Irreducible Complexity

Evolution of an Irreducibly Complex System – Lenski’s E. Coli

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On another thread we have been discussing abiogenesis in particular, but there was also some discussion about the evolution of an irreducibly complex system. Commenter CHartsil indicated that “we actually watched an IC system evolve” in reference to Lenski’s E. coli research. At my request, he has posted a brief summary of the research and his take, which I am now elevating to a new thread on this important topic.

For those who disagree with CHartsil’s take, strong objections on substantive grounds are of course welcome, whether relating to Lenski’s research or CHartsil’s interpretation of it, but not irrelevant personal attacks. Thank you.

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Guest Post by CHartsil:

This is a pro-ID board so I doubt I need to explain irreducible complexity. When arguing against it, most will bring up Ken Miller or Nick Matzke. They have great points but theirs are indirect and theoretical pathways for systems considered IC. That’s why I’m fond of Lenski’s cit* E. coli.

This particular strain of E. coli evolved the ability to metabolize citrate aerobically. While most E. coli can do this anaerobically, part of the definition of wild-type E. coli is actually the inablity to use citrate as a substrate aerobically. This may not have been a terribly fascinating addition of function if not for the frozen fossil records kept by Lenski et al.

These frozen generations allowed Lenski to determine that this trait was not acquired via a single mutation as it could only be repeated after generation 20,000. Given the distinct cladistic division amongst the populations at the border generation, it was determined that there were at least two potentiating mutations prior to the cit* event.

In this third clade a tandem duplication resulting in a novel regulatory module leading to the aerobic cit* could be repeated and verified. It has been noted since that the fitness of the population has been improving without notable upper limit, increasing based on the number of copies of the new regulatory module.

I find this to be sufficient in warranting the dismissal of the concept irreducible complexity. In Lenski’s E. coli, we observe the rise of a new function resulting from a new gene and new gene regulation. This function is comprised of now interdependent components which demonstrably did not exist in parent generations. It is by definition irreducibly complex and it was observed to evolve.

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Nota bene: for purposes of the above discussion, CHartsil is using the following definition of irreducible complexity: “a system comprised of interdependent parts, the removal of any of which will cause the system to cease functioning.”

304 Replies to “Evolution of an Irreducibly Complex System – Lenski’s E. Coli

  1. 1
    Eric Anderson says:

    Joe @83 on the other thread writes:

    CHartsil is confused. All that happened with Lenski’s experiment is that the E coli could now utilize citrate in an oxygen-rich environment. They already had that ability in the an anaerobic environment.

    An IC system did NOT evolve via unguided processes.

    No new genes were formed. An existing gene was duplicated and put under the control of a different promoter, ie a promoter that was on in the presence of O2.

  2. 2
    Eric Anderson says:

    kairosfocus @84 on the other thread writes:

    F/N: On the Lenski counterexample to IC claim, I suggest a glance at CL’s remarks in Sect 5 here (and onwards) in response to Venema:

    http://www.discovery.org/a/17571

    Let me clip Sect 5, as a first example:

    ______________

    >> Section 5: Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information

    In this section, we:

    • Understand why Venema’s citation of Lenski’s “Long Term Evolution Experiments” do not demonstrate that “Complex, specified information can indeed arise through natural mechanisms”
    • Review Michael Behe’s 2010 paper in Quarterly Review of Biology which investigated Lenski’s research and found that “mutations were decreasing or eliminating the protein’s function”
    • Investigate why Lenski’s E. coli bacteria that evolved the ability to uptake citrate under oxic conditions didn’t evolve anything new and likely experienced loss-of-molecular function

    Some critics of intelligent design (ID) misunderstand ID as a denial of natural causes. For example, we have recently seen how theistic evolutionist Dennis Venema wrongly suggests that, in both a scientific and theological sense, ID denies natural causes. Venema imports this misunderstanding into his proposed methods of testing ID, suggesting that if we find natural causes doing anything, then ID is refuted.

    Venema writes: “any natural mechanism that can be shown to produce information would render [Stephen Meyer’s] argument that information only arises from intelligent sources null and void.”

    Dennis Venema’s argument collapses into this: ‘if Darwinian evolution can do anything, then ID is wrong.’ But this is not how we test ID, for ID readily allows that natural selection and random mutation can effect some changes in populations. The right question is not ‘Can natural selection do anything?’ but rather ‘Can natural selection do everything?’

    With this in mind, let’s analyze Dr. Venema’s discussion of Richard Lenski’s Long Term Evolution Experiments (“LTEE”) with E. coli.

    Where’s the Behe?

    Before discussing the LTEE, it’s important to note that from the beginning of his series for BioLogos on evolution and the origin of information, Venema didn’t just purport to critique Stephen Meyer’s arguments in Signature in the Cell. Rather he referred to rebutting the entire “Intelligent Design Movement” or what he called (following Judge Jones?) the “IDM.”

    But if Venema is going to critique the entire “IDM” using Richard Lenski’s “Long Term Evolution Experiments,” then Venema should discuss the most relevant literature of the “IDM” that discusses those experiments. He doesn’t do that.

    In Venema’s discussion of the LTEE, there is no mention of a 2010 peer-reviewed scientific paper written by the most prominent biochemist in the “IDM,” published in a prominent biology journal, extensively critiquing Lenski’s LTEE. Venema fails to note and discuss Michael Behe’s December 2010 paper in Quarterly Review of Biology (QRB), which extensively discusses and critiques Lenski’s Long Term Evolution Experiments. Instead, Venema critiques the writings of Stephen Meyer, who hasn’t commented on Lenski’s LTEE because they weren’t relevant to his arguments in Signature in the Cell about the origin of life.

    By misrepresenting Meyer’s thesis as being refuted by evidence of the power of natural selection, Venema creates a straw man. Meanwhile he ignores the substantive critiques by leading ID proponents of the very evidence he raises.

    Vague Discussions vs. Precise Discussions of Lenski’s LTEE

    As an initial salvo regarding Lenski’s LTEE, Venema writes:

    [T]here were many possible genetic states of higher fitness available to the original strain, and random mutation and natural selection had explored several paths, all leading to a higher amount of “specified information” — information that specifies increased reproduction and survival in the original environment. All this was by demonstrably natural mechanisms, with a complete history of the relevant mutations, the relative advantages they conferred, and the dynamics of how those variants spread through a population. The LTEE is at once a very simple experiment, and an incredibly detailed window into the inner workings of evolution.

    But what exactly was the “specified information” that increased? What new function was gained? Where did natural selection and random mutation produce functional, information-rich genes and proteins? Venema doesn’t say what new functions arose, what changed, or what information was gained. His claim that natural selection produced “specified information” is vague.

    By contrast, in critiquing claims that the LTEE has produced something new, Behe’s 2010 Quarterly Review of Biology paper was anything but vague:

    By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others. In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.

    Several years later, when the cultures had surpassed their 20,000th generation, Lenski’s group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003). The authors stated that “The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)” (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein’s activity.

    The group then decided to concentrate on candidate genes suggested by the physiological adaptations that the cells had made over 20,000 generations. One such adaptation was a change in supercoiling density; therefore, genes affecting DNA topology were investigated (Crozat et al. 2005). Two of these genes, topA and fis, had sustained point mutations. In the case of topA, the mutation coded an amino acid substitution, whereas, with fis, a transversion had occurred at the fourth nucleotide before the starting ATG codon. The topA mutation decreased the activity of the enzyme, while the fis mutation decreased the amount of fis gene product produced.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

    If you weren’t following all the technical language, here’s what’s going on: For the first 20,000 generations of Lenski’s LTEE, very little happened. There were a few molecular adaptations observed, yet whenever we understood their molecular basis, they involved the knocking out of genes, or decreasing protein activity — in essence, a decrease in specificity. Behe summarizes:

    The fact that multiple point mutations in each gene could serve an adaptive role — and that disruption by IS insertion was beneficial — suggests that the point mutations were decreasing or eliminating the protein’s function.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010) (emphasis added).)

    Unlike Venema’s discussion, Behe’s is precise, giving multiple examples and detailed descriptions of the types of changes observed in Lenski’s LTEE. And Behe found that the types of changes taking place in the E. coli tended to decrease or eliminate protein function.

    Before getting into a discussion of the citrate-using strain of E. coli, Behe closes with another specific example that involved decreasing gene activity in Lenski’s LTEE:

    In an investigation of global protein profiles of the evolved E. coli, Lenski’s group discovered that the MalT protein of the maltose operon had suffered mutations in 8 out of 12 strains (Pelosi et al. 2006). Several mutations were small deletions while others were point mutations, thus suggesting that decreasing the activity of the MalT protein was adaptive in minimal glucose media.

    Looking at Table 3 of Behe’s QRB paper, not a single example of an adaptive mutation in Lenski’s LTEE entailed a gain of a new molecular function. In fact, over the course of his entire paper, Behe goes further and explains that most of our known examples of molecular adaptations in bacteria entail “loss-of-function” mutations. Somehow, Venema doesn’t discuss any of these findings.

    E coli. Could Uptake and Metabolize Citrate Before Lenski’s LTEE

    Later, when referring to a different stage of the LTEE, Venema claims that a new function did arise in Lenski’s E. coli bacteria during the experiments: the ability of E. coli to metabolize citrate. Venema claims that “One of the defining features of E. Coli is that it is unable to use citrate as a food source,” but after a series of mutations “bacteria that use citrate dominate the population.” According to Venema, these experiments show “Complex, specified information can indeed arise through natural mechanisms.”

    Yet Venema leaves out important details, creating an inaccurate impression. As we’ll discuss below, normal E. coli already have machinery to uptake and metabolize citrate, so the general fact that Lenski’s bacteria showed this ability is really quite unremarkable.

    Unfortunately, Venema’s readers on the BioLogos will never hear that. They also won’t learn that Michael Behe has written extensively about Lenski’s research, showing that the machinery for E. coli to uptake and metabolize citrate already existed in these bacteria. This isn’t an entirely new biochemical pathway. Venema fails to note that normal E. coli already have the ability to uptake and metabolize citrate. They just can’t normally uptake it under oxic conditions; Lenski’s bacteria evolved the ability to uptake it under oxic conditions used in the experiment. Then the E. coli used their normal metabolic pathways to use citrate as a food source. Behe made this point while commenting on these claims soon after they were first published in 2008:

    Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it’s not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a “citrate permease” which can transport citrate from outside the cell through the cell’s membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.”

    (Michael Behe, Amazon Blog, “Multiple Mutations Needed for E. Coli” (June 6, 2008).)

    Likewise, Behe’s recent 2010 paper in Quarterly Review of Biology provided an extensive critique of claims that Lenski’s LTEE showed the evolution of a new pathway that could metabolize citrate. Venema doesn’t cite or mention Behe’s QRB paper, but it too explains that E. coli already had the ability to metabolize citrate. Behe explains:

    Recently, Lenski’s group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

    Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren’t anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:

    As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

    Thus, previous research suggests that the adaptation which allowed these E. coli to uptake citrate under oxic conditions might be caused “by the loss of the activity of a normal genetic regulatory element.” Here’s what is likely going on here:

    Under normal conditions, E. coli can metabolize citrate; after all metabolizing citrate is an important step in the Krebs cycle, a pathway used by virtually all living organisms when creating energy.
    But under oxic conditions, E. coli lack the ability to transport citrate through the cell membrane into the cell. E. coli can do this under reducing conditions, but under oxic conditions E. coli can’t normally uptake citrate.
    If Lenski’s citrate-using E. coli are like previous E. coli which were discovered uptaking citrate under oxic conditions, then it seems likely that the bacteria underwent a mutation that knocked out the regulation mechanism of a citrate-transport gene, causing over-expression, allowing the E. coli to uptake citrate under oxic conditions.

    In other words, the machinery for both transporting and metabolizing citrate was already present in these bacteria. But a series of knockout mutations broke the regulation of pre-existing citrate transport mechanisms, causing over-expression of a citrate transport gene, allowing citrate to be transported under both oxic and anaerobic conditions. If this is the case, then clearly this example of Darwinian “evolution” entails the loss of a molecular function, not the gain of a new one. And there was no wholesale acquisition of the ability to metabolize or, as Venema put it, “use” citrate.

    In fact, as Behe notes, we don’t really yet understand the precise molecular mechanisms that caused these E. coli to be able to uptake citrate under oxic conditions. So as far as we can tell, these changes entailed the origin of no new functional genes or proteins but might have resulted from a broken regulatory mechanism. We have not seen that natural selection and random mutation can produce functional, information-rich genes and proteins, and Venema is wrong to suggest otherwise.

    Contra Venema, this example hardly shows the Darwinian evolution of a “new function,” especially since E. coli already had the ability to uptake and metabolize citrate. Venema claims that CSI has arisen, but if we don’t even know what mechanisms were involved in this change, how does he know that it is new CSI?

    What do Lenski’s LTEE Really Tell Us?

    In his QRB paper, Behe goes on to explain that to date, the known adaptations that have occurred in Lenski’s LTEE are either modification-of-function or loss-of-function changes:

    The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

    Behe’s paper further suggests that when there are several kinds of potential adaptive mutations that might occur, loss or modification of function adaptations will be far more common than gain-of-function adaptations. He concludes:

    Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

    The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation.

    Consider an imaginary order of insects, the Evolutionoptera. Let’s say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium. The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years. At these rates, every thousand years 1000 species of Evolutionoptera will die off, while one new species will develop–a net loss of 999 species. If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth.

    If Behe is correct, then Darwinian evolution at the molecular level faces a similar problem. If, all other things being equal, a loss or modification of function adaptation is generally 100-1000 times more likely than gain of function adaptations, then eventually an evolving population might run out of molecular functions to lose or modify. Neo-Darwinian evolution cannot forever rely on examples of loss or modification-of-function mutations to explain molecular evolution. At some point, there must be a gain of function.

    Vaguely Appealing to Vast Probablistic Resources Won’t Work

    Venema closes his post on the LTEE by saying: “what the IDM claims is impossible, these ‘tiny and lowly’ organisms have simply been doing — and it only took 15 years in a single lab in Michigan. Imagine what could happen over 3,500,000,000 years over millions of square miles of the earth’s surface.”

    But vague appeals to vast eons of time and huge population sizes are unconvincing. You just have to do the math. As David Abel reminds us:

    Mere possibility is not an adequate basis for asserting scientific plausibility. A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, “Yes.” … One chance in 10200 is theoretically possible, but given maximum cosmic probabilistic resources, such a possibility is hardly plausible. With funding resources rapidly drying up, science needs a foundational principle by which to falsify a myriad of theoretical possibilities that are not worthy of serious scientific consideration and modeling.

    (David L. Abel, “The Universal Plausibility Metric (UPM) & Principle (UPP),” Theoretical Biology and Medical Modelling, Vol. 6:27 (Dec. 3, 2009).)

    In the case of E. coli and citrate, the bacteria already had the ability to uptake and metabolize citrate, and simply found a way to transport it under different conditions. It’s likely this occurred by overexpressing pre-existing transport mechanisms. Does this imply that anything and everything “could happen over 3,500,000,000 years over millions of square miles of the earth’s surface”? Well, ID proponents aren’t interested in making vague and ambiguous appeals to vast amounts of probabilistic resources. They want to test these questions, and follow the evidence where it leads.

    As discussed here, ID proponents have asked just how long it takes to evolve traits that require multi-mutation features. A multi-mutation feature requires multiple mutations to be present before there is any advantage given to the organism. Doug Axe’s research makes assumptions very generously favoring Darwinian evolution. He assumed the existence of a huge population of asexually reproducing bacteria that could replicate quickly — perhaps nearly 3 times per day — over the course of billions of years. Yet even here, complex adaptations requiring up to six mutations with neutral intermediates can become fixed. Beyond that, things become implausible.

    If only slightly maladaptive intermediate mutations are required for a complex adaptation, only a couple (at most two) mutations could be fixed. If highly maladaptive mutations are required, the trait will never appear. Axe discusses the implications of his work:

    [T]he most significant implication comes not from how the two cases contrast but rather how they cohere — both showing severe limitations to complex adaptation. To appreciate this, consider the tremendous number of cells needed to achieve adaptations of such limited complexity. As a basis for calculation, we have assumed a bacterial population that maintained an effective size of 109 individuals through 103 generations each year for billions of years. This amounts to well over a billion trillion opportunities (in the form of individuals whose lines were not destined to expire imminently) for evolutionary experimentation. Yet what these enormous resources are expected to have accomplished, in terms of combined base changes, can be counted on the fingers.

    (Douglas D. Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, Vol. 2010(4):1-10.)

    If Axe is correct then we cannot always assume, as Venema seems to do, that sufficient probabilistic resources exist to produce complex features we see in life.

    Summarizing Venema’s Argument Regarding the LTEE

    In short, Venema’s argument regarding the LTEE collapses into common misconceptions about ID, which go something like this:

    (1) ID holds that Darwinian evolution cannot do anything.
    (2) If Darwinian evolution can do something then it can do anything.
    (3) Lenski’s experiments show Darwinian evolution can allow E. coli bacteria to evolve a “new function” of metabolizing citrate.
    (4) Therefore ID is wrong, and given enough time, Darwinian evolution can do anything we “imagine.”

    At each step in his argument, the facts and/or the logic is wrong:

    Regarding (1): In fact, ID does not hold that Darwinian evolution can’t do anything. Rather it claims that natural selection can do some things, but not everything. ID proponents readily acknowledge (as Behe has) that “if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it.” The problem comes when multiple mutations are required to produce some new structure — and as Axe’s research shows, this is where Darwinian evolution typically gets stuck.
    Regarding (2): Darwin-defenders have a long history of over-extrapolating from the data. ID is scientifically cautious and concludes that no one single experiment can show that Darwinian evolution can do everything we ask of it. A single experiment showing the ability of Darwinian evolution to do X simply shows the ability of Darwinian evolution to do X; it doesn’t necessarily show Darwinian evolution can do Y, Z, and A, B, and C, etc. ID says we need to test hypotheses carefully and not over-extrapolate from observed data.
    Regarding (3): In fact Lenski’s experiments did not show the Darwinian evolution of an entirely new function. E. coli bacteria already had the ability to uptake and metabolize citrate, and the experiments simply showed they evolved the ability to uptake it under oxic conditions. This very likely required the loss of a molecular function.
    Regarding (4) ID proponents do not think it is wise or scientifically accurate to vaguely invoke vast eons of time or vast population sizes to document the alleged power of Darwinian evolution. ID cautions that Darwinian evolutionists often assume that there are sufficiently vast probabilistic resources to accomplish any task imaginable, but that assumption might not be valid. Rather than simply assuming, Doug Axe’s research finds that adaptations requiring more than six neutral mutations, or two maladaptive mutations, to provide a functional advantage would not arise in the history of the earth.

    Subsequent research by Axe and Ann Gauger suggests that it would not be uncommon for Darwinian evolution to face obstacles that exhaust the probabilistic boundaries as found by Axe’s research. In 2011, they published research in BIO-Complexity that found at least seven mutations (probably many more) would be necessary to convert one protein into a supposedly closely-related protein.

    While Darwinians may (or may not) claim that this was a real evolutionary pathway, it’s the type of pathway that is often claimed to have been traversed by natural selection over the course of life’s history. The fact that this simple conversion required more mutations to produce a new function than would be allowed under Axe’s mathematical models shows that there may be real obstacles to the Darwinian evolution of new proteins. Venema’s citation of Lenski’s LTEE certainly does not show otherwise.>>

  3. 3
    Eric Anderson says:

    kairosfocus @85 on the other thread writes:

    F/N part 2: Let’s continue, sect 6:

    ______________

    >>Section 6: Another Bogus Claim of “Novel Function Arising Through Mutation and Selection”

    In this section, we:
    • Understand why Dennis Venema’s citation of Joseph Thornton’s steroid research does do not demonstrate a “fascinating case of a novel function arising through mutation and selection”
    • Review the multiple responses to Thornton’s research from leading ID proponents (all ignored by Venema) who found the changes were not information-rich, not necessarily produced by natural selection, entailed diminishment rather than gain of function, and well within the ‘edge of evolution’
    • See that Venema undercuts his own claims by admitting, “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors”

    In the case of Richard Lenski’s Long Term Evolution Experiments (LTEE) with E. Coli bacteria, we saw that Dennis Venema of BioLogos cited purported examples of natural selection increasing specified and complex information — but intelligent design (ID) proponents had long before critiqued these examples. For example, Lenski’s LTEE had been critiqued by Michael Behe when they first came out in 2008, and then later in Behe’s 2010 paper in Quarterly Review of Biology. Venema, however, discussed none of these critiques.

    But Venema has a second empirical example he cites to supposedly show the Darwinian evolution of what he calls “CSI on Steroids.” Citing research co-published by University of Oregon biologist Joe Thornton in 2006, Venema calls this “a second fascinating case of a novel function arising through mutation and selection.” But here too, ID proponents had extensively critiqued the experiment when it was first published. And again, Venema failed to discuss or respond to any of these prior arguments from ID proponents. It’s hard to ignore responses from the ID camp to Thornton’s research since there are so many of them. These responses were all published back in 2006 when Thornton’s research was first published:

    Michael Behe on the Theory of Irreducible Complexity
    How to Explain Irreducible Complexity — A Lab Manual
    Paul Nelson on Debating the Controversy That Doesn’t Exist
    Bruce Chapman on the Science Stories that Fizzled (and the One that Might Have Been)
    CSC Director Stephen C. Meyer Responds to Research on Irreducible Complexity
    Casey Luskin: Science Plays Politics, but Implies Behe and Snoke (2004) Supports Irreducible Complexity and ID After All

    Many of these responses will be discussed below.

