molecular event. Mutations are internal consequences of internal and external events…they are often last-ditch efforts to achieve stability.

    I consider myself to be an informed supporter of ID and I believe that God is directing every molecule in existence due to their ontological nature of being part and parcel of God. Therefore in my understanding everything in existence is part of God and being directed by God because nothing exists outside of God’s ontological controlling nature e.g nothing has the ability to do anything independent of God’s will because everything exists under the control of and as a part of God whose will is the controlling agent for all actions, i.e. the cause of all causes.

  40. DaveScot is the man. #30. Its true though, no hiding, this cannot be falsified.

  41. 41

    Dave stated:

    “To be fair, I’ll offer you a falsifiable ID hypothesis.

    “Symbolic coding systems can be found in nature in two places. Incorporated in things invented by humans (example: morse code) and incorporated into all living cells (the genetic code). In all cases where the origin of symbolic coding systems can be determined with surety it was via intelligent agency. It is hypothesized that no unintelligent mechanism can produce a symbolic code because symbols are abstract and only an intelligence can create abstractions.”

    This can be falsified by a single observation of an unintelligent process creating a symbolic code.”

    DNA: The Tiny Code That’s Toppling Evolution

    http://www.gnmagazine.org/issues/gn58/tinycode.htm

    Moreover, the copying mechanism of DNA, to meet maximum effectiveness, requires the number of letters in each word to be an even number. Of all possible mathematical combinations, the ideal number for storage and transcription has been calculated to be four letters.

    This is exactly what has been found in the genes of every living thing on earth—a four-letter digital code. As Werner Gitt states: “The coding system used for living beings is optimal from an engineering standpoint. (Gitt, p. 95). ”

    Biophysicist Hubert Yockey determined that natural selection would have to explore 1.40 x 10^70 different genetic codes to discover the (optimal) one found in nature. Yockey estimated 6.3 x 10^15 seconds is the maximum time for the code to originate. Natural selection would have to evaluate roughly 10^55 codes per second to find the (optimal) universal genetic code. (Information Theory and Molecular Biology 1992)
    –(The Cell’s Design pg 273 Rana 2008)

  42. “Let’s try a different example. Suppose some stalking clown throws, monkey-like, a handful of his own poop aimed directly at your pointy little head, Bob.”

    Hah hah hah.

  43. Mentok: “I consider myself to be an informed supporter of ID and I believe that God is directing every molecule in existence due to their ontological nature of being part and parcel of God. Therefore in my understanding everything in existence is part of God and being directed by God because nothing exists outside of God’s ontological controlling nature e.g nothing has the ability to do anything independent of God’s will because everything exists under the control of and as a part of God whose will is the controlling agent for all actions, i.e. the cause of all causes.”

    Well I just have to disagree. I don’t think God is an inteventionalist. I believe God created humans — and other lifeforms — in the image of Himself in the sense that we are all little creators. We’re all conscious, we all have minds, we all have been blessed with the intelligence and molecular tools needed to respond to environmental, social and other assorted worldly events — it is thus not up to God to intervene on our behalf. God no more needs to intervene to digest our food than he does for us to generate a molecular response. God gave all creatures the ability to adapt and respond to environmental circumstances…this means we do it ourselves — we don’t rely on God to do it for us. Having said that, I believe God can work through us and our belief in Him can do and work miracles in our lives.

  44. This seems pretty obvious to me.

    True or False:
    Selection can operate on a non-random mutation.

    If the answer is true, then clearly Lenski’s statement is false.

  45. johnny

    In all fairness to ecoli, is there an observation which, in principle, could NOT be understood by design?

    Not if a designer who can interfere in an undetectable manner is allowed as a possibility. This came up as an objection to Behe’s “Edge of Evolution” in the form “Why can’t a designer be interfering with the evolution of P.falciparum by preventing mutations.” We really have to assume that there is not a designer interfering in real time in an undetectable manner just as we must assume that law and chance is reasonably bounded by statistical mechanics. I’m often asked for a mechanism by which an interfering designer can guide evolution. One possibility I offer is the same way we humans sometimes interfere – using a retrovirus as a vector to modify an organism’s DNA for our own purposes.

  46. “I’m often asked for a mechanism by which an interfering designer can guide evolution. One possibility I offer is the same way we humans sometimes interfere – using a retrovirus as a vector to modify an organism’s DNA for our own purposes.”

    This is a good analogy, and it works for the same reason the watch analogy works for irreducible complexity. We have evidence of humanity. We know that humans create. Therefore, if we see a watch lying on a deserted island, it still makes sense to assume that it was made by humans.