    Venema claims that Thornton’s research shows “a second fascinating case of a novel function arising through mutation and selection.” As we will see, if by “novel function” Venema means “diminishment of function,” then perhaps he is correct. As a brief and cursory summary of problems with the Thornton et al. research, consider the following points:

    The Thornton et al. research cited by Venema merely found that an alleged precursor enzyme could potentially perform two functions, and then supposedly lost the ability to perform one of those functions. At worst it shows loss-of-function through two mutations. At best, this is an example of small-scale change, which the research of ID proponents like Michael Behe readily concedes is possible. Because Thornton et al.’s research only supported small-scale evolution, which ID proponents don’t question, Behe wrote in response: “This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.”
    Christoph Adami reviewed Thornton et al.’s research in Science, claiming it refuted ID. The research was also puffed in the New York Times as addressing intelligent design after the authors issued a press release entitled “Evolution of ‘Irreducible Complexity’ Explained,” purporting to be a direct response to “[a]dvocates of Intelligent Design.” Whether they are right or wrong, this is amusing since we see ID-critics debating over the scientific controversy that they claim does not exist.
    The authors’ press release gave a retroactive confession of ignorance, admitting that “[h]ow natural selection can drive the evolution of tightly integrated molecular systems … has been an unsolved issue in evolutionary biology.” Yet in the New York Times article, Thornton commented that “There’s no scientific controversy over whether this system evolved. The question for scientists is how it evolved.” So before this study they didn’t know how it evolved, yet somehow they knew it did evolve. It sounds like they are assuming the truth of Darwinian theory rather than testing it.
    Before the paper was published, Thornton had stated on his website that his “goal is to illustrate how a complex, tightly integrated molecular system — one which appears to be “irreducibly complex” — evolved by Darwinian processes.” After ID-theorist Paul Nelson pointed out that this implied that Thornton saw irreducible complexity as a legitimate scientific challenge, the words “irreducibly complex” magically disappeared from Thornton’s website. The episode demonstrates that ID raises legitimate scientific challenges of interest to Darwinian evolutionary biologists, even as they sometimes deny that fact for political reasons.
    In sum, this study doesn’t show how Darwinian evolution scales Mount Improbable, as Dawkins has put it. It simply shows that neo-Darwinism can get you the last 10 yards up the mountain after you’ve already spent 10 hours hiking. It’s an exercise in what Behe called “making grandiose claims based on piddling results.”

    But there’s much more to say in response to this research. Since much of the work responding to it has already been done, the best thing is simply to quote from some of these responses:

    Response 1: Michael Behe’s comments:

    The bottom line of the study is this: the authors started with a protein which already had the ability to strongly interact with three kinds of steroid hormones (aldosterone, cortisol, and “DOC” [11-deoxycorticosterone]). After introducing several simple mutations the protein interacted much more weakly with all of those steroids. In other words, a pre-existing ability was decreased.

    That’s it! The fact that this extremely modest and substantially irrelevant study is ballyhooed with press releases, a commentary in Science by Christoph Adami, and forthcoming stories in the mainstream media, demonstrates the great anxiety some folks feel about intelligent design.

    In the study the authors wished to see if two related modern proteins called the glucocorticoid (GR) receptor and mineralocorticoid receptor (MR) could be derived from a common ancestral protein. Using clever analysis the authors made a protein that they thought represented the ancestral protein. That protein binds several, structurally-similar hormones, as does modern MR. They then introduced two amino acid changes into the protein which are found in modern GR. The two changes caused the ancestral protein to bind the different kinds of hormones anywhere from ten- to a thousand-fold more weakly. That protein bound aldosterone about three-fold more weakly than cortisol. The authors note that modern GR (in tetrapods) also binds aldosterone more weakly than cortisol. So perhaps, the thinking goes, an ancestral gene that could bind both hormones duplicated in the past, one copy accumulated those two mutations to become the modern GR, and the other copy became modern MR.

    […]

    Here are number of comments in response:

    1) This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.

    2) The authors (including Christoph Adami in his commentary) are conveniently defining “irreducible complexity” way, way down. I certainly would not classify their system as anywhere near IC. The IC systems I discussed in Darwin’s Black Box contain multiple, active protein factors. Their “system”, on the other hand, consists of just a single protein and its ligand. Although in nature the receptor and ligand are part of a larger system that does have a biological function, the piece of that larger system they pick out does not do anything by itself. In other words, the isolated components they work on are not irreducibly complex.

    3) In the experiment just two amino acid residues were changed! No new components were added, no old components were taken away.

    4) Nothing new was produced in the experiment; rather, the pre-existing ability of the protein to bind several molecules was simply weakened. The workers begin their experiments with a protein that can strongly bind several, structurally-very-similar steroids, and they end with a protein that at best binds some of the steroids ten-fold more weakly. (Figure 4C)

    5) Such results are not different from the development of antibiotic resistance, where single amino acid changes can cause the binding of a toxin to a particular protein to decrease (for example, warfarin resistance in rats, and resistance to various AIDS drugs). Intelligent design proponents happily agree that such tiny changes can be accomplished by random mutation and natural selection.

    6) In the “least promising” intermediate (L111Q) the protein has essentially lost its ability to bind any steroid. In the “most promising” intermediate protein (the one that has just the S106P alteration) the protein has lost about 99% of its ability to bind DOC and cortisol, and lost about 99.9% of its ability to bind aldosterone. (Figure 4C)

    7) Although the authors imply (and Adami claims directly) that the mutated protein is specific for cortisol, in fact it also binds aldosterone with about half of the affinity. (Compare the red and green curves in the lower right hand graph of Figure 4C.) What’s more, there actually is a much larger difference (about thirty-fold) in binding affinity for aldosterone and cortisol with the beginning, ancestral protein than for the final, mutated protein (about two-fold). So the protein’s ability to discriminate between the two ligands has decreased by ten-fold.

    8) One would think that the hundred-fold decrease in the ability to bind a steroid would at least initially be a very detrimental change that would be weeded out by natural selection. The authors do not test for that; they simply assume it wouldn’t be a problem, or that the problem could somehow be easily overcome. Nor do they test their speculation that DOC could somehow act as an intermediate ligand. In other words, in typical Darwinian fashion the authors pass over with their imaginations what in reality would very likely be serious biological difficulties.

    9) The fact that such very modest results are ballyhooed owes more, I strongly suspect, to the antipathy that many scientists feel toward ID than to the intrinsic value of the experiment itself.

    10) In conclusion, the results (and even the imagined-but-problematic scenario) are well within what an ID proponent already would think Darwinian processes could do, so they won’t affect our evaluation of the science. But it’s nice to know that Science magazine is thinking about us!

    Behe’s point (10) is especially noteworthy since Venema writes about Thornton et al.’s research that “Over and against these lines of evidence, however, the Intelligent Design Movement claims that such novelty is inaccessible to random mutation and natural selection.” But Behe has made it clear that these kinds of modest loss-of-function changes are exactly the type of changes we might expect from Darwinian evolution. So Venema is misrepresenting the claims of the ID movement.

    In fact, Venema undercuts his own argument that this research represents significant novel CSI by admitting that: “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors.” This research does not demonstrate that natural selection and random mutation can produce functional, information-rich genes and proteins because what was produced was not information-rich. If anything, function was diminished or lost rather than gained.

    Response 2: Stephen Meyer’s Comments:

    The Bridgham et al. study published in Science is trivial. ID theorists have long known that a few mutations can slightly alter an existing protein fold. What we question is whether mutation and selection are sufficient to search the enormous combinatorial space of possibilities necessary to finding fundamentally new protein folds and structures. This study does nothing to allay our skepticism on that score.

    Contrary to what the authors assume receptor-hormone pairs do not constitute irreducibly complex systems. The receptor-hormone pair is only a small component of a signal transduction circuit that regulates other complex physiological processes. For such pairs to have any selective or functional advantage many other protein components have to be present, including the other components of a signal transduction circuit and the physiological processes that such circuits regulate. If this is the best that Michael Behe’s critics can do after ten years of trying to refute him, then neo-Darwinism is in deep trouble.

    The really interesting thing about this paper is not the science it contains–its scientific results are trivial–but the sociological dynamics surrounding the publication of these papers. The AAAS has repeatedly insisted there is no scientific controversy about intelligent design. Now Science, the AAAS flagship journal, publishes two articles taking positions on a controversy that the AAAS says doesn’t exist. Will Science now allow Michael Behe to respond or will it only publish articles about the controversy which claim that ID is wrong?

    Response 3: “How to Explain Irreducible Complexity — A Lab Manual”:

    Another response to the Thornton et al. research came from various Discovery Institute authors in a fun piece titled How to Explain Irreducible Complexity — A Lab Manual:

    What [Bridgham/Thornton et al.] do say, however, is biologically meaningless.

    A Tutorial in Evolutionary Theory

    To understand why, we need a brief primer in fundamental evolutionary theory. Natural selection preserves randomly arising variations only if those variations cause functional differences affecting reproductive output. Since Bridgham et al. tell their story by invoking natural selection (see below), the system whose origin they claim to explain must have a selectable function for it to qualify as irreducibly complex. Indeed, given that natural selection favors only functionally advantageous variations, Behe has made clear that “function” in a biological context necessarily means a selectable functional advantage, for an obvious reason: a system of well-matched parts that performs a function can’t lose that function unless it possesses one to begin with. Unfortunately, these receptor-ligand pairs do not meet Behe’s definition of irreducible complexity for an equally obvious reason: receptor-ligand pairs do not by themselves confer any selective functional advantage.

    Indeed, in Bridgham et al.’s scenario, the function undergoing natural selection is not simply MR-aldosterone binding, but electrolyte homeostasis, the complex physiological regulation of essential cellular ions such as potassium or calcium. The novel receptor MR evolved, they write, “because it allowed electrolyte homeostasis to be controlled” (p. 100).

    Natural selection is acting, therefore, not on MR-aldosterone binding alone. Indeed, it cannot, because unspecified binding confers no functional advantage.

    But that is what Bridgham et al. do not seem to understand. They think they are explaining the origin of a single receptor-ligand pair, the mineralocorticoid receptor (MR) protein and the steroid hormone aldosterone. But that is biological nonsense. It is nonsense, moreover, strictly on the grounds of evolutionary theory itself.

    Let’s suppose the newly-evolved cellular receptor, MR, interacts with a hormone ligand, aldosterone. This is a novel relationship. Now, will natural selection preserve it?

    Who knows? Without more information — that is, without more details about the cellular or organismal effect of that novel binding — the bare function “aldosterone binds to MR” is biologically vacuous.

    Compare: Pound a nail, we tell you. Where and why? you ask. Never mind that, we say, just go pound a nail. So you hammer a three-penny nail through the power supply of this blog’s server.

    In any case, the receptor-ligand pair by itself is certainly not irreducibly complex. These pairs represent only small components of complex physiological processes such as metabolism, inflammation, immunity, and electrolyte homeostasis. For such pairs to have any selective advantage as part of the regulation of larger physiological processes, many other protein components have to be present. In particular, all the other components of a complete signal transduction circuit have to be present, as well as the component parts of the physiological process that such circuits regulate. (Even the ligand aldosterone itself doesn’t exist apart from a separate enzyme that produces it, and Bridgham et al.’s gene duplication scenario does not account for the origin of this necessary component either.)

    Bridgham et al. appear to grasp the need for more details (albeit in a distressingly loose way) because both early and late in their paper they specify the functional role of MR. The receptor “is activated by aldosterone to control electrolyte homeostasis” (p. 97) they note, and evolved “because it allowed electrolyte homeostasis to be controlled” (p. 100).

    Thus, in Bridgham et al.’s scenario, the actual system undergoing natural selection is electrolyte homeostasis, not simply MR-aldosterone binding. There’s a good reason for that: as noted, the function “aldosterone-MR binding,” considered in isolation, cannot be a target for natural selection. Try it, if you think it can. You’ll quickly find that you are floating in biological limbo. Aldosterone binds to MR…MR interacts with aldosterone…MR and aldosterone…OK, enough of that. Why does MR interact with aldosterone? Hello? Can we get an organism here?

    Back to Biological Reality

    So — is the physiological system of electrolyte homeostasis, of which both MR and aldosterone are small parts, irreducibly complex? Maybe. Take a look at a physiology textbook, or even any review paper on steroid or receptor biochemistry. Bridgham et al. don’t say much about the complexity of electrolyte homeostasis, however, because they are unaware that they have completely misunderstood the relevant unit of selection in their scenario. They write (p. 98):

    It is not obvious how the tight aldosterone-MR partnership could have evolved. If the hormone is not yet present, how can selection drive the receptor’s affinity for it? Conversely, without the receptor, what selection pressure could guide the evolution of the ligand?

    By Bridgham et al. ‘s own account, however — although they don’t realize it — natural selection is not acting at this level (the MR-aldosterone relationship alone) at all. To have any selectable function, many more components need to brought into the story. Genuine irreducible complexity re-emerges, and will be quite unexplained by the Bridgham et al. scenario.

    Response 4: My Own Comments:

    [L]ook at the bottom line of what this research really found: Adami highlights that the lock and key fit of the glucocorticoid enzyme with the cortisol substrate is based upon the specificity of merely two amino acids, where the precursor molecule was also functional (lacking those 2 mutations).

    In other words, one enzyme might have evolved into another via 2 mutations. This would appear to be a fairly simple system–and, assuming it did evolve in this fashion, an unimpresive example of evolution. Two meager mutations (something which even Behe and Snoke’s (2004) simulations found could evolve under mutation and selection) is not an impressive evolutionary leap and there seems no reason to assume that many enzyme-substrate interactions might not require the simultaneous substitution of many more amino acid residues in order to function, vastly decreasing the likelihood of their evolution. (In fact, this research would not address the origin of complex molecular machines requiring many interacting parts, like the bacterial flagellum.) Even if we grant that this present system is “reducibly complex” (with regards to at least 2 meager amino acids, that is), why should we assume that all the other enzyme-substrate interactions in biology follow suit?

    The last two commentaries combine to make two important points:

    First, the fact that one precursor enzyme could potentially perform two functions, and then lost the ability to perform one of those functions, does not imply that all biologically functional enzymes can evolve in this fashion.

    Second, we must keep in mind that the research of Bridgham/Thornton et al. involved intelligently directing mutations in these enzymes. Since they did not identify specific selective advantages, intelligent agents were doing the selection in a goal-directed fashion, hoping to select for future function. This is important when we consider the research of Axe (2010), discussed in Section 3 above. Axe found that when there is no selective advantage to a given mutation, it has a much smaller chance of becoming fixed in a population.[3] Thus, while a series of intelligently directed mutations might lead back to a functional ancestor, Bridgham/ Thornton et al. have not demonstrated that this pathway is likely to have been followed under natural conditions.

    Venema stated that “If any natural mechanism can be shown to produce “functional, information-rich genes and proteins,” then intelligent design is no longer the best explanation for the origin of information we observe in DNA.” But in this example we have seen that:

    The change was not information-rich
    It’s not clear that natural selection produced this change
    Function was diminished or lost rather than gained

    In fact, Venema undercuts his own argument that this research represents significant novel CSI by admitting in a comment that: “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors.” ID proponents would say the same thing, which is why this research does not demonstrate that a “natural mechanism can be shown to produce ‘functional, information-rich genes and proteins.’” >>
    _______________

    In short the story is by no means the slam dunk one sided case as has been presented.

    KF

  4. 4
    CHartsil says:

    “CHartsil is confused. All that happened with Lenski’s experiment is that the E coli could now utilize citrate in an oxygen-rich environment. They already had that ability in the an anaerobic environment.”

    That was already pointed out. It didn’t have the ability in an aerobic environment.

    “An IC system did NOT evolve via unguided processes.”

    It was dependent on multiple changes in multiple systems and cannot function without all of said changes. It’s IC

    “No new genes were formed. An existing gene was duplicated and put under the control of a different promoter, ie a promoter that was on in the presence of O2.”

    It’s a new gene head to tail opposed to the other.

    “Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren’t anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:”

    Except it WAS already known, a head to tail duplication and a novel regulatory module. That’s the point. It’s new information that is reliant on other, also new information.

    “The change was not information-rich
    It’s not clear that natural selection produced this change
    Function was diminished or lost rather than gained”

    It can now metabolize a food source in an entirely new environment.

    As the generations pass, it only becomes more prominnet

    It was due to a duplication. Also, evolution is not directional.

  5. 5
    Andre says:

    Evolution is not directional? Just the other day we read about research that says evolution likes em getting bigger….

  6. 6
    CHartsil says:

    “Evolution is not directional? Just the other day we read about research that says evolution likes em getting bigger”

    Certain traits are favored in a given environment. That does not mean evolution has a goal in mind

  7. 7
    Collin says:

    “It was dependent on multiple changes in multiple systems and cannot function without all of said changes. It’s IC”

    I don’t think that’s the exact definition of an IC system. The system must have multiple co-dependent PARTS. Not multiple, perhaps linear, changes that must occur before some system functions. They must be concurrently functioning codependent PARTS that, the removal of which, would cause the system to cease functioning.

    Is that the case here?

  8. 8
    CHartsil says:

    “The system must have multiple co-dependent PARTS. ”

    It does, if either the new regulatory module or the new duplicate gene are gone, it can’t metabolize citrate aerobically.

  9. 9
    Collin says:

    CHartsil,

    That’s very interesting.

    I’m not sure how others view IC, but to me it has always been a probabilities argument. I never thought that IC systems were impossible, but merely improbable, and when a system’s complexity increased, so did the likelihood that it could not have evolved by chance.

    So perhaps an arch, an IC system with two legs and a keystone, may have evolved over a given period of time, 10 arches on top of each other might not have done so.

    Does Lenski’s experiment tell us anything about how rarely IC systems come about by chance in nature and the probabilities involved for changes to species that multiply far slower than bacteria? Perhaps like hominids to humans in a relatively brief number of generations?

  10. 10
    CHartsil says:

    “Does Lenski’s experiment tell us anything about how rarely IC systems come about by chance in nature and the probabilities involved for changes to species that multiply far slower than bacteria?”

    Well, it could be repeated pretty much at will after the generation containing the (at least) two potentiating mutations.

  11. 11
    Collin says:

    Here is Behe’s response in 2012.

    http://www.evolutionnews.org/2.....66361.html

  12. 12
    CHartsil says:

    He appears to have just made up the idea of ‘functional coded elements’ as an ad hoc rationalization to explain away the clear cut case of the addition of information by Lenski’s E. coli

    He also gets this wrong

    “It turns out that the bacterium is lacking only a protein to transport citrate into the cell in the presence of oxygen; all other enzymes needed to further metabolize citrate are already present”

    The metabolization actually comes from the new regulator conferred by the head-to-tail duplication.

    What he’s saying is akin to claiming that because humans can breathe, humans breathing underwater would not be a new function

  13. 13
    nightlight says:

    @CHartsil — Where exactly did the experiment demonstrate that the mutations or up/down regulations needed were “random” or “aimless” i.e. that the mechanism was neo-Darwinian?

    Evolution is not just a characteristic of biological systems. It is even more obvious in human technologies, sciences, languages, religions, cultures,… But in all cases where the novelty generating mechanism is understood, it is a purposeful, intelligent process.

    What is the essence of the distinction between the E.coli experiment and all other well understood instances of evolution that demonstrates “aimlessness” or “randomness” in the case of E. coli experiment?

    Note that you can’t say that there is no “intelligence” in the cells. After all cellular biochemical networks know/understand physics, chemistry and biochemistry deeply enough to be able to engineer new cells or organisms from scratch (from simple atoms and molecules), something that human best and brightest scientists are not even remotely capable of. Hence, we do have plentiful, well demonstrated intelligence of the cellular biochemical networks which is far beyond anything human scientists could show.

    Why is that well demonstrated intelligence dogmatically excluded (without any empirical evidence) as the most likely intelligence that generated the observed novelties and the novelty mechanism is declared to be “random” or “aimless” mutation?

  14. 14
    bFast says:

    There are four points that I would like to make in this conversation.

    By the most minimal definition of IC, I think this qualifies. Is this a 2 or a 3 mutational step event? In any case, it is within the range of what Behe describes as “The Edge of Evolution.”

    It was noted that the precursor to this success offered the organism advantage. When the precursor offers disadvantage, that’s when the IC case gets interesting.

    The e-coli in this case were offered EXTREME reward for pulling off this example of minimal IC. It would appear to me that most natural systems would not be so generous with the size of the reward.

    It only took 50,000 generations to get there. If the LCA of human and chimp was about 5 million years ago, and if the human lineage averaged 10 years per generation (close enough) then there are about 500,000 generations in in the human lineage from the LCA of human and chimp. So this small IC event took 1/10 that generational time. The HAR1F took on 18 mutations in that period of time. As the HAR1F is ultra-conserved, It is clear that no individual point mutation in the edited region of the HAR1F offered even neutral effects. In fact, based upon the folding of the HAR1F it is difficult to imagine any less than 6 deleterious mutations were required before a positive one could have come about. This one transaction alone is far beyond the scope of the Darwinian prowess demonstrated in Lenski’s E. Coli.