    In the same sense, I agree with you that non-random mutations can and will be selected upon by natural selection.

    However, the problem comes in, where you assume an intelligent designer that you cannot observe.

    God or alien scientists that are potential designers simply cannot (at least not right not, and in my opinion, not ever) be obeserved.

    So, while there is a possibility for non-random mutations (like in human experiments or in the Sripps study) we can only study them scientifically by assuming the ultimate source was non-random mutations that produced a mechanism through which random mutations are possible. If we proceed under this assumption, we can make great strides in the feild of human or even bacterial evolution.

    My point being, that non-random mutations is not evidence of an intelligent designer.

  47. Van, I respect what you believe, but my point was that your claim was not true. You said

    no informed creationist would suggest that God Himself is directing mutations or any other molecular event.

    That is simply not true. In essence you claim that your philosophical or religious beliefs set the standard for what all “informed creationists” should or should not accept as valid when it comes to God and the nature of God’s interactions with the universe. You should know that there are mnay different theories and philosophies held by many different “informed creationists”.

  48. DaveScot says:
    “I don’t share your limited vision of what science can and cannot demonstrate. It appears I have more faith in science than you do.”

    Apparantly so… my belief in God requires faith, but my belief in science requires evidence.

    DaveScot says:
    “Describe an observation which, in principle, could NOT be understood by chance & necessity.”

    Evolution is easily falsifiable in a number of ways.

    If a fossilized organism was found in the ‘wrong’ time period, evolutionary theory would be incorrect. Therefore, something other than random mutations and natural selection is going on (non-random speciation of organisms)

    DNA sequencing could falsify similarity tests between chimps and humans. If we find no significant homology, which is predicted by random genetic mutations, then we’d have to conclude something non-random is occuring.

    Ff an intelligent designer revealed itself, and told us mutations are directed, this would also falsify the idea of randomness.

    Now, lets look at your example:

    “This can be falsified by a single observation of an unintelligent process creating a symbolic code.”

    Ah, but this is not exaclty true. How can we be sure that an intelligent designer isn’t producing the code, unseen by us? What appears to a randomly produced code, could in fact be being produced by a designer.

    There is no way to observe if this is true and therefore cannot be falsified.

  49. dumb question:

    If we agree that in Lenski’s e. Coli experiment where citrate metabolism is one significant evolutionary event, where there is a detectable
    phenotypic change (DPC), and

    we consider it took 40K generations over 20 years;

    and we consider that human generations are 20 years, then 40K human generations would take 800K years
    and if it’s 5 to 8 mya that humans and chimps broke off from each other, let’s say 8M,
    then 8 M / 800 K = 10

    so, we might expect about 10 DPC events during that time,
    but the website listed here:

    http://www.whyevolution.com/chimps.html#chimp

    would seem to list a few more than 10 such events, maybe 100′s.

    the brain discussion there, or the discussion of the sugar in the cells are very interesting

  50. 50

    E-coli states:

    “Evolution is easily falsifiable in a number of ways.”

    No it is not!

    Even though the fossil record is totally contrary to what evolutionary theory predicted, with sudden appearance, rapid diversity, and then a gradual loss of diversity and variability over long periods of time, it “mutates” into punctuated equilibrium. Overwhelmingly detrimental mutation rates don’t seem to phase evolutionists in the least as well. When ENCODE took away the junk DNA for evolutionists to play with on their hypothetical papers, the obfuscation I encountered by them was astonishing. When complexity for the DNA code is revealed that far, far surpasses man’s ability to produce as such, evolutionists, I debate, shrug their shoulders and say evolution is true no matter what. The evidence has little effect on what they believe.

    Yet here we are debating whether a preexisting citrate utilizing ability that is brought into service by e-coli under stress should be considered solid proof for evolution.
    The bill that evolutionists owe for evidence is far, far greater than this supposed novel ability they are trumpeting. Indeed evolutionists are scientifically bankrupt as far as compelling evidence is concerned!

    Indeed what the Lord said of the ancient religious teachers can be applied to the modern evolutionary priesthood.

    King James Bible
    Ye blind guides, which strain at a gnat, and swallow a camel.

    which means:

    A forcible image of those who are very conscientious over small matters that don,t matter, and careless of the great matters that should be obvious to them.

  51. bornagain:
    “No it is not!”

    Nothing you described in your post contradicted what I said about how evolution could be falsified, so I’m not sure why you’re taking objection to what I stated.

    Detrimental mutations occur, but obviously, these usually aren’t selected for, and are rare in natural populations. And I fail to see what it had to do with my proposed falsifications, at any rate.