  15. 15
    CHartsil says:

    “Where exactly did the experiment demonstrate that the mutations or up/down regulations needed were “random” or “aimless” i.e. that the mechanism was neo-Darwinian?”

    Where it could not be repeated prior to the 20,000 generation

    “But in all cases where the novelty generating mechanism is understood, it is a purposeful, intelligent process.”

    False equivocation and affirming the consequent. In technology, objects that are not subject to replication with variation are designed or improved upon with known, testable mechanisms of design.

    “What is the essence of the distinction between the E.coli experiment and all other well understood instances of evolution that demonstrates “aimlessness” or “randomness” in the case of E. coli experiment?”

    Can you refine this question?

    “Why is that well demonstrated intelligence dogmatically excluded (without any empirical evidence)”

    That which is asserted without evidence can be summarily dismissed without evidence.

  16. 16
    Box says:

    CHartsil #12,

    Behe: It turns out that the bacterium is lacking only a protein to transport citrate into the cell in the presence of oxygen; all other enzymes needed to further metabolize citrate are already present.

    CHartsil: He also gets this wrong. The metabolization actually comes from the new regulator conferred by the head-to-tail duplication.

    It might have been more accurate for Behe to have stated that the gene for the citrate transporter, citT, only needs a promoter that functions in the presence of oxygen. IOW the gene for the citrate transporter protein is already present it just lacks a promotor – which is also present as we will see later. In fact Behe is too kind, for the gullible reader it may seem as if a whole new protein is needed.

    Blount et al: One reason that E. coli cannot grow aerobically on citrate is its inability to transport citrate24,31,32. The origin of the Cit+ phenotype therefore required expression of a citrate transporter.

    Behe: The gene for the citrate transporter, citT, that works in the absence of oxygen is directly upstream from the genes for two other proteins that have promoters that are active in the presence of oxygen.

    Okay, so the gene for the citrate transporter needs to get near one of those promotors. How?

    Behe: A duplication of a segment of this region serendipitously placed the citT gene next to one of these promoters, so the citT gene could then be expressed in the presence of oxygen.

    Did we witness an evolutionary miracle? A whole new protein? Are we talking irreducible complexity? Of course not:

    Behe: Gene duplication is a type of mutation that is known to be fairly common, so this result, although requiring a great deal of careful research to pin down, is unsurprising.

  17. 17
    Zachriel says:

    bFast: By the most minimal definition of IC, I think this qualifies. Is this a 2 or a 3 mutational step event? In any case, it is within the range of what Behe describes as “The Edge of Evolution.”

    Irreducible complexity is normally defined as a complex and irreducible system. The derived citrate system fits this definition. The question is whether such a system can evolve. And it clearly can.

  18. 18
    CHartsil says:

    “It might have been more accurate for Behe to have stated that the gene for the citrate transporter, citT, only needs a promoter that functions in the presence of oxygen.”

    Again, wrong. At least two potentiating mutations were also necessary as a genetic drift building block to the duplication and new regulation.

    “Did we witness an evolutionary miracle? A whole new protein? Are we talking irreducible complexity? Of course not”

    Did a system evolve that serves a function which requires multiple interacting components? Yes

    Define IC for us again

  19. 19
    Box says:

    CHartsil #18,

    CHartsil: Again, wrong. At least two potentiating mutations were also necessary as a genetic drift building block to the duplication and new regulation.

    What do you mean ‘wrong’? So it took at least two mutations to get next to the promoter. And? Where did Behe (or anyone) deny that?

  20. 20
    Zachriel says:

    CHartsil: At least two potentiating mutations were also necessary as a genetic drift building block to the duplication and new regulation.

    Not that it matters. If you have a Roman arch built with a scaffold, then remove the last support, it’s only a single step, but the final product is irreducibly complex.

    The question isn’t how many steps are involved, but whether the final product is both complex and irreducible.

  21. 21
    CHartsil says:

    “What do you mean ‘wrong’? So it took two mutation to get next to the promoter. And? Where did Behe (or anyone) deny that?”

    >only needs a promoter that functions in the presence of oxygen.

  22. 22
    Box says:

    CHartsil,

    Box: What do you mean ‘wrong’? So it took two mutation to get next to the promoter. And? Where did Behe (or anyone) deny that?”

    CHartsil: >only needs a promoter that functions in the presence of oxygen.

    That is a correct statement which obviously does not imply that it takes only one mutation to get there. In fact it doesn’t say anything about the number of mutations needed.

  23. 23
    CHartsil says:

    “That is a correct statement which obviously does not imply that it takes only one mutation to get there. In fact it doesn’t say anything about the number of mutations needed.”

    >Only

    http://www.merriam-webster.com/dictionary/only

    >alone in a class or category : existing with no other or others of the same kind

  24. 24
    PaV says:

    CHartsil:

    This is NOT an IC system. In the Discovery response, they point this out.

    Here’s the definition being used: ““a system comprised of interdependent parts, the removal of any of which will cause the system to cease functioning.”

    So, two questions: (1) What exactly was “removed” from the system? and (2) if the bacteria “cease[d] functioning,” then how did it “evolve”? That is, if it ceased functioning, then it would die. Dead things don’t “evolve.”

  25. 25
    CHartsil says:

    “What exactly was “removed” from the system?”

    The potentiating mutations prior to the 20,000th generation. Also, if either the duplicate gene or the new regulator is removed, the cit* ceases functioning.

    “if the bacteria “cease[d] functioning,” then how did it “evolve”? That is, if it ceased functioning, then it would die. Dead things don’t “evolve.””

    It’s talking about individual systems, not the organisms in which the systems reside.

  26. 26
    humbled says:

    The Lenski experiment does nothing other than to show one particular preexisting strain became dominant when an artificial set of environmental conditions were forced on them. No evolution took place.

    If this is the best you’ve got you’re in trouble.

  27. 27
    nightlight says:

    #15 CHartsil

    “Where exactly did the experiment demonstrate that the mutations or up/down regulations needed were “random” or “aimless” i.e. that the mechanism was neo-Darwinian?”

    Where it could not be repeated prior to the 20,000 generation

    How many generations of humans it took to intelligently design cars, airplanes, computers, smart phones…? Intelligence does not imply or require instant success or no failures. Some problems are hard and require many intelligent, yet unsuccessful tries before they are solved. Even mearly realizing that there is a solvable problem and formulating it can take many generations for otherwise intelligent beings.

    Hence, the number of generation before the needed capability is produced does not demonstrate neo-Darwinian mechanism for novelty generation i.e. that it was “random” or “aimless” mutation that generated it.

    The cellular biochemical networks may have well been seeking to optimize their biochemistry to the environment. It just took them that many generations to figure out how to get there from what they had initially. James Shapiro calls this intelligent process “natural genetic engineering” (NGE).

    More generally, the cellular biochemical networks are the same kind of distributed self-programming computers as the networks of neurons making human brains.

    From the research of neural networks, which are mathematical models of such adaptable networks, it is known that when exposed to punishments and rewards, the create and run anticipatory algorithms to optimize their net ‘rewards – punishments’ utility function. These algorithms look ahead, try various actions in their internal model space, follow them up and evaluate consequences, then pick the action in the real world that yields the optimum value for their utility function.

    “But in all cases where the novelty generating mechanism is understood, it is a purposeful, intelligent process.”

    False equivocation and affirming the consequent. In technology, objects that are not subject to replication with variation are designed or improved upon with known, testable mechanisms of design.

    Merely calling new E.coli tries “replication with variation” does not demonstrate that the process was “aimless” or “random”.

    The early PCs had 2MHz single core processors and 4K of RAM, 160K floppy disk. Today, billions of “copies with variation” (if you wish to call it that way) of PCs later, they have 4 or more cores per PC, each running several thousand times faster with tens of thousands more RAM and permanent storage (also accessible thousands times faster).

    There is no essential difference in the requirement and availability of intelligent processes for novelty generation between these “copies with variation” of PCs and “copies with variation” of E. coli. The main difference is the particular implementation of the distributed computers (cellular biochemical networks for E. coli vs networks of neurons forming human brains for PC evolution) and their anticipatory algorithms. But each process was intelligent (in the sense of creating and running anticpatory problem solving algorithms) in its own problem domain.

    In technology, objects that are not subject to replication with variation are designed or improved upon with known, testable mechanisms of design.

    You are defending “randomness of gaps” (ROG) theory — just because our present science hasn’t yet figured out how to “decompile” (reverse engineer) the algorithms used by the cellular biochemical networks to generate novelty, then the process is declared “random” and “aimless”.

    That is as anti-scientific as ‘god of gaps’ since it amounts to saying — move on, nothing to see beyond this point, it is just some “random” and “aimless” chemical reactions that did it, end of story. In fact, neo-Darwinian dogma was repeatedly the major impediment and science stopper for decades, among others in the research of epigenetics and “junk” DNA.

    While we don’t know yet how to decompile (reverse engineer) anticipatory algorithms for most real world adaptable networks, such as brain or cellular biochemical networks, that is possible with our mathematical models (abstractions) of such distributed computers, neural networks.

    Such decompilation of internal algorithms produced by neural networks (when exposed to abstract punishments & rewards) shows that the adaptable networks create internal models of their environment, with self actor (representing the ‘system itself’ in the model space) and the model environment, which may also include other intelligent actors.

    The algorithms (which are self-programmed by the network in the unsupervised learning mode) then run these self actors in the model space forward in model time, just like chess player moving chess pieces several moves forward in his mental model of the chess position, and evaluating resulting final positions in order to decide which move to play on the real chess board.

    Note that J. Shapiro’s NGO represents the decompilation only of few low level disjoint “subroutines” of the algorithms performed by the cellular biochemical networks. Over time, the higher level functions that “call” these “subroutines” will be figured out, then gradually the entire anticipatory algorithms tying them all together will be decompiled as well.

    The neo-Darwinist priesthood will fight this progress every step of the way, just as they fought epigenetic and “junk” DNA research and discoveries. Eventually, though, as always they will quietly submit while morphing their marvelously flexible language, finally declaring, yes, of course, that’s what we actually meant all along.

    “Why is that well demonstrated intelligence dogmatically excluded (without any empirical evidence)”

    That which is asserted without evidence can be summarily dismissed without evidence.

    There is vast amount of evidence for intelligence of cellular biochemical networks.

    Start for example with engineering and synthesizing of new live cells from ‘scratch’ (from simple molecules used as ‘food’). Why don’t you try doing it in the lab without using live cells or their components, but just from basic ‘food’ and ‘light’ that say photosynthetic bacteria use to synthesize new cells.

    Not only you couldn’t do it, but you could take all the world’s best biochemists and molecular biologists together, in one all star team, give them all the resources they ask for, and they won’t be able to synthesize from scratch one live organelle, let alone the whole live cell from scratch. All you will get for the investment will be hundreds of conferences, thousands of papers and millions of words, but not a single live cell to show.

    Yet, while you were reading the above paragraph, your own cellular biochemical networks have achieved such mind-boggling feats of molecular scale bioengineering thousands of times.

    One cell in your little toe knows more physics, chemistry and biochemistry needed for molecular scale bioengineering than all the world’s scientists and sciences put together.

    Of course, needless to mention the vastly greater intelligence needed to construct the live cells plus whole live organism such as animal, plant or human. Our science is light years behind of even dreaming about such feats of molecular engineering.

    So, why is this plainly evident (e.g. from cell reproduction to ontogeny) intelligence in the cells excluded by the neo-Darwinian dogma as the designer and engineer of the genetic novelty behind evolutionary phenomena?

    Note that existence of biological evolution is the strongest argument for Intelligent Design since it takes far more underlying intelligence to engineer and build a system that not only functions well in the initial environment, but that changes over time to adapt to new environments.

  28. 28
    wd400 says:

    The Lenski experiment does nothing other than to show one particular preexisting strain became dominant when an artificial set of environmental conditions were forced on them. No evolution took place.

    Have you read the paper? Or a summary of it? There are lots of mutations, so which have been fixed in different populations, some of those by selection. And there’s ongoing change in mean fitness. That’s evolution.

  29. 29
    wd400 says:

    Nighlight,

    Have you heard of the Luria Delbruk experiment? It’s a pretty clear demonstration that benificial mutations can arise without design (unless, I guess, organisms can see into the uture!)

  30. 30
    Piotr says:

    What he’s saying is akin to claiming that because humans can breathe, humans breathing underwater would not be a new function

    Land artiodactyls —> protocetids —> whales

    Whew! still mammals. Trivial post-flood variation within a kind. (I actualy heard this argument from Robert Byers.)

  31. 31
    Box says:

    WD400: Have you read the paper? Or a summary of it? There are lots of mutations, so which have been fixed in different populations, some of those by selection. And there’s ongoing change in mean fitness. That’s evolution.

    I’ll offer you my summary:

    an already available gene needs to be next to a nearby promoter to express its protein. By way of gene duplication it gets in place. The end.

    Behold the power of evolution! How many generations did this take?

  32. 32
    nightlight says:

    #29 @wd400 “It’s a pretty clear demonstration that benificial mutations can arise without design (unless, I guess, organisms can see into the uture!)”

    Nothing in that or any other experiment demonstrates that mutations were “random” or “aimless”. Exactly the same kind of statistical analysis can be done on evolution of languages or technologies, even though we recognize that intelligent processes were guiding those changes. The evolution of languages is in fact reconstructed in the same way as evolution of biological organisms via measurements of distances, linguistic or genetic.

    As explained in the previous post, there is plenty of clearly evident intelligence in the cells to account for design of the needed biochemical changes in DNA. Cellular biochemical networks are far smarter in problem domain of molecular design and bioengineering that all the human science and technology put together.

  33. 33
    Piotr says:

    Exactly the same kind of statistical analysis can be done on evolution of languages or technologies, even though we recognize that intelligent processes were guiding those changes.

    Interesting. So when, for example, speakers of mainstream British English began to drop their final or preconsonantal /r/’s regularly in words like CAR and CARD in the eighteenth century, it was an intelligently designed process? Or when speakers of Old Latin began to rhotacise intervocalic /s/’s, which led to odd alternations like FLOS/FLORIS, was it deliberate design on their part?

  34. 34
    nightlight says:

    #33 @Piotr ” …it was an intelligently designed process?”

    For the long past changes we can’t generally reconstruct who first came up with some linguistic variation and why. You would need to find who did it first and ask them how did they come up with it. But we can see the process going on today on the web where new words are routinely coined via deliberate process.

    Note also that intelligent process generating novelty need not be conscious in all its steps. In fact the most revolutionary ideas and the most productive intelligent processes are subconscious, in one’s sleep or just ideas that work themselves out in the background and suddenly pop into one’s consciousness while doing something else.

    But even in such cases, the discoverer had often spent great deal of time and effort on the problem, then left it alone, even gave up, then the solution came to him out of a blue as it were.

  35. 35
    wd400 says:

    Nothing in that or any other experiment demonstrates that mutations were “random” or “aimless”. Exactly the same kind of statistical analysis can be done on evolution of languages or technologies, even though we recognize that intelligent processes were guiding those changes. The evolution of languages is in fact reconstructed in the same way as evolution of biological organisms via measurements of distances, linguistic or genetic.

    Did you read the page? It’s hard to believe that you could write this after doing so.

  36. 36
    nightlight says:

    #35 @wd400 “Did you read the page? It’s hard to believe that you could write this after doing so.

    Read that paper ages ago and revisited it since in numerous “debates” as well. Explain where exactly that or any other experiment show that the mutation was “random” or “aimless”. The Luria-Delbruk experiment merely shows that mutants with right resistance to particular phage existed in the population before the experimenters exposed them to the phage. So what? It’s like you running into a question similar to something you have seen before.

    In technological evolution, which we understand to be intelligently guided, that is perfectly analogous to engineer having figured out how to solve some problem (or had developed technique for that type of problem) before the same or similar problem turned up at his new job.

    The pre-existence of either the mutation in biological case or solution in engineering case, doesn’t demonstrate that the mutation/solution was previously produced by a random or aimless process as neo-Darwinian dogma postulates.

    Hence, that experiment is non sequitur regarding the question whether the process generating evolutionary novelties is “random” (“aimless”) or deliberate and intelligent (i.e. in algorithmic language, computed via anticipatory, goal directed algorithms).

    To demonstrate “aimlessness” and “randomness” of novelty generating process in biological systems you need some biological phenomenon that doesn’t have direct analogies in intelligently guided instances of evolution, such as those of technologies or languages.

  37. 37
    wd400 says:

    Well, you might have read the page or indeed the paper. But you haven’t understood the experiment at all.

    (the populations in the experiment start from a single cell. The variance in viable cells that the experiment measures tests exactly the hypothesis you describe)

  38. 38
    nightlight says:

    #37 wd400

    You are welcome to explain how “random” or “aimless” nature of the mechanism behind mutation responsible for phage resistance follows from that experiment. Bacteria has been battling phage for over 3 billions years.

    Why is it implausible that some technique bacteria developed over those billions of years, which it encoded into its DNA, might not happen to be effective against some phage that experimenters in 20th century chose to expose it to?

    There is nothing in that experiment that sheds any light on the mechanism behind the novelty generating process. They only show that the mutation already existed in some bacteria before their exposure. That is a non sequitur regarding the nature of the mechanism that produced those mutations at some earlier time.

    Go ahead, explain how exactly do you deduce from their findings that the mutation was produced (at some earlier time) by a random, aimless process. Such conclusion simply doesn’t follow.

  39. 39
    wd400 says:

    I added a little in an edit that may have crossed with your post Nightlight.

    THe experiment starts from a single cell, so the results can’t be explained by variation that existed before the experiment started.

  40. 40
    CHartsil says:

    “The Lenski experiment does nothing other than to show one particular preexisting strain became dominant when an artificial set of environmental conditions were forced on them. No evolution took place.”

    It was a change in heritable traits and the change was irreducibly complex by any definition.

    I’m even giving IC enough credit to imply it warrants debunking. It’s still just a gap argument.

    nightlight, you missed the point of my post. If you’re claiming that the E. coli was designed and aimed to change in a certain direction, that’s your burden to show that.

  41. 41
    nightlight says:

    #39 @ wd400
    THe experiment starts from a single cell, so the results can’t be explained by variation that existed before the experiment started.

    That’s not correct. They say it was more like 50-500 bacteria:

    “In order to be reasonably certain that the resistant bacteria found in the test had not been introduced into the test culture with the initial inoculum, the test cultures were always started with very small inocula, containing between 50 and 500 bacteria from a growing culture.”

    But even if the culture was grown from a single bacterium, what they have shown was that mutation arose in some bacteria of the colony they grew from the initial culture before the exposure to the phage. That’s all they were trying to prove and then managed to demonstrate experimentally.

    Their experiment demonstrates absolutely nothing about the nature (intelligently guided/computed or “random”, “blind”, “aimless”…) of the process that produced those mutations, at whatever point in time-space they occurred.

    The number of the initial bacteria in the culture, be it 1, 50 or 500, is completely irrelevant for the question about nature of the process that generated the mutation. The contested hypothesis of the neo-Darwinism is that this process is “random” or “aimless”, but that was never demonstrated, either empirically or theoretically.

    Note that “guiding intelligence” need not be some gigantic, non-material hand coming down from heavens to “intelligently” tweak the genes, as Mayer or others from Discovery Institute imagine. Yes, Luria-Delbruk did demonstrate that nothing of that sort (such as any visible heavenly intervention) happened during their experiment.

    But the intelligence in the domain of molecular scale bioengineering is already more than evident in the cell itself. It doesn’t need to come down from heavens as some ancient mideastern shepherds and their modern day followers from Seattle have theorized.

    After all the cell can engineer and construct new live cells from scratch (from simple ‘food’ molecules), which is a feat of biochemistry and molecular biology light years ahead of anything our science knows how to do. To say nothing of the even more mind-boggling intelligence needed to first build trillions of such cells and then compose them into a live organism. The intelligence and depth of understanding of physics, chemistry, biochemistry, programming,… that are required for such project are beyond anything we can presently even imagine doing.

    Just try designing and building from scratch a nano-scale electric motor with performance characteristics comparable to flagellum or ATP synthase that your cells build by the thousands every second without breaking a sweat, as it were.

    Or just type randomly, aimlessly on your keyboard and see whether the instructions on how to do it come through by chance. After all, in the infinitely many among the infinitely many universes, infinitely many of your replicas will surely get it the first time. Any of your infinitely many successful replicas can then report to my replicas in those particular universes what the correct construction procedure is. Give it a shot, you’re sure to hit the jackpot.

  42. 42
    wd400 says:

    I guess I was wrong about the published L-D experiment, though I (and many thousands of undergrads) have done it from 1 cell.

    Note that “guiding intelligence” need not be some gigantic, non-material hand coming down from heavens to “intelligently” tweak the genes, as Mayer or others from Discovery Institute imagine. Yes, Luria-Delbruk did demonstrate that nothing of that sort (such as any visible heavenly intervention) happened during their experiment.

    But the intelligence in the domain of molecular scale bioengineering is already more than evident in the cell itself. It doesn’t need to come down from heavens as some ancient mideastern shepherds and their modern day followers from Seattle have theorized.

    In this scenario the cells have to predict they will face a phage soon. But only some of them, in some lines of the experiment.

  43. 43
    nightlight says:

    #40 CHartsil you missed the point of my post. If you’re claiming that the E. coli was designed and aimed to change in a certain direction, that’s your burden to show that.

    I think you missed my point. The experiment didn’t demonstrate that the phage resistance was result of “random” or “aimless” mutation subsequently filtered by natural selection. There is nothing shown in that experiment (or any other) about the nature of the mutation generating process (random/aimless or intelligent/directed aka J. Shapiro’s NGE process).

    Hence, the experiment doesn’t show that the neo-Darwinian process (RM+NS) is capable of producing or has produced that particular adaptation (whether one calls it IC adaptation or just XY adaptation or anything else). The experiment is simply non sequitur regarding the neo-Darwinian conjecture you are trying to support with it.

  44. 44
    CHartsil says:

    Again, if you’re claiming it was designed to evolve, the burden is on you to show that.

  45. 45
    Andre says:

    This post is ludicrous on so many levels its not even funny……

    The Lenski experiments is nothing more than good old adaptation……. We have seen this with the Galapagos finches, once hailed the definitive proof of a very suspect theory…. The same will happen to the e-coli, when the environmental pressures ease they will revert back to their original form, perhaps we can get Lenski to test that? All biological systems are preloaded with an amount of variables for its environment. There is no single system that can write its own code, it gets that information elsewhere on what it has to do……..

  46. 46
    CHartsil says:

    Andrew, which part are you not understanding?

    It’s a system that evolved that requires multiple interdependent parts

  47. 47
    nightlight says:

    #42 wd400 In this scenario the cells have to predict they will face a phage soon. But only some of them, in some lines of the experiment.

    What’s the difference between that and example of some group of students studying the same school materials, then in the finals some of them can solve particular problem while others can’t, even though they all might be using all their intelligence to figure it out. It is additionally irrelevant whether they all came from the same common ancestor (some ancient Adam and Eve or some such), or even if they are siblings or twins.

    The experiment (along with any other done so far) is simply non sequitur regarding the neo-Darwinian conjecture about the nature of novelty generating process (intelligent/directed vs random/aimless). That is simply a conjecture not backed by any empirical evidence.

    What is even worse than the mere lack of empirical evidence (one can always hope something will turn out eventually) is that simultaneously the conjecture is contrary to the nature of novelty generating processes in any other evolutionary phenomena in which we understand how the novelty is generated, such as evolution of technologies or sciences. In all instances of evolutionary phenomena in which we understand the nature of the novelty generating mechanism we always find the intelligent process as the generator.

    Hence, neo-Darwinist conjecture not only lacks supporting empirical evidence, but it outright contradicts all the existent empirical knowledge about novelty generating processes needed in all other evolutionary phenomena that we understand.

  48. 48
    Andre says:

    CHartsil

    There is no new parts ….. It did not poof out of nowhere, it is existing systems altered and changed to cater for a specific environmental pressure, this is an absolute sure fire sign of a designed system because what we empirically observe here is the following;

    a Risk management strategy, redundancy and a serious amount of fault tolerance!

  49. 49
    CHartsil says:

    And trolling…

  50. 50
    nightlight says:

    #44 CHartsil “Again, if you’re claiming it was designed to evolve, the burden is on you to show that.”

    I am saying that contrary to your claim, the experiment you brought up has no bearing on the question about the nature of the novelty generating mechanism (random/aimless vs intelligent/guided). It sheds no light on the question whether the neo-Darwinian mechanism (RM+NS) suffices to produce the required mutations as you claim it to do.

  51. 51
    CHartsil says:

    “What’s the difference between that and example of some group of students studying the same school materials, then in the finals some of them can solve particular problem while others can’t,”

    Did the students that can solve it get an entirely new brain part which aided them in solving it?

  52. 52
    Andre says:

    Chartsil

    I hope you’re not calling me a troll…… if that is the case you’ve lost this argument that you brought up. I can simply not phantom how somebody that sees purpose in nature all the time deny that purpose and I simply cannot accept this drivel you call aimless or directionless, if this was the case we would see biological systems falling into gooey slops all over the place all of the time, but that’s not the case now is it?

    We observe purpose, we observe direction and we do so empirically.

  53. 53
    nightlight says:

    #51 CHartsil “Did the students that can solve it get an entirely new brain part which aided them in solving it?

    It is irrelevant for the nature of the “novelty generator” (aimless/random vs directed/intelligent), which is the problem being argued in that subthread, how the particular new problem solving capability is encoded.

    As a matter fact, though, the memories are encoded as molecular differences at low enough level.

  54. 54
    computerist says:

    well said nightlight.

  55. 55
    CHartsil says:

    It’s entirely relevant. You compared the addition of functional genetic information to someone being smarter than someone else.

  56. 56
    wd400 says:

    What’s the difference between that and example of some group of students studying the same school materials, then in the finals some of them can solve particular problem while others can’t, even though they all might be using all their intelligence to figure it out?

    Every detail? Is your position really that cells are, in every generation, delibertly trying (and almost always failing) to create specific mutations that will protect them from a phage on the next part of the experiment they are part of?

    What experiment could prove the randomness of mutation to you?

  57. 57
    Andre says:

    Of course there are anomalies in a system (random mutations! Any system with parts are prone to failure and for things to go wrong! If there is no error correction, redundancy or any type of strategy the system will simply fall apart……. We recognize this in biological systems too……..

    If you think I’m talking crap let the science speak!

    http://www.ncbi.nlm.nih.gov/pubmed/22522932

  58. 58
    Upright BiPed says:

    Chart,

    Your attack on IC is misinforned and pointless, as are all such attacks. IC is an intractable fact of biology. In order to organize the cell into an autonomous self-replicator capable of open-ended evolution, you must have — regardless of any particular individual’s beliefs about origins — prescriptive control over matter. In other words, you have to have the translation of information.

    You cannot translate information without IC.

    To translate information into physical effects requires two irreducibly sets of matter. One set must serve as a representational medium (i.e. encode the information) and the other set must establish what the effects of that encoding will be (i.e. have the capacity to produce the specified effect). The organization of the system must accomplish this task while preserving the necessary physicochemical discontinuity between the medium of information and its post-translation effect. All instances of translation have this specific architecture, including the translation of information inside the living cell. It’s a necessity dictated by physical law.

    You are simply unaware of it.

  59. 59
    Paleysghost says:

    Hartsil has had this misguided argument up on his fake group for over a year and it’s been ripped apart Ad Nauseam (just like it has been done above in this thread).

    Why is UD even entertaining this troll?

  60. 60
    Paleysghost says:

    The FACT that nobody else on the entire planet has ever claimed this to be an example of an IC system (including Lenski) should be a tell tale sign of this rambling nonsense.

    Hartsil lies on facebook about having a degree in Cell Biology (while using a fake name) and misunderstands even basic biochemistry.

    UD needs to stop entertaining every troll of the street and stick to reporting actual ID news.

  61. 61
    Upright BiPed says:

    Good grief, is this guy involved in the Facebook crap?

    Goodbye

  62. 62
    nightlight says:

    #56 wd400 Every detail?

    Just the relevant aspects being discussed — the nature of the novel capability/solution generator: is it aimless random process or intelligently guided process. Neither the L-D experiment nor the analogous students example can addresses that question.

    Namely, you brought up the fact that in L-D experiment only some bacteria developed resistance and asserted that this fact somehow implies that mutation was “random” or “aimless”. I brought up the counterexample with students which shows that intelligently guided process (trying to answer the test questions) can also yield only sporadic successes. Intelligently guided does not imply sure success in every try. Hence, the mere generic presence of failures or sporadic successes of some problem solving process sheds no light on the nature of the underlying process. Lot more homework needs to be done before one can connect the two (as described later in this post).

    Is your position really that cells are, in every generation, deliberately trying (and almost always failing) to create specific mutations that will protect them from a phage on the next part of the experiment they are part of?

    Consider processes in your brain which you can introspect directly. There are constantly some flows of thoughts and internal dialogues going on. That doesn’t mean you’re constantly divining and solving some problem that might come up in the finals or in debates at UD. But the thinking process may well be an exercise for something that might come up.

    Similarly, the cellular biochemical networks are constantly computing (thinking) their next optimal action using anticipatory algorithms encoded and accumulated by themselves and their ancestors for billions of years of computations and problem solving. The constant flux of biochemical changes in the these networks (which include DNA and its occasional mutations, although it’s mostly epigenetic activity tweaks) is the molecular manifestation of their computational process, their optimization of the internal state for anything their algorithms anticipate might come next. Your brain does the same kind of anticipatory self-optimization of its internal state for whatever its algorithms anticipate might come next, consciously and unconsciously, and its self-optimization similarly leaves molecular traces throughout the brain.

    The only scientifically demonstrably “random” mutations would be those induced via randomized mutagenic process by the researchers, just as “randomized” drug trial requires researchers to randomize test subjects between placebos and drugs. Anything else can introduce uncontrollable biases and spurious correlations.

    What experiment could prove the randomness of mutation to you?

    Consider an example of someone claiming to toss fair dice randomly. How would you test that claim experimentally?

    You would first construct the model space that contains all the final states for the dice, assign probabilities to each final state of the allegedly “fair dice” (such as 1/6-th to each final face). Then you let them “randomly” toss the dice and if the observed frequencies deviate “too far” (for given certainty level) from the predicted for the random tosses of the “fair dice”, then you know that process wasn’t random in some way. Either the person was tossing it in some particularly “skillful” way, or the dice was loaded i.e. it wasn’t a “fair dice.”

    For DNA molecule no one can presently compute such probabilistic model of “random” mutations since that would require full quantum mechanical treatment of the large molecule and computation of all possible transition probabilities to nearby states within some distance from the initial state (or accessible within some time interval relevant for the experiment). Since such computations even for much smaller molecules is out of reach of present technology, and the dimension of Hilbert space (which is the state space of quantum system) grows exponentially with number of particles, computing such transition probabilities for DNA is astronomically farther out of technological reach.

    Further, on the experimental side of the proof, controlling and measuring the initial microscopic quantum state of each molecule in each test of the model so it matches the initial quantum state used for the model computations (the analogue of letting the person “randomly” toss his “fair dice”) is even harder for our present technology than figuring it out in the model space.

    Note also that over decades under the pressure of falsifying evidence, the neo-Darwinian priesthood has gradually backed off from the above “random toss of fair dice” semantics of their “random” mutation, while retaining the terminology unchanged. The semantics was relaxed into more flexible but more vacuous and even less falsifiable claim: mutation is “random” or “aimless” with respect to “fitness” (a term which either is used as tautology or as another unquantifiable “quantity”).

    Note that merely measuring the actual rate of different “spontaneous” mutations sheds no light on the nature of the underlying “spontaneous” process that generated them (intelligently guidied or undirected random). Anything that can be concluded or reasoned from such empirical rates holds equally well for empirical rates of attempted innovations in any example of intelligently guided evolution (such as that technologies, languages, sciences…).

    In short, there is no presently a way for testing “randomness” or “aimlessness” of the mutation conjecture of the neo-Darwinism, whether one means the stronger or the weaker form.

    Hence, “random mutation” is a vacuous, purely ideological add on (in order to prop atheistic ideology) with no connection to any empirical or theoretical facts or demonstrations. It’s an empty bluff of the neo-Darwinian priesthood imposed via bullying of doubters and heretics into submission.

    For the sake of fairness, neo-Darwinist RM conjecture is no more or less scientifically demonstrable than the Seattle version of ID, in which the “intelligent mind” allegedly sneaks in and out of the “material universe” every now and then, at its whim apparently, to help out the “natural laws” by tweaking some molecules into “irreducibly complex designs” or to inject, somehow, large quantities of “specified complexity.”

    Between the two ideologies, neo-Darwinism is on top for now only because it has bigger and louder bullies on its side. That, plus the hand on the main levers for research funding and peer reviewed publishing. But they are both relics from the centuries past, forever locked in their ancient battle. Both should have been mothballed by 1950s, at the latest, when the DNA structure and some of its functionality were discovered.

  63. 63
    Joe says:

    CH:

    Again, if you’re claiming it was designed to evolve, the burden is on you to show that.

    Again, if you’re claiming it evolved by accumulations of genetic accidents, the burden is on you to show that.

  64. 64
    Joe says:

    This is not an IC system and no one can demonstrate that gene duplications arise via blind and undirected processes.

  65. 65
    Zachriel says:

    humbled: The Lenski experiment does nothing other than to show one particular preexisting strain became dominant when an artificial set of environmental conditions were forced on them.

    They were clones of an initial population, and genetic analysis shows the mutations were not there in the original population.

    nightlight: Nothing in that or any other experiment demonstrates that mutations were “random” or “aimless”.

    That is incorrect. The experiment shows a constant rate of random mutations, roughly r/m – ln(m) = 1.24, where m is the mutation rate, and r is the number of mutants.

    nightlight: Exactly the same kind of statistical analysis can be done on evolution of languages or technologies, even though we recognize that intelligent processes were guiding those changes.

    Evolution of language accents is not due to any overall design.

    nightlight: Similarly, the cellular biochemical networks are constantly computing (thinking) their next optimal action using anticipatory algorithms encoded and accumulated by themselves and their ancestors for billions of years of computations and problem solving.

    The Lederberg Experiment elegantly shows that mutation is random with respect to fitness. See Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

  66. 66
    Joe says:

    They were clones of an initial population, and genetic analysis shows the mutations were not there in the original population.

    Even baraminology accepts the changes that occurred.

    The Lederberg Experiment elegantly shows that mutation is random with respect to fitness.

    Gibberish. The experiment did not show the mutations were genetic accidents, errors or mistakes.

  67. 67
    wd400 says:

    Nightlight,

    “Every detail” was an answer to your question, not a request for clarification. The two scenarios differ in every detail, so don’t make for a good analogy.

    I sincerely think you’ve lost the plot. The scenario you describe is so bizarre (cells predicting the next step of the experiment they are in, then trying (with very low success) to induce a mutation to deal with that next step) that I have trouble believing anyone could sincerely hold it.

    It certainly demonstrates that you are so dedicated to your belief that mutation is not random with respect to fitness that no evidence will sway you (which you more ore less admit your strange passage about quantum mechanics — why should we need a quantum explanation of the distribution of discrerte outcomes for mutation but not for dice rolls?).

    So I’ll leave you to your beliefs.

  68. 68
    Joe says:

    Being “random with respect to fitness” means nothing in a debate about whether or not all mutations are accidents, errors and mistakes.

  69. 69
    Andre says:

    WD400

    I cited a paper that shows that mutations are not random with good evidence. What do you do? You ignore it…. why? Does it challenge your religious beliefs?

  70. 70
    wd400 says:

    Andre,

    This one? It shows the rate of mutation is non-random (which is true) not that mutations are not random with respect their fitness.

    The mainstream evolutionary biology understanding of mutations is that organisms can’t induce the specific mutations they need for a given environment. Simlpy upping the mutation doesn’t conflict with that position.

    (In fact, there are many non-random patterns to mutation that can be explained by evolutionary biology by are hard to understand otherwise — why should mutation rate correlate to effective population size for instance?)

  71. 71
    nightlight says:

    #65 Zachriel

    nightlight: Nothing in that or any other experiment demonstrates that mutations were “random” or “aimless”.

    That is incorrect. The experiment shows a constant rate of random mutations, roughly r/m – ln(m) = 1.24, where m is the mutation rate, and r is the number of mutants.

    The Lederberg Experiment elegantly shows that mutation is random with respect to fitness. See Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.

    Constant rate of spontaneous mutations conferring a phage (or antibiotic) resistance, before and after phage (or antibiotic) challenge, has no bearing on the question whether such mutation is intelligently guided or not.

    For example, in evolution of technologies, the annual rate of say new patents for data storage and data compression algorithms (these are some of innovations in the technological evolution) may remain the same before and after YouTube popularity rose, even though the need for larger storage or better compression increased (since consumers are storing larger and more files than before).

    But that constancy of innovation rate, whether they are genetic mutations or technological inventions, doesn’t shed any light on the nature of the novelty generating mechanism i.e. whether

    ==> a) those novelties were the result of aimless, random errors in production of hard disks or due to algorithm source code copying and typing errors which turned out upon testing by shear luck to improve the storage capacity (analogue of RM+NS), or

    ==> b) the novelties were result of creative, intelligent processes in the brains of the engineers who came up with the techniques for improved storage capacity (better packed disks or better compression of videos).

    But the question (a) vs (b) type of mechanism is precisely the point of contention between the neo-Darwinist hypothesis of type (a), and Intelligent Design hypothesis of type (b), about the nature of the evolutionary novelty generating mechanism.

    In your response, you are basically conflating the terms:

    1) “spontaneous” or “random” in the sense of uncontrolled, unpredictable by the researchers (hence uncorrelated with the fitness attributes researchers chose to measure later), with

    2) “aimless”, “purposeless” in the sense of not being intelligently guided.

    The #1 is attribute of the obserer of the system while #2 is attribute of the system itself.

    What those and other similar experiments which have observed the constant empirical rate of particular spontaneous mutations (that happen to confer improved fitness upon subsequent challenge) demonstrate is the presence of “spontaneous” mutations in the sense #1, while their alleged support for the neo-Darwinist conjecture (a) is “deduced” via equivocation of such observation with the meaning #2 (the unintelligent, aimless mutations).

    Neither L-D nor L & L nor any later experiments shed any light on this point of contention, whether the nature of novelty generating mechanism is of type (a) or of type (b).

    The phenomenon of constant empirical innovation rate for some mutations which happened to confer better fitness under subsequent challenge is no different regarding (a) vs (b) question than the phenomenon of constant empirical rate of some kind of technological patents that just happen to confer greater profitability under subsequent market demands.

    In the latter case (evolution in technologies or sciences) we know that the innovations generating mechanism is an intelligent, anticipatory and creative process in the brains of the innovators. The constant empirical rate for some kind of patents has generally nothing to do with the question whether the innovation process that produced those kinds of patents is intelligently guided or not.

    But the neo-Darwinist dogma insists that the novelty generating mechanism in the evolution of biological systems is the sole exception to the uniform pattern observed in all other cases of evolutionary processes in which we understand the novelty generating mechanism (which is always the result of intelligent processes).

    Hence, the neo-Darwinist conjecture of “random” mutation in the sense #2, is not only unsupported by any direct empirical evidence, but it is also contrary to all other observations of evolutionary phenomena in all other domains in which the novelty generation mechanism is well understood.

    Another counterexample illustrating why such experiments may but need not be able to distinguish between novelty generating mechanisms (a) and (b) could be students doing some multiple choice tests.

    Say, you give elementary school students a college level math test with five answer choices per question. The lazier students may just do their usual thing, randomly circle one of the five choices and move on. The “random” guessers will thus get 20% of correct answers. In contrast, the more diligent or more intelligent students may struggle, try to figure it out, but the problems are just too hard to solve using their clumsy, naive technique in the short amount of time given, so despite their best efforts and intelligence, they too may get only 20% correct answers.

    On the other hand, if you give the same students problems which are at the difficulty level of the materials previously taught in the class, the random guessers will still get 20% answers right, while the intelligent solvers will get much higher percentage of correct answers.

    Note that the same ‘problem difficulty effect’ in this student tests example is observed also in the discussed type of E. coli experiments that compare the empirical rates of favorable mutations before and after some challenge.

    For example, in the famous (and controversial) Cairns et al 1988 E. coli experiments on evolution of lactose metabolism, they found that the exposure to lactose did yield the higher rate of favorable mutations compared to the rate of such mutations in the absence of the challenge. Hence, these experiments were analogous to the above students doing the math test that is at their level, while the earlier L-D or L-L experiments are analogous to the elementary school students struggling with college level math tests, where the random guessing and the intelligent attempts yielded the same test performance.

    nightlight: Exactly the same kind of statistical analysis can be done on evolution of languages or technologies, even though we recognize that intelligent processes were guiding those changes.

    Evolution of language accents is not due to any overall design.

    That’s a straw-man argument. Intelligent Design hypothesis doesn’t require “overall design” either i.e. the deistic front-loading by an omniscient and omnipotent being. That type of ID, which is a theological thesis rather than a scientific hypothesis, is usually promoted by the major mainstream religions.

    But the scientific ID can be based on “intelligence” working incrementally and continuously from within the systems (i.e. performing anticipatory computations of the next state of the system) such as James Shapiro’s “Natural Genetic Engineering” or SFI’s “Complex Adaptive Systems” (adaptable networks) or Stephen Wolfram’s NKS automata & networks etc.

    The scientific, “inside-out” variant of ID is perfectly analogous to the role of intelligent agents in the evolution of languages, sciences, technologies, religions,… In all such cases, the individual intelligent agents don’t provide an upfront “overall design” for the whole language or science or technology, but merely intelligently and incrementally contribute to the “overall design” small bits and pieces, and no single contribution needs to amount to an “overall design.”

    The essential difference between the two kinds of ID, deistic vs “inside-out” ID, is that the latter requires much less front loading i.e. it needs to postulate much less as the basis for its system of knowldge. In the inside-out ID only the simple elemental computing building blocks are postulated as front loaded, then these, rather than some omniscient being, compute the rest as they go, rather than upfront, all at once.