    I’m also not following your statements on how the fossil record doesn’t follow with predictions of evolution. Perhaps you will read this? http://www.talkorigins.org/faqs/punc-eq.html

  52. Mentok: “That is simply not true. In essence you claim that your philosophical or religious beliefs set the standard for what all “informed creationists” should or should not accept as valid when it comes to God and the nature of God’s interactions with the universe. You should know that there are mnay different theories and philosophies held by many different “informed creationists”.

    ok, well I would change the wording if I could. But since I can’t I’ll put it this way: until today I’ve not read of a creationist who believes God steps in and performs molecular, digestive or other bodily functions. That’s not to say some aren’t out there. God Bless.

  53. I am getting into this discussion kind of late but two things:

    In the Jablonka and Lamb book, I believe there is a section on directed mutations occurring in bacteria. It may be some of what has already been presented here but if someone has the book, then they could look it up. My book is home and I will be away for a few days more. Allen MacNeill has talked here about these directed mutations when bacteria are put under stress.

    Second, there is no need for mutations to happen for selection to take place. If the capability is already in the gene pool then a change of environment could favor some members of the population over others because they have an already existing capability. This is obviously not the case with citrate transport but could be the case for other environmental changes. In other words the population could change dramatically in just a few generations and not be the result of any mutations taking place.

    Larry Fafarman has already talked about recombination in sexual reproduction as a potential source for new genes not through mutations. And theoretically the new gene that is the result of recombination could be a basis for selection.

    I know next to nothing about this but wouldn’t horizontal gene transfer be another non mutation creation of new genetic material. While the genetic material transferred is not new in itself, the combination with the other genetic material in the new organism could possibly be new and this combination could be subject to selection.

  54. ecoli, (48)

    You said, “If a fossilized organism was found in the ‘wrong’ time period, evolutionary theory would be incorrect.
    How far out of place would it have to be? Would it matter which way? What you have said sounds daring and wonderful, but you haven’t put numbers on it.

    Here’s the problem with taking your statement seriously. If we find, say, a coelocanth, some 60 to 80 Ma after the last one is supposed to have died out, evolutionary theory acts surprised, and continues on. Same for the horseshoe crab, the gingko, and other organisms. If we find vertebrates at the time of the Cambrian explosion, or spiders way earlier than we had thought, evolutionary theory just adapts. If we find chains or bells in lumps of coal, the veracity of the finds are questioned, to put it mildly. Nothing must be allowed to derail evolutionary theory–nothing.

    It isn’t anywhere near as easy to falsify evolutionary theory as your quote would suggest.

  55. 55

    e-coli you stated:

    “And I fail to see what it had to do with my proposed falsifications, at any rate.”

    Be careful dude you almost admitted the truth that you blind to any contrary evidence.

    The entire fossil record when looked at soberly is, as Paul Geim briefly illustrated, completely “out of place” as far as what Darwin predicted.

    It is a commonly known fact that more phyla were present at the end of the Cambrian explosion than are present today, whereas Darwinism predicts it should be exactly the opposite!. So much for fossils being out of place falsifying the theory of evolution e-coli.

    Then you say something about, what I consider evolutions strongest piece of “suggestive” evidence, sequence similarities. I don’t follow your logic for falsification but let me show you how sequence similarity is actually falsified by the evidence.

    Naturalists always try to establish scientific validity for evolution by pointing to suggestive genetic similarities while ignoring the foundational principles of science (genetic entropy; conservation of information) that contradicts their preconceived philosophical bias.

    For example, naturalists/evolutionists say that evolution is proven true when we look at the 98.8% similarity between certain segments of the DNA in a Chimpanzee and compare them with the same segments of DNA of a Human. Yet that similarity is not nearly good enough to be considered “conclusive” scientific proof. For starters, recent preliminary comparisons of the complete genome of chimps and the complete genome of man yield a similarity of only 96%. As well, the December 2006 issue of PLoS ONE reported that human and chimpanzee gene copy numbers differ by a whopping 6.4% (Hahn). Whereas, Dr. Hugh Ross states the similarity may in actually be closer to 85% to 90% when the entire genome is considered. Secondarily, at the protein level only 29% of genes code for the exact same amino acid sequences in chimps and humans (Nature, 2005). As well, our DNA is 92% similar to mice as well as 92% similar to zebrafish (Simmons PhD., Billions of Missing Links). So are we 92% mouse or are we 92% zebrafish? Our DNA is 70% similar to a fruit fly; So are we therefore 70% fruit fly? Our DNA is 75% similar to a worm; So are we 75% worm?