    Note that there is also a third variant of ID, the Seattle ID (aka Discovery Institute’s ID). In that variant the “intelligent agency” makes allegedly its mind to somehow jump in and out of the “material universe” every now and then, at its whim, to help out the “natural laws” by injecting large amounts of “specified complexity” into some systems or twiddling some molecules it decided to favor into “irreducibly complex designs” while leaving other less favored molecules to follow “natural laws.” Seattle ID is basically an absurd, incoherent “god of gaps” position based on fundamental misunderstandings of both, natural science and theology.

    It is in fact a mirror image of its nemesis, the neo-Darwinian “randomness of gaps” perspective. These two anti-scientific relics should have been boxed in a museum long ago.

  72. 72
    Piotr says:

    #62 nightlight,

    Note that merely measuring the actual rate of different “spontaneous” mutations sheds no light on the nature of the underlying “spontaneous” process that generated them (intelligently guidied or undirected random).

    This is not very different from saying that if you flip a fair coin many times, trying to force it psychokinetically to come up heads, psychokinesis works about 50% of the time. The fact that in the remaining tosses the coin comes up tails so consistently must be attributed to some invisible intelligent force thwarting your efforts.

  73. 73
    CHartsil says:

    “The FACT that nobody else on the entire planet has ever claimed this to be an example of an IC system (including Lenski) should be a tell tale sign of this rambling nonsense.

    Hartsil lies on facebook about having a degree in Cell Biology (while using a fake name) and misunderstands even basic biochemistry.”

    Genetic fallacy. You have yet to attempt to show which part of the two potentiating mutations, the duplicate gene and the new regulator can be removed while retaining cit* function.

  74. 74
    CHartsil says:

    Amusing buttmad spyhoppers are amusing and buttmad. All those scientific illiterates (Tiny Tim et al.) on ‘that other’ ID page implying that they’ve done anything but stumble and bumble at Lenski’s E. coli while simultaneously having me blocked, not allowing me to correcting them

  75. 75
    drc466 says:

    CHartsil,

    Let’s try an analogy to Lenski’s experiment, and see if you agree:

    Imagine a car engine that can run on injections of oxygen and nitrogen. There is a LED tied to the injection valve that switches between the two – it runs on oxygen during the day and nitrogen at night. This is an IC system – the engine and all its parts running together. The valve itself is not – by itself a valve switching between oxy and nitro is of no value.

    Now, imagine a “mutation” duplicates the valve, just without the LED control – it is a simple opening direct to nitrogen only. It is not, however, open in to the engine, just out to the oxy/nitro. This does not damage the IC engine at all, nor is it relevant to the overall operation. Nor is this new “stuck valve” IC in and of itself – it is not a system of multiple parts, it is a duplication of a single part.

    Now, a second “mutation” occurs. This mutation causes the original valve to be destroyed, and the new nitro-only valve to connect in to the engine. You now have a “new” IC engine, one that only runs on nitro. It is a “nitro*” engine.

    To your point – the entire engine is still IC, as you can’t just destroy any one part and have it still run – including the new valve. And it took multiple “mutations” to create the new nitro* engine, of which the new valve is one part.

    Questions:
    1) Do you agree that this is a fair analogy to the cit* mutation? Why or why not?
    2) Has any “new” information been created? Does a defective copy of an original count as new information?
    3) Is the valve IC? By analogy, is the mutation in Lenski’s e. coli by itself IC? Or does it need the (existing) IC system already in place (the ability to process citrate)?
    4) In your opinion, does a mutation to an existing IC system count as a “new” IC system? Using the Behe standard – if I modify an existing mousetrap to use a slightly-defective trigger rather than the original trigger, creating a “new” mousetrap that is IC, does that count as the random evolution of an IC system?

    I think you can tell what I think, and why I think Lenski’s experiment doesn’t come even close to qualifying as demonstrating the random evolution of an IC system. And I am sure you don’t agree. But hopefully you can see my point, if you are intellectually honest with yourself.

    [Edited for grammar]

  76. 76
    CHartsil says:

    Strawman. It’s not a switch going back and forth from aerobic to anaerobic. It’s an entirely new system, gene, regulator and all.

  77. 77
    Paleysghost says:

    Top Kek at UD last week.
    Moving right along.

  78. 78
    Joe says:

    CHartsil- It is not a new gene. It is not a new regulator. It is an existing system being used in a different environment.

  79. 79
    CHartsil says:

    It’s a new, duplicate gene and a new regulator in the spots that exactly allowed for cit*

    To the spyhoppers

    “Kid is still going on about this over at UD, but for some reason hasn’t been able to comprehend that the consecutive “STEPWISE” mutations form a very reducible “Pathway” and not even an “Apparatus” of any kind, let alone an IC one.”

    So then which of the two potentiating mutations, one duplication and new regulator can be removed while the cit* can still be conferred? Be specific.

  80. 80
    Zachriel says:

    nightlight: Constant rate of spontaneous mutations conferring a phage (or antibiotic) resistance, before and after phage (or antibiotic) challenge, has no bearing on the question whether such mutation is intelligently guided or not.

    If it’s random, then ascribing intelligence to the process would be an extraneous property.

    nightlight: For example, in evolution of technologies, the annual rate of say new patents for data storage and data compression algorithms …

    Those innovations aren’t random.

    nightlight: Neither L-D nor L & L nor any later experiments shed any light on this point of contention, whether the nature of novelty generating mechanism is of type (a) or of type (b).

    Luria–Delbrück showed the mutations were random. We now know the mechanisms by which mutations occur.

    nightlight: In your response, you are basically conflating the terms: 1) “spontaneous” or “random” in the sense of uncontrolled, unpredictable by the researchers (hence uncorrelated with the fitness attributes researchers chose to measure later), with 2) “aimless”, “purposeless” in the sense of not being intelligently guided.

    No, we used the term random as a probability distribution.

    nightlight: Neither L-D nor L & L nor any later experiments shed any light on this point of contention, whether the nature of novelty generating mechanism is of type (a) or of type (b).

    Sources of mutation include deamination, slipped strand mispairing, error prone replication by-pass, etc.

    nightlight: The constant empirical rate for some kind of patents has generally nothing to do with the question whether the innovation process that produced those kinds of patents is intelligently guided or not.

    If it were guided, it wouldn’t form a random probability distribution.

    nightlight: On the other hand, if you give the same students problems which are at the difficulty level of the materials previously taught in the class, the random guessers will still get 20% answers right, while the intelligent solvers will get much higher percentage of correct answers.

    Which is what we don’t see.

    nightlight: For example, in the famous (and controversial) Cairns et al 1988 E. coli experiments on evolution of lactose metabolism, they found that the exposure to lactose did yield the higher rate of favorable mutations compared to the rate of such mutations in the absence of the challenge.

    Cairns results show the effects of hypermutation under stress, not any sort of intelligent process. The confusion occurs because if you assume a standard rate of mutation, you will see far more beneficial mutations than expected; however, that’s only because there are more mutations overall.

  81. 81
    Zachriel says:

    CHartsil: It’s an entirely new system, gene, regulator and all.

    That’s right. It’s a new IC system that evolved incrementally from a precursor system.

  82. 82
    Joe says:

    It is a duplicate of an existing gene that was placed under the control of an existing regulatory system.

    You evos have absolutely no clue.

  83. 83
    Joe says:

    Luria–Delbrück showed the mutations were random.

    They did not show the mutations were accidents, errors and mistakes- that is the question.

  84. 84
    nightlight says:

    72 Piotr

    #62 nightlight — Note that merely measuring the actual rate of different “spontaneous” mutations sheds no light on the nature of the underlying “spontaneous” process that generated them (intelligently guided or undirected random).

    This is not very different from saying that if you flip a fair coin many times, trying to force it psychokinetically to come up heads, psychokinesis works about 50% of the time. The fact that in the remaining tosses the coin comes up tails so consistently must be attributed to some invisible intelligent force thwarting your efforts.

    Glad you brought that up since the second example I gave with student tests and a note of Cairns 1988 experiments was meant to help preempt that very objection. But it apparently didn’t connect at least with one reader, so let me explain more explicitly why what I stated is very different.

    My statement is that merely observing the constant spontaneous rate in some experiments doesn’t suffice in distinguishing between “random” (aimless) mutations vs intelligently guided mutation. Much more homework needs to be done before one can use such experiments in distinguishing between the two.

    Namely, consider a statement: I weighed myself before and after 4 weeks of using diet pills X, yet there is no difference in my weight. Hence, diet pills X don’t work.

    Does the mere characterization “weighed myself” suffice to draw the conclusion that diet pills X don’t work?

    My point is that such conclusion may, but need not follow. It depends on what exactly “weighed myself” consisted of. For example, if you “weighed yourself” on a postal scale with range of up to 5 pounds, all that such “weighing yourself” will tell you is that before and after the pills you weighed more than 5 pounds.

    Similarly, if you “weighed yourself” on a scale for ships with units of 100 pounds, then all that such “weighing” will tell you is that before and after the pills you weighed approximately 200 pounds +/- 50 pounds, hence no difference again.

    In order for ‘weighing yourself’ to tell you something meaningful about the effectiveness of some diet pills X, you need a scale with suitable range and suitable units.

    That’s precisely what my example with student tests followed by reference to Cairns et al 1988 E. coli experiments was meant to clarify and guard against.

    For example, if you don’t wish to know which of two groups of students is smarter but you still wish to make a confident seemingly empirically based claim about the two groups, you might chose a test which is too hard so nobody will solve any of the problems, or too easy so everyone will solve all the problems.

    That way you can claim “the latest studies show that there is no difference in intelligence” between these two groups of students, even though your tests don’t show anything of the sort. Your tests are telling you more about the tests themselves (revealing their inadequacy) than about the capabilities of the two groups of students.

    That’s exactly how neo-Darwinists (ab)use and equivocate the about ancient L-D and L-L experiments which were not tuned at all for distinguishing between neo-Darwinian “Random Mutation” hypothesis and the alternatives such as intelligently guided mutations. These experiments were meant to prove something entirely different (chiefly that bacteria also follows Mendelian inheritance rules via genes which was a matter of some contention back then since some argued that bacteria doesn’t have genes for inheritance).

    The challenges in those experiments were too hard for the amount of time & population sizes given to the bacteria to solve it reliably via some complex new mechanism, hence their phage (or antibiotic) defense observed were the baseline defaults which worked only probabilistically.

    On the other hand, the Cairns at al 1988 experiments were tuned toward the more sensitive and more relevant range for the question of “random” (aimless) vs intelligently guided mutations. Namely, the amount of time for the gradual starvation was sufficient for at least some of the intelligent novelty generating mechanisms (Shapiro’s NGE) to prove their value and come up with the needed fitness improving mutations with higher empirical rates than the baseline rates of those mutations.

    But if instead, the researchers gave the bacteria only few minutes to adapt or die, or gave them some more time but chose a challenge that requires dozens of new coordinated mutations (instead of just couple) to adapt and survive, they wouldn’t have uncovered any among more intelligent novelty generating mechanisms but would have seen only the default defense mechanisms (the nature of which the experiment wasn’t designed to probe) which may or may not work for the given challenge.

    In short, it is easy to not see what you don’t wish to see i.e. it is trivial to come up with experiments that won’t find some subtle effect (such as intelligent guidance of mutations) if you don’t wish to find it in order to claim it doesn’t exist. You just pick the wrong range of experiment sensitivity which will obliterate any difference, and you’ve got the desired ‘move on, nothing to see here’ result that neo-Darwinians sought.

  85. 85
    CHartsil says:

    “It is a duplicate of an existing gene that was placed under the control of an existing regulatory system.”

    >This led the researchers to conclude that there had been at least two potentiating mutations involved in Cit+ evolution. The researchers also found that all Cit+ clones sequenced had in their genomes a duplication mutation of 2933 base pairs that involved the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem, resulting in two copies that are head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk.

    >by creating a new regulatory module

  86. 86
    CHartsil says:

    “My statement is that merely observing the constant spontaneous rate in some experiments doesn’t suffice in distinguishing between “random” (aimless) mutations vs intelligently guided mutation. Much more homework needs to be done before one can use such experiments in distinguishing between the two.”

    If you’re claiming they’re guided or the result of design, that burden is on you.

  87. 87
    fifthmonarchyman says:

    zac says,

    That’s right. It’s a new IC system that evolved incrementally from a precursor system.

    I say,

    head slap.

    where to start

    The problem is the blatant equivocation of the term “evolution”. The new system does not evolve from the precursor system.

    Think about a reservoir.

    In a sense it is an IC system in that it requires a river and a dam to “function”. However we would never say that a reservoir evolved from a precursor river.

    A river and a reservoir are two separate systems.

    The reservoir is not the result of a random variation in the river filtered by natural selection. Indeed it can’t be so.

    Instead The reservoir resulted from the joining of two separate non related components (the river and a dam).

    That is the jest of the concept of IC.

    Now because in this case we only have two simple naturally occurring components it is not impossible for them to combine spontaneously from time to time and form a new system.

    But the combining is not “evolution” it is a totally different process

    The more integrated components in a system and the more intricate the fit the less likely the system arose by chance. But “evolution” can’t enter the picture at all until after the combination takes place

    I can’t believe the critics still don’t understand what is being argued

    peace

  88. 88
    drc466 says:

    CHartsil,

    So, basically you are claiming that an aerobic citrate permease is, by itself, an IC system – the facts that:
    1) it acts as a “valve” to a larger IC system (the ability to metabolize citrate)
    2) it serves no beneficial function in and of itself (bacteria full of unusable citrate would be counterproductive)
    3) it is a change in the conditions under which an existing function (the ability to uptake citrate) occurs rather than a novel/unique function
    are not relevant.

    An interesting argument. Not buying it, we’ll have to agree to disagree (#2 is a killer, in my mind).

  89. 89
    Zachriel says:

    fifthmonarchyman: The problem is the blatant equivocation of the term evolution. a new system does not evolve from a precursor system.

    And yet the evidence indicates it has happened many times in the history of life.

    fifthmonarchyman: The reservoir is not the result of a random variation in the river filtered by natural selection.

    Have no idea why you brought up a reservoir. But, yes. River systems can be said to evolve, but certainly not by the same process as biological organisms.

  90. 90
    Box says:

    Joe:

    It is a duplicate of an existing gene that was placed under the control of an existing regulatory system.

    Perfect summation.

  91. 91
    fifthmonarchyman says:

    Zac says,

    River systems can be said to evolve, but certainly not by the same process as biological organisms.

    I say,

    Rivers do evolve but they don’t evolve into reservoirs. Indeed they can’t.

    It amazes me that this is not obvious.

    Zac said.

    And yet the evidence indicates it has happened many times in the history of life.

    I say,

    You were responding to a now corrected Typo, At present I’m not claiming that universally no system can change to another only that an IC system is not the result of evolution. Indeed it can’t be. unless you twist the term evolution beyond recognition

    peace

  92. 92
    Zachriel says:

    fifthmonarchyman: Rivers do evolve but they don’t evolve into reservoirs.

    Of course they can. They’re called lakes.

    fifthmonarchyman: At present I’m not claiming that universally no system can change to another only that an IC system is not the result of evolution. Indeed it can’t be.

    Of course it can. One way is through a scaffolding, a complicated but reducible system that is then optimized. Another way is through addition and specialization.

  93. 93
    nightlight says:

    #80 Zachriel

    Constant rate of spontaneous mutations conferring a phage (or antibiotic) resistance, before and after phage (or antibiotic) challenge, has no bearing on the question whether such mutation is intelligently guided or not.

    If it’s random, then ascribing intelligence to the process would be an extraneous property.

    You are using term “random” in the sense #1 from previous post, i.e. as attribute about the knowledge of the researchers about detailed causal chain that generated those mutations. In that sense my term “spontaneous” is equivalent to random #1.

    But then that “random #1” doesn’t have any relevance regarding the contention between the neo-Darwinian conjecture of “aimless random mutation” vs intelligently guided mutation of ID conjecture.

    Namely, your random #1 merely means that researchers have no idea how exactly the mutation was generated and they cannot predict which one and when it will happen. Thus, “random #1” is a fact about researchers’ state of knowledge (lack of knowledge about detailed causal chain behind particular mutation), not about the nature of the mechanism proper.

    But it is precisely the nature of this novelty generating mechanism behind evolutionary phenomena that is at issue between the neo-Darwinism and ID. Is the mechanism intelligently guided or is it aimlessly random?

    To address that question, you need semantics of “random #2” from the previous post i.e. semantics pertinent to the very issue of contention above. That is not the “random #1” as unpredictable or merely spontaneous mutation.

    Hence, something can be “random #1” yet intelligently guided. For example, scientific discoveries or technological inventions are intelligently guided. Yet they are “random #1” in the sense that they happen spontaneously and unpredictably. A researcher of patenting rates may know that there will be 5000 +/- 300 software patents filed this year and may call those filing events “random #1” since he has no idea what exactly will be patented and when. Yet, each of those filings and the inventions being described are results of the intelligent processes.

    Measuring hose patent filing rates and how they change year after year still has no bearing on what is the nature of the process which generated them: where the inventions described in them result of intelligent activity (ID) or of random copying and typing errors (neo-Darwinism).

    Hence the concept of “random” in the sense #1 (which is what you are using) lacks resolution to distinguish the contentious issue between ID and neo-Darwinism.

    nightlight: For example, in evolution of technologies, the annual rate of say new patents for data storage and data compression algorithms .

    Those innovations aren’t random.

    They are random in the sense that they are spontaneous, and each one unpredictable i.e. random in the same sense that L-D and L-L mutations were as far as researchers could tell.

    Just as one can’t know what, when and by whom will be invented, those researcher didn’t know what or when mutation will happen. That type of “random #1” (as unpredictable, uncontrollable process) is equally consistent with intelligent guidance and aimless, undirected event. The semantics of “random #1” simply lacks the resolution to even formulate the problem.

    No, we used the term random as a probability distribution.

    Probability distributions are elements of the mathematical models used for describing randomness which is completely irrelevant for the contentious issue between ID and neo-Darwinism.

    You can have probability distribution of number of technological innovations (e.g. # of filed patents) by year or by country, etc. Yet those innovations are generated by the intelligent processes.

    Hence, the fact that one uses probability distributions to mathematically model “randomness” has no relation with the nature of the novelty generating mechanism — were those innovations results of activity of intelligent processes or of aimless copying and typing errors followed by “natural selection” out of the gibberish of stuff that made sense. The rates or frequencies of the innovations can be modeled via probability distributions in either case.

    Therefore, your “explanation” (“as a probability distribution”), while not false, is completely vacuous regarding the question being debated.

    nightlight: The constant empirical rate for some kind of patents has generally nothing to do with the question whether the innovation process that produced those kinds of patents is intelligently guided or not.

    If it were guided, it wouldn’t form a random probability distribution.

    A guided processes can and are often modeled by probability distributions and treated as random processes, which they are from the perspective of the modeler who doesn’t have inside information about the guidance.

    As a trivial counterexample to your “theory” about relation between concepts “guided” and “random” — consider someone who measures and researches traffic volumes and their various probability distributions over time and locales. For that researcher, these processes are random and are describable by probability distributions. Yet, the path of each car is an intelligently guided process (from the perspective of its driver). Similarly, to each driver whether some car ahead will turn this way or that way on an intersection is “random” yet that other car is simultaneously intelligently guided by the other driver.

    nightlight: On the other hand, if you give the same students problems which are at the difficulty level of the materials previously taught in the class, the random guessers will still get 20% answers right, while the intelligent solvers will get much higher percentage of correct answers.

    Which is what we don’t see.

    Not true. The bacteria can and do control their mutation rates and use that capability to improve their survival odds (Cairns et all 1988). The variety of more recently uncovered mechanisms that James Shapiro named “natural genetic engineering” provide much richer repertoire of levers for finer, more intelligent guiding of the mutations. Similarly the epigenetic effects on DNA can also be categorized as intelligent, targeted and heritable modifications of the cellular biochemistry.

    Cairns results show the effects of hypermutation under stress, not any sort of intelligent process.

    But if a stock broker increases rate of sale of the stocks based on some general sell signal in his charts, then it is called an action of an intelligent agent. You’re merely playing with the semantics of “intelligent” in order to biological processes just bunch of random, unintelligent chemical reactions.

    The confusion occurs because if you assume a standard rate of mutation, you will see far more beneficial mutations than expected; however, that’s only because there are more mutations overall.

    I explicitly said that intelligent guidance need not manifest itself as increased rate of particular beneficial mutations under all circumstances.

    That’s what the students test example was meant to illustrate. The test needs to be calibrated for the students’ level of competence before it can show difference between the intelligent efforts by some students and random guessing by others. If the problems are too hard for any student at a given level to come up with correct solutions in the time provided, the results will show no success dependence on intelligent guidance.

    The intelligent guidance does not imply sure success on every try, or even merely the more successful outcomes under all circumstances or all challenges.

  94. 94
    rhampton7 says:

    I’m having a discussion with Timaeus on another thread and this issue came up.

    Material processes alone (absent an intelligence or will or intent that is at least in part supernatural/non-material) can not generate IC or SC (again, speaking as a proximal cause).

    Now there certainly are a lot of opinions (including those of Meyer, Dembski, Behe et. al.) as to the truth of this statement, but what specifically does the theory of Intelligent Design claim (or the suppositions its built on)? It seems to me that it is agnostic on the matter — it allows that material causation alone may be a sufficient explanation for generating instances of IC or SC.

  95. 95
    Joe says:

    CHartsil- Yes it was a new module as the two were never paired together before.

  96. 96
    nightlight says:

    #86 CHartsil

    “My statement is that merely observing the constant spontaneous rate in some experiments doesn’t suffice in distinguishing between “random” (aimless) mutations vs intelligently guided mutation. Much more homework needs to be done before one can use such experiments in distinguishing between the two.”

    If you’re claiming they’re guided or the result of design, that burden is on you.

    You’re arguing against your own strawman, since your objection has nothing to do with my statement you quoted. I am saying only that the experiment lacks resolution to answer such question. But that’s not equivalent to picking one or the other answer as you suggest I am doing.

  97. 97
    Joe says:

    rhampton- If materialistic processes could produce SC, CSI and IC ID wouldn’t have an argument as ID claims all three are hallmarks of intelligent design.

  98. 98
    rhampton7 says:

    Joe,

    That’s a presumption on your part. Remember, I’m asking specifically what ID theory claims.

    The nests of the Weaver bird would be considered examples IC and SC. So the question becomes, is the intelligence of the Weaver bird sufficiently explained by material processes alone. If yes, then materialism does indeed generate IC/SC. (Weaver birds are representative of any known non-human intelligence, be it mammal, fish, insect, etc.)

    Since we do not know that answer, and ID theory does not claim to provide one, its an open scientific question. Therefore ID is agnostic on the matter.

  99. 99
    Zachriel says:

    nightlight: You are using term “random” in the sense #1 from previous post, i.e. as attribute about the knowledge of the researchers about detailed causal chain that generated those mutations.

    No. Lederberg & Lederberg used it in the sense of uncorrelated with fitness, but Luria & Delbrück used it in the sense of a random probability distribution.

    nightlight: But then that “random #1? doesn’t have any relevance regarding the contention between the neo-Darwinian conjecture of “aimless random mutation” vs intelligently guided mutation of ID conjecture.

    Just curious, what’s ‘intelligent’ about a process that is random with respect to fitness?

    nightlight: Namely, your random #1 merely means that researchers have no idea how exactly the mutation was generated

    Nowadays, we have a great deal of understanding of how mutations occur.

    nightlight: Yet they are “random #1? in the sense that they happen spontaneously and unpredictably.

    While the events of technological innovation and the event of mutations are both random, technological innovation has a non-random effect, while mutations are random.

    nightlight: The bacteria can and do control their mutation rates and use that capability to improve their survival odds (Cairns et all 1988).

    The rate changes, and the rate can vary across the genome, but the mutations are still random with respect to fitness.

    nightlight: But if a stock broker increases rate of sale of the stocks based on some general sell signal in his charts, then it is called an action of an intelligent agent.

    Good analogy.

    No. If he bought or sold randomly, it wouldn’t be considered intelligent. Increasing the rate of buying and selling, such as during periods of market volatility, wouldn’t make him more successful.

  100. 100
    fifthmonarchyman says:

    Zac said,

    Of course they can. They’re called lakes.

    I say,

    How do you think lakes arise? Do you honestly think they arise naturally when rivers “evolve”?

    Lakes are the result of the combination of two separate components a river and an obstruction/dam.

    I can’t believe this is not obvious.

    It’s really difficult to have a discussion with someone who attributes every conceivable change to evolution.

    you say,

    Of course it can. One way is through a scaffolding,

    I say,

    Scaffolding is not evolution it is an entirely different process. A stone does not become an archway by evolving through scaffolding.

    A scaffold combines stones into an archway.

    use your head

    you say,

    Another way is through addition and specialization.

    I say,

    Addition and specialization are not evolution. That is unless you twist the term evolution until it simply means any thing that can possibly happen

    geez

    Can you name a single natural process that you would not consider to be “evolution”?

    peace

  101. 101
    Joe says:

    What ID claims, from Darwinism, Design and Public Education page 92:

    1. High information content (or specified complexity) and irreducible complexity constitute strong indicators or hallmarks of (past) intelligent design.

    2. Biological systems have a high information content (or specified complexity) and utilize subsystems that manifest irreducible complexity.

    3. Naturalistic mechanisms or undirected causes do not suffice to explain the origin of information (specified complexity) or irreducible complexity.

    4. Therefore, intelligent design constitutes the best explanations for the origin of information and irreducible complexity in biological systems.

    rhampton:

    The nests of the Weaver bird would be considered examples IC and SC. So the question becomes, is the intelligence of the Weaver bird sufficiently explained by material processes alone. If yes, then materialism does indeed generate IC/SC. (Weaver birds are representative of any known non-human intelligence, be it mammal, fish, insect, etc.)

    Exactly. However, first material processes have to be capable of producing a living organism.

  102. 102
    nightlight says:

    #99 Zachriel

    what’s `intelligent’ about a process that is random with respect to fitness?

    Intelligent actions in my semantics are those which on average improve survival odds (or for general kind of system, improve relevant ‘rewards – punishments’) compared to the actions which are picked randomly out of all possible actions. Note that survival odds are used here as a synonym for fitness.

    But the intelligent action doesn’t imply improved performance or fitness under all circumstances or all kinds of experiments.

    Hence, merely finding an experiment in which bacterial mutagenic activity doesn’t improve their survival odds could only mean that their “natural genetic engineering” toolkit (manifesting among others in their mutagenic and epigenetic activities) wasn’t up to the challenge posed in the particular experiment. That’s analogous to giving first graders the college level multiple choice math test — results of such tests can’t tell you whether students were randomly guessing among the offered choices or exerting intelligent efforts before picking.

    As long as there are some experiments in which mutations improve their survival odds, there is intelligent guidance (anticipatory computation of some sort) of the mutagenic activity, since the average performance will improve vs that of pure random guesser.

    Consider for example chess playing programs. If the program A picks on average better moves than a program B which always picks randomly among available legal moves, the program A would be classified as “intelligently guided”. Further, among such intelligently guided programs, those which pick better moves on average than some other such programs, they would be considered “more intelligent” than the lower performing ones.

    Regarding intelligence of bacterial, or generally of cellular biochemical networks, my point is that these networks are far more intelligent about the molecular scale bioengineering than all the human biochemist and molecular biologists put together into one all star team. Just give both sides the ‘IQ test’ which requires each to engineer a new live cell from scratch, i.e. from atoms and simple molecules (the ‘food’).

    By the time you read the above paragraph your cellular biochemical networks have achieved this feat thousands of times. In contrast, the ‘all star team’ of human molecular biologists and biochemists, even years later, won’t have a clue how to engineer from scratch a single live organelle, let alone a whole live cell from scratch.

    These cellular biochemical networks (which are mathematically the same kind of distributed self-progamming computers as human brains, just faster and specialized in different domain of problems) understand physics, chemistry and biochemistry of molecular scale engineering at depths that we can only dream about approaching in some far away future.

    Therefore, I find the neo-Darwinian dogma that these networks are modifying cellular biochemistry “aimlessly” and “randomly” as absurd as novice chess player declaring that as far as he can see, the moves picked by the chess grandmaster are random and aimless since he can’t see the rime and reason behind those moves. The cellular biochemical networks are grandmasters of grandmasters in the game of molecular scale bioengineering while humans are novices of novices.

    Any time I see neo-Darwinian priesthood squirming again to hastily explain away yet another finding contradicting their “just some random, dumb chemistry” theory of life and its evolution, it’s like watching the above chess novice trying to explain away yet another checkmate he just got from that randomly moving grandmaster, by going into the Monty Python ‘flesh wound’ routine.

  103. 103
    Joe says:

    The theory of intelligent design (ID) neither requires nor excludes speciation- even speciation by Darwinian mechanisms. ID is sometimes confused with a static view of species, as though species were designed to be immutable. This is a conceptual possibility within ID, but it is not the only possibility. ID precludes neither significant variation within species nor the evolution of new species from earlier forms. Rather, it maintains that there are strict limits to the amount and quality of variations that material mechanisms such as natural selection and random genetic change can alone produce. At the same time, it holds that intelligence is fully capable of supplementing such mechanisms, interacting and influencing the material world, and thereby guiding it into certain physical states to the exclusion of others. To effect such guidance, intelligence must bring novel information to expression inside living forms. Exactly how this happens remains for now an open question, to be answered on the basis of scientific evidence. The point to note, however, is that intelligence can itself be a source of biological novelties that lead to macroevolutionary changes. In this way intelligent design is compatible with speciation. page 109 of “The Design of Life”

    and

    And that brings us to a true either-or. If the choice between common design and common ancestry is a false either-or, the choice between intelligent design and materialistic evolution is a true either-or. Materialistic evolution does not only embrace common ancestry; it also rejects any real design in the evolutionary process. Intelligent design, by contrast, contends that biological design is real and empirically detectable regardless of whether it occurs within an evolutionary process or in discrete independent stages. The verdict is not yet in, and proponents of intelligent design themselves hold differing views on the extent of the evolutionary interconnectedness of organisms, with some even accepting universal common ancestry (ie Darwin’s great tree of life).
    Common ancestry in combination with common design can explain the similar features that arise in biology. The real question is whether common ancestry apart from common design- in other words, materialistic evolution- can do so. The evidence of biology increasingly demonstrates that it cannot.- Ibid page 142 (bold added)

  104. 104
    velikovskys says:

    FFM:
    Lakes are the result of the combination of two separate components a river and an obstruction/dam.

    Actually some rivers do “evolve” into oxbow lakes,

  105. 105
    rhampton7 says:

    Joe,

    I hope you apprecaite that the either or choice “between intelligent design and materialistic evolution” strongly implies that intelligence is non-material — that intelligence is supernatural.

    Now if some intelligences can be strictly material, like the weaver bird, then the best proximal explanation is that nature (materialism) can produce IC/SC even if the ultimate cause can be traced to an intelligent Creator. This is no different than saying lightning is best explained by natural forces even though God created natural forces. It only becomes a stark either-or proposition if you categorically reject any possibility that intelligence can be entirely material.

    Once you make that a priori claim, however, you have committed the same error as materialism. Additionally, by necessity you have forced Intelligent Design theory into being a supernatural proposition since, by definition, intelligence must be non-material. And ID Theory does not make any such claim.

  106. 106
    Joe says:

    rhampton:

    I hope you apprecaite that the either or choice “between intelligent design and materialistic evolution” strongly implies that intelligence is non-material — that intelligence is supernatural.

    Why supernatural? The weaver bird’s intelligence is not strictly material. What gave you that idea?

    Look your very limited point of view doesn’t mean anything. Pre-natural, non-natural are also in play. Artificial also works. We just don’t know- Do you understand that? And science doesn’t care.

  107. 107
    Silver Asiatic says:

    rhampton7

    Intelligence is not what we would call a materialist cause. Materialism is equivalent to a blind, unintelligent cause.

    For example, there is a difference between a pile of logs in a stream and a beaver dam. One is created by intelligence, the other through blind, physical forces.

    The term ‘nature’ is tricky because it can be said that human beings are part of nature. But forensics makes a distinction between a natural cause (accidental) and an intelligent act.

    So, I don’t think it’s correct to consider an animal intelligence as purely material. To do so, we’d have to find somewhere in an animal’s brain, the mechanism that causes a bird to create a nest. But there is some sense of purpose and deliberation in what the bird does — and that cannot be found in materialism alone.

  108. 108
    rhampton7 says:

    How do we know, scientifically, that the weaver bird’s intelligence can not be explained solely by material causation? I understand the philosophical and theological arguments that appeal exclusively to non-material intelligence, but there is no scientific reason to rule out material intelligence.

    Do you believe that ID theory actually refutes any possibility of a purely material intelligence?

  109. 109
    Joe says:

    Demonstrate that purely materialistic processes can produce intelligence and ID would be falsified.

  110. 110
    rhampton7 says:

    I can neither demonstrate that purely materialistic processes can produce intelligence nor that purely materialistic processes can not produce intelligence.

    Because I can not demonstrate either condition, I can not reject the hypothesis that (some) intelligence is non-material, nor that (some) intelligence is material.

  111. 111
    fifthmonarchyman says:

    velikovskys says,

    Actually some rivers do “evolve” into oxbow lakes,

    I say,

    Notice how we have now moved from talking about reservoirs to talking about oxbow lakes. I suppose next you will be saying the pacific ocean is one big reservoir.

    Twisting language like this makes honest communication impossible.

    Are you really willing to pay that price to avoid actually addressing the IC claim on it’s merits?

    Oxbow lakes happen when a body of water is separated from a river. What’s left is no longer a river by definition.

    This is not the same thing as the combination that goes on with IC systems but it’s not evolution.

    It can’t be. That is as long as words have meaning

    Peace

  112. 112
    velikovskys says:

    FFM:
    Notice how we have now moved from talking about reservoirs to talking about oxbow lakes. I suppose next you will be saying the pacific ocean is one big reservoir.

    Actually you were talking about lakes” FFM:
    Lakes are the result of the combination of two separate components a river and an obstruction/dam.

    I was merely pointing out that not all lakes have two components, but yes one of the definitions of reservoir ” a place where fluid collects, especially in rock strata or in the body.” would apply to the Pacific Ocean now that you mention it

    Twisting language like this makes honest communication impossible.

    Not twisting anything,

    Oxbow lakes happen when a body of water is separated from a river. What’s left is no longer a river by definition.

    But that transition required no intelligent design, but the lake has many similarities to the river

    This is not the same thing as the combination that goes on with IC systems but it’s not evolution.

    Unless both are the result of natural forces, taking something that had one function a using it for another .

    It can’t be

    The question is whether that is true

    That is as long as words have meaning

    Sure but just because you call something irreducible doesn’t make it so,

  113. 113
    Eugen says:

    “It appears to be a quite general principle that, whenever there is a randomized way of doing something, then there is a nonrandomized way that delivers better performance but requires more thought.”

    E. T. Jaynes

  114. 114
    CHartsil says:

    “Yes it was a new module as the two were never paired together before.”

    No, it was a new module produced in the lineage of the cit* exclusively.

  115. 115
    nightlight says:

    It seems some member here got offended by something I said and reported me to FB for using pseudonym there, where I also discuss on ID related groups under pseudonym (perhaps “CHartsil” due to recent comments on FB ID group by another member about this thread). So I will drop FB and won’t be posting to those ID groups any more.

  116. 116
    Andre says:

    I know our materialist friends think they understand evolution. Truth is they don’t here is a rebuttal not only for CHartsil but pretty much every other person rooting for Darwin…..

    It is interesting to note that a purely retrospective analysis could easily have concluded that only the rnk-citG and dctA* mutations were involved in the evolution of the Cit++ phenotype. This would imply an adaptive trajectory in which evolution crossed a fitness valley or plateau. However, the earlier evidence (4, 7) for the existence of potentiating mutation(s) shows that this is not necessarily the case. This argues for a degree of caution in interpreting other retrospective analyses of epistasis among mutations that underlie the evolution of any given trait. Later refining mutations can mask the effects of earlier steps, making them difficult to detect and leading to a qualitatively incorrect picture of the evolutionary history. Even in this system, where the existence of potentiating mutation(s) is already suspected, the masking effect of the dctA* mutation makes them difficult to find. Thus far, their identity remains an intriguing mystery.

    http://www.pnas.org/content/111/6/2056.full

    Can I ask those that are good at explaining things to others what this means….. I am not good at that….. Only that it’s an adaptation and who ever argues about those?

    I Trust Chartsil and co, will now count their losses and apologise for wasting people’s time with absolute nonsense they conjured up in their spare time….

  117. 117
    nightlight says:

    #109 Joe Demonstrate that purely materialistic processes can produce intelligence and ID would be falsified.

    There is nothing to demonstrate about it since your request hinges on adherence to one’s personal view that mind and matter are apart (dualism). But your request is vacuous to all the rest of us who have other opinions (panpsychism which is my view, but also idealism and materialism, or generally any monistic view).

    Note that Discovery Institute’s version of ID which your post echoes (that’s what Meyer keeps repeating, too), is also incoherent to anyone who doesn’t share dualist philosophy. That’s a completely needless self-inflicted handicap regarding their acceptance that they chose to impose upon themselves.

    Their message could reach far beyond their little circle of dualists (which is one of the most inelegant among philosophies in history) if they would drop that philosophical monkey off their backs.

  118. 118
    fifthmonarchyman says:

    velikovskys says

    But that transition required no intelligent design

    and

    Unless both are the result of natural forces, taking something that had one function a using it for another .

    I say,

    I will ask you the same question I asked Zac. Are there any natural processes at all that you are not willing to call “evolution”?

    The argument has always been that an IC system can not be the result of evolution not that they can’t arise by other natural processes.

    We see IC systems arising by natural processes all the time think reservoirs or molecules

    Or take a look at fire an IC system with three parts the fuel oxygen and the ignition source.

    Fire can occur by natural processes but it does not occur because the fuel “evolves”. It can not happen that way by definition

    The more independent parts in a IC system and the more intricate the connection the less likely such a system will arise by chance.

    But an IC system can never be the result of evolution. Evolution can only be a factor after the system already exists.

    I can’t believe after all this time this simple basic premise of the argument is not understood by the critics.

    peace

  119. 119
    Joe says:

    rhampton:

    I can neither demonstrate that purely materialistic processes can produce intelligence nor that purely materialistic processes can not produce intelligence.

    Sounds like your position is untestable.

  120. 120
    Joe says:

    nightlight:

    There is nothing to demonstrate about it since your request hinges on adherence to one’s personal view that mind and matter are apart (dualism).

    They are apart.

    But your request is vacuous to all the rest of us who have other opinions (panpsychism which is my view, but also idealism and materialism, or generally any monistic view).

    Find support for your opinions and someone will care.

  121. 121
    Joe says:

    It is very entertaining watching CHartsil misrepresent what happened in the Lenski lab…

  122. 122
    Hangonasec says:

    fmm @ 118

    I can’t believe after all this time this simple basic premise of the argument is not understood by the critics.

    But an IC system can never be the result of evolution. Evolution can only be a factor after the system already exists.

    If you mean ‘true IC’, a pair of parts neither of which could have ever existed independently of the other, then of course evolution can’t go there. But it is not a trivial matter to establish ‘true IC’. Consider the case where part A exists, then part B subsequently arises linked to it, and the pairing proves more successful than A alone. Now, both A and B can subsequently be tuned by the presence of the other, because it is the pairing that is functioning as an evolutionary unit under selection. Initially, B was an ‘optional extra’. But if the pairing evolves in tandem, at some point the option of getting rid of B may be lost completely, because A has come to depend upon it. A form of co-evolution, in other words.

    We come along, in ignorance of history, and declare the system to be IC. But we’re wrong (in the example).

  123. 123
    Joe says:

    IC has been established. And two part systems need not apply. To refute IC as an indicator of ID you have to show the most irreducibly complex structure can arise via blind and undirected processes. You cannot demonstrate a 40 part structure can evolve via blind and undirected processes by showing a two part structure can

  124. 124
    Piotr says:

    #123 Joe,

    2 = 1+1
    3 = 2+1
    4 = 3+1

    38 = 37+1
    39 = 38+1
    40 = 39+1

    Which step in this sequence is impossible?

  125. 125
    Hangonasec says:

    If a 2 part structure can evolve, any additional number of parts can be added serially by the same means. Once A+B has arisen in such a co-dependent manner, AB + C can arise, then ABC + D, and so on. And parts can be lost. Evolution is a bugger for erasing history.

  126. 126
    kairosfocus says:

    DEF’N, adapting Behe slightly:

    What type of biological system could not be formed by “numerous successive, slight modifications?” Well, for starters, a system that is irreducibly complex. By irreducibly complex I mean a single system composed of several well-matched interacting parts that contribute to the basic function, wherein the removal of any one of the [core] parts causes the system to effectively cease functioning. [DBB, 1996, p. 39, emphases and parenthesis added.]

    –> I would have preferred, multiple and specifically arranged and coupled . . .

  127. 127
    kairosfocus says:

    H & P:

    The issue is, that multiple specifically matched core parts need to be correctly arranged and coupled for function in a context where if one is missing, no function. Thus incremental achievement is blocked. And, exaptation runs into Menuge’s C1 – 5:

    For a working [bacterial] flagellum to be built by exaptation, the five following conditions would all have to be met:

    C1: Availability. Among the parts available for recruitment to form the flagellum, there would need to be ones capable of performing the highly specialized tasks of paddle, rotor, and motor, even though all of these items serve some other function or no function.

    C2: Synchronization. The availability of these parts would have to be synchronized so that at some point, either individually or in combination, they are all available at the same time.

    C3: Localization. The selected parts must all be made available at the same ‘construction site,’ perhaps not simultaneously but certainly at the time they are needed.

    C4: Coordination. The parts must be coordinated in just the right way: even if all of the parts of a flagellum are available at the right time, it is clear that the majority of ways of assembling them will be non-functional or irrelevant.

    C5: Interface compatibility. The parts must be mutually compatible, that is, ‘well-matched’ and capable of properly ‘interacting’: even if a paddle, rotor, and motor are put together in the right order, they also need to interface correctly.

    ( Agents Under Fire: Materialism and the Rationality of Science, pgs. 104-105 (Rowman & Littlefield, 2004).]

    That makes blind arrangement and coupling — especially in an automaton that is self-assembling — highly unlikely to the point of effectively impossible, especially when one blends in population genetics and available timeline.