    Decoding the dogma of DNA similarity
    http://creationontheweb.com/content/view/5111

    No, of course not!! This type of reasoning is simple minded in its approach and clearly flawed in establishing a solid scientific foundation on which to draw valid inferences from! Clearly, we must find if the DNA is flexible enough to accommodate any type of mutations happening to it in the first place. This one point of evidence, (The actual flexibility of DNA to any random mutations), must be firmly established, first and foremost, before we can draw any meaningful inferences from the genetic data we gather from organisms!! Fortunately we, through the miracle of science, can now establish this crucial point of DNA flexibility. The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation! (Gerrish and Lenski, 1998, Bataillon, 2000, Elena et al, 1998).

    “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.” (Sanford; Genetic Entropy page 24)

    The fate of competing beneficial mutations in an asexual population (Philip J. Gerrish & Richard E. Lenski)

    “Clonal interference is not the only dynamic that inhibits the progression of beneficial mutations to fixation in an asexual population. A similar inhibition may be caused by Muller’s ratchet (Muller, 1964; Haigh, 1978), in which deleterious mutations will tend to accumulate in small asexual populations. As shown by Manning and Thompson (1984) and by Peck (1994), the fate of a beneficial mutation is determined as much by the selective disadvantage of any deleterious mutations with which it is linked as by its own selective advantage.”

    http://myxo.css.msu.edu/lenski.....Lenski.pdf

    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.

    High Frequency of Cryptic Deleterious Mutations in Caenorhabditis elegans ( Esther K. Davies, Andrew D. Peters, Peter D. Keightley)

    “In fitness assays, only about 4 percent of the deleterious mutations fixed in each line were detectable. The remaining 96 percent, though cryptic, are significant for mutation load…the presence of a large class of mildly deleterious mutations can never be ruled out. ”

    ” 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.”

    Trying to find an actual “hard” number for the “truly” beneficial mutation rate is, in fact, what Dr. Behe tried to do in his book “The Edge of Evolution”.

    Dr. Behe states in 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 explain the generation of the complexity 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 (births) of the malarial parasite, by Dr. Behe.

    Thus, the actual rate for “truly” beneficial mutations, that would account for the complexity we see in life, is far in excess of one-hundred-billion-billion mutational events.

    Thus, this one in a million number, that is often bantered about for “truly” beneficial mutations, is actually far, far too generous for the evolutionists to be using for their hypothetical calculations.

    In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biology, with no exceptions at all, and that the belief in “truly” beneficial mutations is nothing more than wishful speculation on the naturalists part that has no foundation in empirical science whatsoever:

    The foundational rule of Genetic Entropy for biology can be stated something like this:

    All 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 original integrated complex information in the parent species genome.

    Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is clearly overwhelming, for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker).

  56. ecoli

    You’re conflating common descent with evolution. I don’t have any problem with common descent from one or a few common ancestors over hundreds of millions or billions of years.

    How do you propose we can falsify evolution by random mutation & natural selection?

    If it can’t be falsified, at least in principle, it’s dogma not unlike explaining things by saying it was done by an omnipotent god. This is where the term “chance worshipper” comes from.

  57. I missed Bob’s attempt at an argument, but I thought I’d throw my piece in as well.

    From a coder’s perspective, there are various scenarios where I’d want to generate a pseudorandom result at varied rates. I could also have a mechanism that tweaks this based upon my foreknowledge.

    random(0,1000,rate)

    random(0,10,rate*5)

    The second instance is a specialized case where I want only a smaller pool of results generated at a faster rate. The narrowed focus is the direction. But if we go by Bob’s argument somehow all these changes are still 100% random even though I’m purposefully increasing the rate and focus of the pseudorandom generator.

  58. Patrick:
    “The second instance is a specialized case where I want only a smaller pool of results generated at a faster rate. The narrowed focus is the direction. But if we go by Bob’s argument somehow all these changes are still 100% random even though I’m purposefully increasing the rate and focus of the pseudo random generator.”

    Increasing the focus could be a winning strategy in the short run, but it’s a bit like trying to anticipate the market based on recent history, or using things learned in the last war to fight the next one.

  59. Petrushka,

    Obviously the conditions under which the modified generator(s) would run would be detected. There can be multiple such conditional sets based upon foreknowledge of various likely scenarios. You’re correct that not all scenarios can be anticipated, but I would think that’d be the point of using a directed pseudo-random response instead of an explicit pre-scripted response since that’d increase the likeliness of hitting upon a “winning strategy”.

  60. Having a directed response seems a bit like using brute force to win at chess. It’s a perfect strategy if you can list all the moves and countermoves.

    So the question is, can all the possible future conditions in the game of life be listed, and is the list of a manageable length?

  61. jerry

    Actually E.coli does already have the capability for citrate transport – citrate permease. Its expression is repressed in the presence of oxygen for some reason in the wild. Lenski’s strain expresses it in the presence of oxygen. His is not the first strain known to do this. His is the first one to be closely observed changing from repression to expresson. There was likely no real “evolution” but rather just run-of-the-mill gene induction which is a rather common occurence. It’s really kind of mind boggling that anyone would think to make a big deal out of it. It’s sort of like making a big deal out of turning on the air conditioner in a car and thinking that this was somehow was a fundamental change in the automobile’s construction. If there was a “potentiating mutation” this is also analogous to the car where you first have to turn on the air conditioner then adjust the thermostat lower. If you don’t first turn on the air conditioner then lowering the thermostat does nothing.

    You are correct that no genetic mutations need take place for selection to operate. Gene induction through methylization is heritable but does not involve changing any DNA bases. And of course recombination in sexual reproduction can cause all sorts of preexisting traits to be repressed or expressed. It used to be thought that the gene was everything and modifications in their amino acid sequence was the major source of descent with modification. Now its not changes in the gene that is the major driver but rather changes in when and how much of the particular protein or enzyme product is produced.

    Horizontal gene transfer creates nothing new, it just shuffles preexisting things from one organism to another like sexual recombination without the sex.

  62. 62

    Lets talk about common ancestry here people, shall we?

    I think (and it goes well with the article posted by Bill on apes with rights) that materialistic Darwinian evolution is really just a way of finding the LOWEST common denominator amongst living (or all) things. You can think that people and apes are in the same class of mammals all you want. That’s your right, but I have news for you; all things are in the same class- its called “matter.” In other words human beings are NOT apes just like apes are not fish but if you want to group everything by it’s interconnected significance via evolutionary linage then all things are in the same class. In fact apes to me are closer to insects than they are to people because the dominion that human beings have over apes in the animal kingdom. You see, genes and lineages in the GRAND scheme are beside the point- and btw every one knows this, all you have to do is go to a zoo and see what a mere 2% difference can get you. That is why DE is less about lineages and more about “ purposelessness and chance.” You cannot practically compare a person to an ape- the differences are obvious to a one year old, but if you can bring their independent significance closer together by lowering the value of the PROCESS and mechanisms by which they both arise- and then throw in their obvious interconnectedness and play it off as the clincher, you have a much better shot at holding life’s apparent design down and in a much darker light.

    Yes, indeed, all things and events truly can (as far as empirical science is concerned) be looked as existing in a world ruled by so called “chance” — as is done in the philosophical mode of the Copenhagen interpretation of quantum physics. However, “chance” is merely a way of “using data to predict and build ratios.” Chance cannot purchase itself nor can it explain symmetry and laws and constants. In fact of what chance there is, it alone can be looked at as a form of a constant itself. For example say you were talking about mutations and you wanted to see if they were totally “chance based”- it wouldn’t take long to see that “necessity” is required as well in order for chance to give us ANYTHING! We need all kinds of physical stipulations in order for life forms and or “anything” to exist. First of all matter is necessary, then you need light, and matter “in all of its forms” and “the right ratios” before life can have a chance to exist. Where all of this geometry and algebra comes from no one knows. This is essentially what the “privileged planet” is all about. Chance alone cannot purchase itself, nor can it explain necessity. I should also add that chance and necessity as viewed by many including Mike Behe and Bill are not event enough by them selves. That is event omitting the mathematical design of the world in conjunction with “unpredictable” events, there still may not even be enough to support a design ess universe.

    The interconnectedness of all things, assuming some chain of common ancestry is correct, is merely one “small” and tiny little stipulation that pales in the face of the complexity and specified design of the final product. Interconnectedness is not a powerful value- think about any object such as a penny. A penny is not very interesting and it wasn’t when it was merely some “unrefined” copper either. “It is not the lowest common denominator that is significant about life and life forms it is the glory and complexity of the final product.” This part of the story is the part that is not being told in modern evolutionary theory.

    All the laws in the universe, all of the molecular machines, genetic patters and efficient systems are not the result of “interconnectedness” and or “common denominators” they are the apex of what the grand design schemata has to offer.

    So all of this stuff about how apes are only 5 or 2% different than human beings is greatly beside the point. If i was to randomly remove 2% of you genetic code or alter it you might not even be able to survive much less fire rockets at the moon. It is the product that design encompass, while DE is too busy trapped inside a steel cage of denial…

    at the amusement of all those sociopathic people running the political zoo.

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