    KF

  128. 128
    Joe says:

    Piotr @ 124- what is your point?

    If you have a 5 component structure that requires all 5 components before it achieves the function what do you do? And if all the parts have to be specific, ie can’t be just any part, what do you do?

  129. 129
    Joe says:

    Hangonasec:

    If a 2 part structure can evolve, any additional number of parts can be added serially by the same means.

    Talk about being naive. If a 2 part structure does one thing and you need another function tat the two part structure doesn’t have, then what?

  130. 130
    kairosfocus says:

    F/N: To get an idea, consider the main gear of the 6500 C3 reel (and the gear train and drag).

    Just the geat. Set up an exact coord system, and acurately locate and align a brass disk with circularity, and accurately alighned sides. Hard already and with multiple IC requisites.

    Then, define a gear tooth profile and cut it along a precise trajectory along the rim. Increment to the next. Continue and have a precise integer number of teeth around the disk. HALT at just the right number.

    Cut a precisely centred keyway and a precisely machined cylindrical cut-out for the drag disk stack.

    Notice, this is already well beyond 125 bytes to describe much less to execute. Real world IC usually implies FSCO/I.

    Proceed in a similar manner for the rest of the parts, then assemble correctly for function.

    IC is a reality and a commonplace.

    In the world of life, things like the flagellum are notorious, but so are co-ordinated communication and control networks, and of course in that context the von Neumann kinematic namomolecular self replicator integrated with a metabolising, encapsulated automaton with smart gating.

    IC is relevant, starting with OOL.

    Go on to any number of systems in complex body plans, of which bird flight is perhaps the clearest and most familiar.

    You may want to quibble on borders and definitions, but the reality is there, staring you in the face.

    KF

    PS: Don’t overlook the implications of the transcendental number nature of pi, a gear can be precise but not exact. Something has to give in circumference or diameter as the two are not commensurate.

  131. 131
    Hangonasec says:

    KF – nonetheless, the incremental argument needs to be addressed, not wafted away. Given that incremental interaction, mutual tuning and loss of prior supporting structures has the potential to generate apparent IC, we would need to eliminate that possibility.

    The heart of the system is the ‘motor’, a rotary ATPase. It has the capacity to generate weak directional motion alone, which would certainly be beneficial against stationary competitors, but would soon be eliminated by swifter, better-steered ones. Attachment of spindle fibres would enhance the efficiency of coupling, and so those weaker movers would soon be outcompeted, and that step of evolutionary history erased.

    Nearly all the proteins in the flagellar assembly have homology with other cellular proteins, so virtually nothing new is evidenced. I know that designers bodge as well, but the point is that little fundamental evolutionary novelty is displayed by the flagellar system, rendering it at least potentially within reach of evolutionary tinkering and tuning. Knocking out one of the proteins now says little about its optionality when first incorporated.

  132. 132
    Hangonasec says:

    Joe:

    Talk about being naive. If a 2 part structure does one thing and you need another function tat the two part structure doesn’t have, then what?

    Who said anything about ‘need’? If you have a 2 part structure, another part can be added to it. If that triumvirate is beneficial, or at least minimally detrimental, you’ve taken a step. If it isn’t, you stay where you are.

  133. 133
    kairosfocus says:

    H, I have to go now, on of those doctor wait type days — long wait, painful, expensive, and you are out of your own control. With bureau -rats on the other sides of the desks, likely hostile. The issue is simultaneity of multiple well matched parts as a pivotal issue. As Menuge highlighted. And BTW, without a viable mechanism for ATP energy battery molecules or the equivalent no cell, then you have to explain the bridge to the present state on observational evidence, yet another chicken egg puzzle that cannot be waved away with a just so story. KF

  134. 134
    Hangonasec says:

    KF – if one is arguing for a particular case declared IC, it is a diversion to demand how some component or other came into existence in the first place. The existence of competent ATPase activity can be taken for granted in all cellular life. How it got there is not a question of direct relevance to the question of whether flagella are or are not IC, in the sense of being ‘unevolvable’ from a non-IC precursor state.

  135. 135
    Joe says:

    Hangonasec:

    Who said anything about ‘need’?

    Organisms have needs. They need functioning systems and subsystems.

    If you have a 2 part structure, another part can be added to it.

    maybe and maybe not. It all depends.

    If you need 5 parts and all you have are two, you lose.

  136. 136
    Zachriel says:

    fifthmonarchyman: How do you think lakes arise?

    All sorts of ways. As rivers and landscapes evolve, lakes can occur due to landslides, oxbows, sinkholes, tectonic forces, glaciers, even volcanoes.

    fifthmonarchyman: Lakes are the result of the combination of two separate components a river and an obstruction/dam.

    There is no river without geology.

    fifthmonarchyman: It’s really difficult to have a discussion with someone who attributes every conceivable change to evolution.

    As we stated, the evolution of rivers is not the same thing as biological evolution. You’re the one who introduced rivers, after all, claiming “we would never say that a reservoir evolved from a precursor river.” But this has nothing to do with biological evolution. Not sure why you brought it up.

    fifthmonarchyman: Scaffolding is not evolution

    Scaffolding in biology can occur when a structure undergoes duplication and mutation, then parts are knocked out. So you might have A then A-A then A-A-A1 then A1-A2-A3 then A1-A3; wherein the complex A1-A3 can’t evolve directly, but is irreducible. A2 is the scaffold.

    fifthmonarchyman: Addition and specialization are not evolution.

    Of course it is. For example, we have A, then a helper is added B. Then some of the function migrates from A to B, so we have A1-B1; wherein the complex A1-B1 is irreducible.

    fifthmonarchyman: Can you name a single natural process that you would not consider to be “evolution”?

    If you mean biological evolution, then anything not biological.

  137. 137
    Joe says:

    Hangonasec:

    Nearly all the proteins in the flagellar assembly have homology with other cellular proteins

    So what? You need the correct number of subunits. You need the correct configuration of those parts and you need some way to communicate with it so it can be controlled.

  138. 138
    Joe says:

    Rivers do not evolve as evolution requires reproduction.

  139. 139
    Zachriel says:

    nightlight: Intelligent actions in my semantics are those which on average improve survival odds (or for general kind of system, improve relevant ‘rewards – punishments’) compared to the actions which are picked randomly out of all possible actions.

    Has to be better than a random distribution, then. There’s no evidence that genetic mutations are intelligent.

    fifthmonarchyman: The argument has always been that an IC system can not be the result of evolution not that they can’t arise by other natural processes.

    “Can not” is a very strong claim. We showed where irreducible complexity can occur in biology through two different processes.

  140. 140
    Joe says:

    Having a random distribution does not mean they are all accidents, errors and mistakes.

    We showed where irreducible complexity can occur in biology through two different processes.

    You don’t even know what you are trying to demonstrate.

  141. 141
    Hangonasec says:

    Hangonasec:

    Who said anything about ‘need’?

    Joe: Organisms have needs. They need functioning systems and subsystems.

    And if they are already viable and competent, those immediate needs are met, by iterated replication of the current blueprint. You are talking about the ‘need’ for an alteration, and then inventing some kind of Universal Block to that need ever being met. One change is OK? Right, evolutionist, try 2! 3! 40! How do ya like them apples!

    Me: If you have a 2 part structure, another part can be added to it.

    Joe: maybe and maybe not. It all depends.

    If you need 5 parts and all you have are two, you lose.

    So, if that is what you really ‘need’, you go extinct. Who cares? The space of possible genomes is littered with places evolution cannot go, or cannot stay long when the environment changes. This does not define the entire space. Modern life is populated exclusively by lineages that did not go extinct. If there was an unfulfillable ‘need’ in some other lineage, it has been erased from the page and need not trouble us. All one has to do is assert that there was not such an unfulfillable need in ours. That is, at least, a perfectly valid logical possibility. You can make the counter-assertion that there was, but the evidence is against you – here we are!

  142. 142
    Hangonasec says:

    Me: Nearly all the proteins in the flagellar assembly have homology with other cellular proteins

    Joe: So what?

    So it substantially increase the likelihood that serial additions can occur. If every component has to be invented afresh, that’s a much bigger problem.

    You need the correct number of subunits. You need the correct configuration of those parts and you need some way to communicate with it so it can be controlled.

    For the Full Monty modern E Coli version, perhaps. But this is a derived state, where the modern parts have been subject to a long history of the co-evolutionary process outlined above. Each amendment causes tuning of the existing components in view of the overall interaction. If A alone had a function, then B is added, A evolves in the presence of B, to the point where B can no longer be removed.

  143. 143
    kairosfocus says:

    H,

    I am not particularly arguing about particular cases, I have noted objections and have identified that IC is both real and relevant. That is a baseline, it really has to be faced.

    I am not satisfied that ever so many objectors are willing to admit even that much. Same, for the deeper challenge, FSCO/I.

    Multiple, matched interacting parts that all have to be present then properly arranged and coupled to achieve function. Function, that if just one of the multiple core parts is missing, will fail.

    The claimed counter example is a case of two components to achieve a function, not several. E Coli already can address citric acid, it already has promoters, just the TWO need to come together.

    For me, the first interesting issue would be how do we get to the two functions and to the mutual fit, the real innovation.

    The coupling of the two components is then in effect one join, and it seems hard to find . . . significant.

    That, to my mind, does not seem to be a test of what IC is about. But, as here we have A + B –> AB, that will be trumpeted as dismissing the real issue.

    That rather reeks of a strawman to me, with all due respect.

    KF

  144. 144
    Piotr says:

    Joe,

    If you need 5 parts and all you have are two, you lose.

    Why? You start with a primitive function, add more parts, and get a more complex system with new secondary functions (exaptations) which may be selected for and fine-tuned.

  145. 145
    PaV says:

    CHartsil:

    PaV: “What exactly was “removed” from the system?”

    Response: The potentiating mutations prior to the 20,000th generation. Also, if either the duplicate gene or the new regulator is removed, the cit* ceases functioning.

    How do you know they were removed?

    PaV: “if the bacteria “cease[d] functioning,” then how did it “evolve”? That is, if it ceased functioning, then it would die. Dead things don’t “evolve.””

    Response: It’s talking about individual systems, not the organisms in which the systems reside.

    I guess you missed my point. If the organism “must” use citrate in an anaerobic environment, and it does not have this putative IC system, then how could it possibly survive??

    If you think it through, the answer is likely that the bacteria has a very reduced ability to synthesize the citrate; but, nonetheless, a reduced ability is there, otherwise it could not survive. The logical conclusion is that the ones that “survive,” survive because they already have some kind of reduced ability to synthesize the citrate. This seems to mean that the ‘added’ mutations simply enhance this reduced capacity. Given enough time, we would expect that through neutral drift, and perhaps some kinds of directed mechanisms, a much greater ability to process the citrate would develop (not ‘evolve’).

  146. 146
    Andre says:

    I apologise this is off topic but news maybe you want to look into this?

    http://www.nature.com/nature/j.....14172.html

  147. 147
    wd400 says:

    Hey Andre, did you miss my reply in #70?

    (I assume, since you said this “I cited a paper that shows that mutations are not random with good evidence. What do you do? You ignore it…. why? Does it challenge your religious beliefs?” that you weren’t simply ignoring it)

  148. 148
    Andre says:

    WD400

    I did miss it. Apologies your link is not working please repost.

  149. 149
    wd400 says:

    Link was to here: http://www.ncbi.nlm.nih.gov/pubmed/22522932

    Confirming this was the paper you were taking about, since it does nothing to show mutations are not rando with respect to fitness.

  150. 150
    wd400 says:

    I guess you missed my point. If the organism “must” use citrate in an anaerobic environment, and it does not have this putative IC system, then how could it possibly survive??

    The medium has a small amoung of glucose. They can survive absent a way to use citrate, than can prosper with a way to use it.

    That put’s pay to most of the rest, but this passage seems to invent a new meaning for the word evolve.

    his seems to mean that the ‘added’ mutations simply enhance this reduced capacity. Given enough time, we would expect that through neutral drift, and perhaps some kinds of directed mechanisms, a much greater ability to process the citrate would develop (not ‘evolve’)

    A change in genotype leading a change in phenotype is evolution. I don’t know how you think drift would find it (or even how that makes any sense at all, since a mutation that adds to efficient use of citrate will have a selective advantage)

  151. 151
    Box says:

    WD400: Confirming this was the paper you were taking about, since it does nothing to show mutations are not random with respect to fitness.

    I have to say that this is not quite true. Martincorena et al argue for non-random mutations with regard to fitness. Although it is also true that they sugarcoat their message with political correctness and extreme caution.

    Thus, although mutations are generally assumed to occur independently of their fitness effect, it is conceivable that local mutation rates themselves might evolve, resulting in genomes whose mutations occur non-randomly: more frequently where they are more often advantageous and less frequently where they are most deleterious.
    Currently, however, there is little evidence that local mutation rates have been optimized during evolution, with the limited exceptions of bacterial contingency loci and somatic hypermutation in the vertebrate immune system.
    Our understanding of how the mutation rate varies along a genome has been restricted by the lack of reliable approaches to measure local mutation rates on a large scale. Experimentally, absolute mutation rates can be determined using gene reporters in fluctuation tests, but
    these are unsuitable for measurements in native genes. Alternatively, in theory,relative mutation rates can be estimated from the accumulation of mutations at selectively neutral positions. Indeed, synonymous or non-coding sites are often used as proxies 7,8 and intriguing correlations between local synonymous substitution rates and gene function or fitness cost have been reported 8,9. However, because selection can act on these sites through factors like codon-usage preference, RNA-folding stability and cis-regulatory elements, interpretation of these observations in support of optimized mutation rates has remained contentious.

  152. 152
    wd400 says:

    The conjecture is that mutations rates can be tweaked in different genomic regions, not that mutations in a given region could be non-random with respect to fitness.

  153. 153
    PaV says:

    wd400:

    The medium has a small amoung of glucose. They can survive absent a way to use citrate, than can prosper with a way to use it.

    From the Wikipedia article on Lenski’s experiment, the bacteria were grown on a minimal growth medium. I suspect that, though “minimal,” there was still plenty of glucose available. Hence, the cit+ mutations were simply, shall we say, a ‘bonus.’ So I still don’t see how this could be considered IC.

    I don’t know how you think drift would find it (or even how that makes any sense at all, since a mutation that adds to efficient use of citrate will have a selective advantage)

    From the Wikipedia page on Lenski’s experiment:

    The authors interpret these results as indicating that the evolution of citrate use in this one population depended on one or more earlier, possibly nonadaptive “potentiating” mutations that had the effect of increasing the rate of mutation to an accessible level.

    There was likely NO selective advantage here because clones taken from before the 20,000th generation could not develop cit+, and the cit+ didn’t develop until the 31,000th generation; hence, as the authors say, they were “possibly nonadaptive.” (In fact, they were likely “nonadaptive.” The fitness did not go up substantially until the cit+ mutation appeared [duplication])

    As to a new definition of evolution, why use the word “evolution” when ‘change’ is just as good? Evolution implies some progressive movement. What “progress” has been made? Is E. Coli now not E. Coli? Should we call it something else?

    The growth medium was “minimal”. What if they grew the Cit+ populations on a glucose rich medium, then what would happen? I suspect the E. Coli would lose the cit+ ability and go back to wild-type E. Coli. So, then, we’re back where we started from. And this is evolution?

    Why not call it what they call it at Wikipedia: “adaptation”?

    Here’s the Webster’s Dictionary definition of “adaptation”: a change in a plant or animal that makes it better able to live in a particular place or situation.

    So, I’ll stick with the word “change.”

    From Wiki:

    The researchers also found that all Cit+ clones sequenced had in their genomes a duplication mutation of 2933 base pairs that involved the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem, resulting in two copies that are head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activates expression of the citrate transporter when oxygen is present, and thereby enabling aerobic growth on citrate.

    There wasn’t a ‘new’ gene that developed, there was an already present gene that was duplicated and put under the regulation of another module. The “potentiating” mutations quoted above had the effect of “increasing” the mutation rate. Everything that happened looks to me to have happened in some kind of a relatively ‘ordered’ way. It reminds of Shapiro’s NGE. I suspect that when we know more, we’ll find out that bacteria, when cultured for so long in a somewhat restricted feeding environment will turn on certain mechanisms that allow certain areas of the genome to start moving relevant parts of the genome around. Then, in a random way, something that increases the fitness will be found. But this smacks of “engineering,” as in NGE.

  154. 154
    Box says:

    Follow up #151,

    Martincorena et al:

    Our observations suggest that purifying selection has driven the evolution of the local point mutation rate in E. coli to reduce the risk of deleterious mutations. This contrasts with most earlier theoretical work that proposed variants of bet-hedging in which frequent positive selection in changing environments leads to the emergence of hypermutators1–3. Instead our observations are in line with an evolutionary risk-management strategy26 in which sustained stronger purifying selection at specific genes favours individuals with preferential protection or repair at these loci, even at a cost of reduced protection of other genes (see Supplementary Information, section 4.3, for a detailed description of the model). In this way, the rate of deleterious mutations in the genome can be efficiently reduced without excessive investment in protection or repair. In addition, this could increase the rate of nondeleterious mutations, so raising the adaptive potential of the population in case of an environmental change.
    We can only speculate about the molecular mechanisms underlying the localized reduction in spontaneous mutations.

  155. 155
    wd400 says:

    Your definition of evolution is… wrong.

    There’s not much point talking abut the mistakes that stem from it.

    I’m pretty sure this is also misleading:

    “The “potentiating” mutations quoted above had the effect of “increasing” the mutation rate”

    Not the mutation rate generally, just the rate at which the cit+ phenotype arose. In other words, the potentiating mutations don’t change the rate at which the cit+ mutations arise, they just create the background in which cit+ mutations can work so when the turn up they are selected for. Contingency.

  156. 156
    franklin says:

    PAV

    Everything that happened looks to me to have happened in some kind of a relatively ‘ordered’ way.

    yes, like point mutations at every possible nucleotide….sometimes more than once…;ordered way;…not so much.

    pav

    The growth medium was “minimal”. What if they grew the Cit+ populations on a glucose rich medium, then what would happen? I suspect the E. Coli would lose the cit+ ability. So, then, we’re back where we started from. And this is evolution?

    Why would you suspect that? Citrate is a suitable source for metabolism and being able to utilize both glucose and citrate would be advantageous over a single food source…….and it appears you don’t understand why citrate is included in bacteria culture media…hint it is to supply necessary iron to the bacteria.

    Which is why, in Lenski’s expt., the evolution of the ability to transport citrate across the cell membrane, in the presence of oxygen, conveyed an advantage to the cultured bacteria allowing them to utilize the additional food source, i.e., citrate.

    pav

    There was NO selective advantage here because there was enough glucose available and because the mutations, as the authors say, were “nonadaptive.”

    there was enough glucose available for the cultures to survive between passages but replication was resource-limited. The evolution of the ability to utilize citrate in the presence of oxygen promoted increased replication due to the ability to utilize citrate as a food resources..

  157. 157
    franklin says:

    wd400

    Not the mutation rate generally, just the rate at which the cit+ phenotype arose. In other words, the potentiating mutations don’t change the rate at which the cit+ mutations arise, they just create the background in which cit+ mutations can work so when the turn up they are selected for. Contingency.

    If I recall correctly the mutations that are being referenced are the ones that occurred to the DNA repair mechanisms in this specific linage.

  158. 158
    fifthmonarchyman says:

    Zac says,

    If you mean biological evolution, then anything not biological.

    and

    We showed where irreducible complexity can occur in biology through two different processes.

    I say,

    So if occurs in biology it is the result of evolution no mater what the process that gave rise to it.

    There you have it in black and white. According to Zac if it occurs in biology it must be the result of evolution.

    It should be obvious that given these presuppositions “evolution” is the only game in town.

    Given this mindset IC structures must arise by evolution because obviously they exist.

    Talk about circularity

    peace

  159. 159
    fifthmonarchyman says:

    wd400 says,

    A change in genotype leading a change in phenotype is evolution.

    I say,

    Well there you have it. GMOs are evolution. HGC is evolution transposons are evolution. Apparently everything biological is evolution.

    I’ll ask you the same question I asked Zac. Is there any natural process that you would not consider evolution?

    peace

  160. 160
    fifthmonarchyman says:

    Hangonasec says,

    If you mean ‘true IC’, a pair of parts neither of which could have ever existed independently of the other, then of course evolution can’t go there.

    I say,

    That is not the definition of IC. A system is IC if the system can’t exist with out all the parts. The individual parts may or may not exist on their own.

    Think of an archway the individual stones can exist but a structure is not an archway until all the stones are present and interacting with each other.

    It is impossible for such a structure to arrive via evolution this should be obvious.

    you say,
    Consider the case where part A exists, then part B subsequently arises linked to it, and the pairing proves more successful than A alone.

    I say

    More successful at what? We need to define what we are talking about System(A union B) is not the same system as part A alone.

    This should be obvious. Part A can not “evolve” into system (a union B) by definition.

    This is not to say that it is not possible for system (A union B) is arise by natural processes only that it can’t arise by “evolution”

    The more parts and the more intricate the union the less likely a system can arise by chance. But an IC system can never arise by evolution.

    This is unless you define evolution as anything that happens in biology and render intelligent communication impossible.

    peace

  161. 161
    wd400 says:

    I’ll ask you the same question I asked Zac. Is there any natural process that you would not consider evolution?

    Countless. If we restrict ourselves to biology and changes in populations (not individuals) the changes brought about by the same genes expressed in a different environment (so called phentypic plasticity) aren’t evolutionary changes. Likewise some animals responses to climate change (migration, change in mating effort/time) are probably not evoltionary changes either (just the same genes in new environment).

    Would you seriosuly argue a change in genotype leading to a change in phenotype is not as example of evolution?

  162. 162
    franklin says:

    fmm

    More successful at what? We need to define what we are talking about System(A union B) is not the same system as part A alone.

    Might be. Myoglobin/hemoglobin and the loading/unloading of oxygen.

  163. 163
    fifthmonarchyman says:

    Wd400 says,

    Would you seriosuly argue a change in genotype leading to a change in phenotype is not as example of evolution?

    I say

    If a change is not ultimately the result of random variation filtered by natural selection then it is not evolution. Would you claim otherwise?

    you say,

    The changes brought about by the same genes expressed in a different environment (so called phentypic plasticity) aren’t evolutionary changes.

    I say,

    So at least we agree on one process that is not evolution. That is something I guess. Can you think of any permanent biological change that is not evolution?

    peace

  164. 164
    fifthmonarchyman says:

    franklin says,

    Might be. Myoglobin/hemoglobin and the loading/unloading of oxygen.

    I say,

    Are you honestly claiming that because Myoglobin and hemoglobin both handle oxygen that they are the same system?

    Are a donkey and a pickup truck the same system because they both can carry cargo?

    peace

  165. 165
    wd400 says:

    If a change is not ultimately the result of random variation filtered by natural selection then it is not evolution. Would you claim otherwise?

    It may still be evolution, though not evolution by natural selection. (There were once many theories of evolution, after all).

    Can you think of any permanent biological change that is not evolution

    Can you? The only “permanent” biological change I can think of is extinction, and that’s certainly a change in allele frequencies (to zero!)

  166. 166
    franklin says:

    fmm

    Are you honestly claiming that because Myoglobin and hemoglobin both handle oxygen that they are the same system?

    In order to understand my example you would have to know something about how myoglobin and hemoglobin function. Once you understand that you will clearly see how that example answers your question:

    More successful at what? We need to define what we are talking about System(A union B) is not the same system as part A alone

  167. 167
    fifthmonarchyman says:

    Wd400 asks,

    Can you?,

    I say,

    Of course, Off the top of my head
    Things like HGT are not evolution. Combining two systems into a new third system is not evolution. Cope’s rule is not evolution if the changes are the result of innate tendencies.

    peace

  168. 168
    wd400 says:

    Well, I guess if you want to make up your own definitions of words that’s fine. But it makes it hard to talk to others when you do that.

  169. 169
    Joe says:

    Piotr:

    You start with a primitive function, add more parts, and get a more complex system with new secondary functions (exaptations) which may be selected for and fine-tuned.

    And if it takes 5 parts before some primitive function exists? What about systems that require thousands of parts- systems that cannot be built up slowly? Bacterial flagella only have 30-50 different proteins but some of those have thousands of subunits. And you have to avoid cross reactions during formation.

  170. 170
    Joe says:

    Hangonasec:

    And if they are already viable and competent, those immediate needs are met, by iterated replication of the current blueprint.

    So now you are arguing against evolution. LoL!. How did they get to be viable and competent? Those IC systems that make them so had to come about some way.

    And the rest of your post is evidence-free wishful thinking.

  171. 171
    Joe says:

    How was it determined that gene duplications are blind watchmaker processes?

  172. 172
    PaV says:

    wd400:

    Your definition of evolution is… wrong.

    That’s interesting, because I think your understanding/definition of evolution is wrong.

    There’s not much point talking abut the mistakes that stem from it.

    Do you mean that I deviate from the orthodoxy that evolutionary biologists impose? Is that a correct understanding of what you wrote?

    I’m pretty sure this is also misleading:

    “The “potentiating” mutations quoted above had the effect of “increasing” the mutation rate”

    Think again. I didn’t say that the mutation rate of cit+ went up all by itself; I said that the mutation rate went up, which, of course, would mean E. coli could find the necessary mutations for the cit+ easier/faster.

  173. 173
    PaV says:

    franklin:

    Why would you suspect that? Citrate is a suitable source for metabolism and being able to utilize both glucose and citrate would be advantageous over a single food source…….and it appears you don’t understand why citrate is included in bacteria culture media…hint it is to supply necessary iron to the bacteria.

    Citrate is a suitable source for metabolism in organisms that can metabolize them. But in a minimal growth medium, a “limited” growth medium, where glucose serves as the carbon source, citrate is present at a very low level, and is not the carbon source.

    When the E. coli attains the ability to metabolize the citrate, then, and only then, does it become an advantage to the E. coli with this ability, an advantage it exercises over the E. coli that can’t metabolize the citrate. Hence the relative fitness increases.

    Now, I’ve already noted that the growth medium being used was “limited” in the glucose available to all the bacteria experiencing growth, so that, in effect, there is some advantage to be able to metabolize citrate. Now, throw all kinds of glucose at the organism that can metabolize citrate, and, I would suspect the E. coli will return to its wild type.

    Again, evolution? Run the experiment I’m proposing. Prove me wrong.

    The rest of your post is just obvious.

  174. 174
    wd400 says:

    That’s interesting, because I think your understanding/definition of evolution is wrong.

    I’m certainly very confident that one of us doesn’t know very much about evolution. You are just wrong to think evolution means “progress” or enough progress to change a species name(!).

    I don’t know why I bothered filling in the gaps in your knowledge of the Lenski experiment, it’s obvious you have no need of just details in creating your opinions.

  175. 175
    PaV says:

    wd400:

    Well, I guess if you want to make up your own definitions of words that’s fine.

    And I guess if you want to define meaningless statements as actually having meaning, you can do that, too.

  176. 176
    PaV says:

    Here’s Michael Behe’s take on the Lenski experiment. Why hasn’t this been talked about?

  177. 177
    franklin says:

    pav

    Citrate is a suitable source for metabolism in organisms that can metabolize them. But in a minimal growth medium, a “limited” growth medium, where glucose serves as the carbon source, citrate is present at a very low level, and is not the carbon source.

    In the Lenski expt glucose levels in the culture media were 25 ppm yet, contrary to your claim, citrate levels were over 350 ppm. Hardly low levels by any consideration. So, pav, you were wrong on this issue as well as the other details that have been pointed out to you. One gets the feeling you aren’t really familiar with the Lenski expt(s) or the ‘animal’ model being used.

    At a concentration of >350 ppm the citrate represents a significant food resource if it can be utilized by the bacteria.

    pav

    When the E. coli attains the ability to metabolize the citrate, then, and only then, does it become an advantage to the E. coli with this ability, an advantage it exercises over the E. coli that can’t metabolize the citrate. Hence the relative fitness increases.

    All e coli have the ability to metabolize citrate. The fitness increase in the Lenski expt(s) was not due to the bacteria developing the ability to metabolize citrate…it already had that ability! Wrong again, PaV.

  178. 178
    Eric Anderson says:

    Joe:

    Rivers do not evolve . . .

    Sure they do.

    You just have to use one of the ever so many definitions of that slippery word: “change over time.”

    The word “evolution” has so many disparate definitions in practice (and I’m talking about the literature, not just blogs and lay commentary), that it is a real challenge just to keep track of them.

  179. 179
    Eric Anderson says:

    CHartsil:

    Here is the bottom line.

    First of all, thank you for taking time to post your thoughts about Lenski’s E. coli experiments. There has been much discussion, and several commenters have addressed the details of those experiments. Unfortunately you continue to persist in assertions that a new irreducibly complex system evolved right before our eyes and that, therefore, Lenski’s experiments somehow refute Behe’s notion of irreducible complexity specifically, and the design inference generally.

    At the risk of restating some of the points that have already been made in this thread, there are three key issues that need to be brought to the fore.

    1. Your position appears to be based more on enthusiastic pro-evolutionary commentary than on the actual science. Again, I would refer you to Behe’s 2010 paper or at least the discussion posted by kairosfocus @2-3 above to get a more objective view as to what actually occurred via the evolutionary mechanisms. The adaptive changes were small in both number and scope, did not result in the creation of any information-rich structure, and likely resulted from a loss of function of pre-existing parts.

    2. You are implying, if not directly stating, that Lenski’s experiments refute Behe. That is a misrepresentation of Behe’s arguments. Behe has certainly never argued that if a significant adaptive advantage can be obtained by making a small number of mutations to a pre-existing irreducibly complex structure, in a large population, over thousands of generations, under extreme selective pressure, that a trial-and-error process like random mutations plus natural selection could never produce such a change. Indeed, Behe himself has looked at similar situations with malaria and sickle-cell anemia, and such changes are well within what he has termed the “edge of evolution.”

    And that is setting aside for a moment the fact that subsequent research suggests that the adaptations in Lenski’s E. coli might well be instances of loss of pre-existing function – breakage of cellular mechanisms – rather than gain of additional function. Such a result would follow Behe’s “First Rule of Adaptive Evolution,” which says (roughly paraphrasing) that if a selective advantage can be obtained either by breaking a pre-existing functional structure or by building a new structure, then evolution will break the pre-existing structure. Thus, if anything, Lenski’s experiments support both Behe’s notion of irreducible complexity, as well as his rule of adaptive evolution.

    3. Finally, and perhaps most importantly, we need to step away from the angels-on-the-head-of-a-pin claim that we are dealing with a “new” IC system, rather than a minor adaptation of an existing IC system. Although the latter is clearly the case, I will defer for a moment, just for purposes of discussion. Let’s assume, as you vocally insist, that Lenski’s E. coli experiments show a “new” IC system, just for argument’s sake. What does that teach us?

    Ultimately, what we are dealing with is this:

    According to the Darwinian storyline, complex, functional, information-rich structures are supposed to arise by evolution all the time. Yet after decades of dedicated research to find the smoking gun of evolution and after billions of dollars collectively spent by the evolutionary community on the effort, what does evolutionary theory have to show for it?

    Well, for one thing we have Lenski’s results: A small number of beneficial mutations to a pre-existing biological system that eventually occurred after thousands of generations in a large population that was subject to extreme selective pressure. This is an interesting result, to be sure. But in the context of the larger claims of evolution’s grand creative power, it is a pittance, a rounding error, the exception that proves the uncomfortable rule. It is well within the edge of evolution that Behe has proposed, and does nothing to suggest that the Darwinian mechanism has any great creative power.

    Conclusion:

    When viewed objectively, without the blinders of materialistic philosophy, Lenski’s experiments are strong evidence for, and a powerful vindication of, Behe’s arguments in particular, and the skeptics of Darwinism in general.

    At the end of the day, Lenski’s E. coli are just another in a long line of Darwinian claims that, upon closer inspection, fail to live up to their hype: from moth coloration to finch beaks to antibiotic resistance in bacteria. In each case, when these examples are carefully studied, instead of supporting the grander claims of the evolutionary creation story, they inadvertently demonstrate the pathetic impotence of Darwinian mechanisms and underscore the need for an alternative source of innovation in the history of life.

  180. 180
    Upright BiPed says:

    …and of course, there is that one other little tidbit where Darwinian evolution requires IC to even exist.

    🙂

  181. 181
    Mung says:

    Mere details UBP. With sufficient imagination they can be overcome.

  182. 182
    Paleysghost says:

    “The Darwin camp has found a new mechanism, thanks to their supporter Christopher Hartsil (real name withheld to protect the identity of a minor) and his wonderful discovery of “Reducible Simplicity”.

    Lenski’s Cit. observations involve an extremely simple biochemical pathway which is formed from 2 consecutive (easily reducible) mutations, thus proving Darwinian evolution is true!!

    …as highlighted by Michael Behe in 1996 and 2007.

    Keep up the good work there, buddy.”

  183. 183
    Paleysghost says:

    End thread//

  184. 184
    Zachriel says:

    fifthmonarchyman: So if occurs in biology it is the result of evolution no mater what the process that gave rise to it.

    No.

    The argument based on irreducible complexity is that there are no plausible intermediate steps. We provided two plausible scenarios where irreducible complexity can evolve step-wise.

    fifthmonarchyman: Is there any natural process that you would not consider evolution?

    Only biological organisms are subject to biological evolution. Are you conflating this with other uses of the word evolution, as you did with rivers above?

    fifthmonarchyman: Think of an archway the individual stones can exist but a structure is not an archway until all the stones are present and interacting with each other. It is impossible for such a structure to arrive via evolution this should be obvious.

    Yet archways can form naturally.

    fifthmonarchyman: Part A can not “evolve” into system (a union B) by definition.

    Argument by definition is not an argument.

    fifthmonarchyman: This is not to say that it is not possible for system (A union B) is arise by natural processes only that it can’t arise by “evolution”

    Scare-quotes don’t constitute an argument either.

    fifthmonarchyman: The more parts and the more intricate the union the less likely a system can arise by chance.

    It’s not chance, but posited incremental adaptation leading to step-wise evolution of irreducible complexity.

    PaV: Here’s Michael Behe’s take on the Lenski experiment.

    Behe, Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,Quarterly Review of Biology 2010: “If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.”

  185. 185
    Zachriel says:

    Paleysghost: Lenski’s Cit. observations involve an extremely simple biochemical pathway which is formed from 2 consecutive (easily reducible) mutations, thus proving Darwinian evolution is true!!

    Um, no. See Blount et al., Genomic analysis of a key innovation in an experimental Escherichia coli population, Nature 2012: “The Cit(+) trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter. The clades varied in their propensity to evolve this novel trait, although genotypes able to do so existed in all three clades, implying that multiple potentiating mutations arose during the population’s history.”

  186. 186
    PaV says:

    wd400:

    You are just wrong to think evolution means “progress” or enough progress to change a species name(!).

    With all due respect, no, I am not wrong. To say a worm “evolved” into a worm makes no sense.

    Here’s the Webster Dictionary definition (quibble with them):

    1. the process by which different kinds of living organisms are thought to have developed and diversified from earlier forms during the history of the earth.

    [synonyms: Darwinism, natural selection
    “his interest in evolution”
    ]
    2. the gradual development of something, especially from a simple to a more complex form.

    If you want to talk about “microevolution” and “macroevolution,” then that’s something different. But why equivocate when it comes to the meaning of “evolution”?

    wd400:

    I don’t know why I bothered filling in the gaps in your knowledge of the Lenski experiment, it’s obvious you have no need of just details in creating your opinions.

    Again, with all due respect, I know of no “gaps” that you filled in.

    Your concern is with, and only with, allele frequencies. Well, if you’re a population geneticist, and you are, then this has been the object of your adult professional life. Does this alone give you the right to call it “evolution,” and then say that this is what science says? I say, “no.”

    For example: in the case of Cit+ the “allele” frequency of the transport protein for citrate has increased. Is this ‘change’ in “allele frequency” the cause of aerobic citrate metabolism? No. It’s the position of the duplicated allele. This should just be obvious.

    All of this should clearly indicate that it is the regulatory mechanisms of an organism that are running the show, and that “allele frequencies” play more of a secondary role; not a primary one.

    franklin:

    All e coli have the ability to metabolize citrate. The fitness increase in the Lenski expt(s) was not due to the bacteria developing the ability to metabolize citrate…it already had that ability! Wrong again, PaV.

    Why the bluster?

    You know darn well that what we’re talking about here is aerobic citrate metabolism, which E. coli does NOT have; it must acquire. Per your statement, Lenski’s experiment showed nothing. Again, why the bluster?

    franklin:

    In the Lenski expt glucose levels in the culture media were 25 ppm yet, contrary to your claim, citrate levels were over 350 ppm

    If this is so, then they didn’t use a “minimal growth medium,” but, instead, should have said they used a “minimal growth medium with a high citrate concentration in the form of a chelating agent.” They didn’t say that. I looked around. I don’t know where you get the figure for citrate, I can only find a pnas paper where they say the citrate concentration was “high,” giving no ppm. [Blount-Borland-Lenski, 2008] That actually makes more sense of the experiment, and why the fitness increased so greatly once the citrate transport protein was activated.

    So the problem is that the authors did not do a good job—at least in the papers I looked at briefly and searching for citrate concentration—of telling people what the “minimal growth medium” consisted of. Maybe you can point this out to the authors.

  187. 187
    Zachriel says:

    PaV: So the problem is that the authors did not do a good job—at least in the papers I looked at briefly and searching for citrate concentration—of telling people what the “minimal growth medium” consisted of.

    They discuss the medium in their paper on contingency under Methods and Materials, Blount et al., Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli, Proceedings of the National Academy of Sciences 2008.

    You can read more about protocols on their website.
    http://myxo.css.msu.edu/ecoli/standprot.html

  188. 188
    franklin says:

    Pav

    If this is so, then they didn’t use a “minimal growth medium,” but, instead, should have said they used a “minimal growth medium with a high citrate concentration in the form of a chelating agent.” They didn’t say that. I looked around. I don’t know where you get the figure for citrate, I can only find a pnas paper where they say the citrate concentration was “high,” giving no ppm. [Blount-Borland-Lenski, 2008] That actually makes more sense of the experiment, and why the fitness increased so greatly once the citrate transport protein was activated.

    Of course the authors used a minimal growth media for the species they were workiing with, i.e., E coli. The authors did an excellent job of providing the details of their methodology. That you aren’t familiar with what a ‘DM25’ culture media consists of is not their fault. You could have, after all, looked up what the DM25 media consists of….it is information that is readily available and to have them spell it out would be a waste of $$ in additional page costs.

    The funny thing is that you’ve gotten everything wrong about the details of the expt.

    pav

    If this is so, then they didn’t use a “minimal growth medium,” but, instead, should have said they used a “minimal growth medium with a high citrate concentration in the form of a chelating agent.” They didn’t say that

    They did say that quite explicitly in their Mat. and Met section as Zachriel has also pointed out. It is only your ignorance of the contents of the paper and your lack of understanding about the methodologies and purpose of the expt. that is getting in the way of any fruitful discussion. Instead ‘we’ are left with pointing out your lack of knowledge of this expt evidenced by all the details you’ve gotten wrong.

    Of course the results make more sense once you understand the contents of the paper outlining the expt.

  189. 189
    Piotr says:

    #186, PaV

    With all due respect, no, I am not wrong. To say a worm “evolved” into a worm makes no sense.

    Of course it does. There are about a dozen different phyla of “worms”. “Worms” have been diversifying for more than half a billion years, evolwing into hundreds of thousands of species. You are just about as closely related to a sea urchin as one worm (e.g. an earthworm) is to another (e.g. the nematode Caenorhabditis elegans).

    And, please, whatever the merits of Webster’s dictionary, it isn’t the right reference book for checking up scientific terminology.

  190. 190
    Joe says:

    See Blount et al., Genomic analysis of a key innovation in an experimental Escherichia coli population, Nature 2012: “The Cit(+) trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter. The clades varied in their propensity to evolve this novel trait, although genotypes able to do so existed in all three clades, implying that multiple potentiating mutations arose during the population’s history.”

    No one knows if that means the mutations were accidents, mistakes and errors, or not.

  191. 191
    Joe says:

    Worms evolving into worms fits in with baraminology. And perhaps Piotr is closely related to worms and he should speak for himself.

  192. 192
    PaV says:

    Zachriel:

    Behe, Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,Quarterly Review of Biology 2010: “If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.”

    Fine. Yes, this IS the “edge of evolution.” Alas. As Eric points out, this is a pittance of neo-Darwinian evolution needs to be.

    And, certainly, it’s “not” an IC situation.

  193. 193
    PaV says:

    Piotr:

    And, please, whatever the merits of Webster’s dictionary, it isn’t the right reference book for checking up scientific terminology.

    The problem, Piotr, is that there is a common sense notion of evolution, and then there is a “scientific” understanding of evolution. The supposed scientific definition, as used by wd400, is at odds with the “common sense” notion, and ends up confusing the issue. It is my impression that evolutionary biologists, otherwise known as Darwinists, like it just this way; however, the general public, and science itself, is not served by using equivocal terms. Adaptation can be demonstrated; but not evolution. We would be better served reserving the word “evolution” for a kind of progressively more complex development of phenotype.

    You say that worms “evolve.” That there are all kinds of phyla. wd400 says that “evolution” is changing allele frequencies (which, of course, in any given species, as in humans, can already be found, though there is no “evolution”). I don’t think anyone associated “evolution” with either of these notions. Why not try to be clear in what we are saying: such as, “adaptation,” and “diversification.” That the chordate lineage produced such things as dinosaurs, birds, apes and humans—now that is “evolution.”

    As I stated before, a caterpillar (I wonder the phyla) becomes a butterfly. Can you think of any greater phenotypic diversity in all of nature? No. And it happens in a matter of weeks or days. And yet there are NO allelic frequencies changing because it’s the exact, same genome that produces both.

    With this simple observation, all of Darwinian theory should be thrown out.

  194. 194
    bornagain77 says:

    Innovation or Renovation? By Ann Gauger – Sept. 24, 2012
    Excerpt: But how significant was this innovation (citrate; Lenski)? In his paper in Quarterly Review of Biology, Dr. Michael Behe pointed out that E. coli was already capable of using citrate for anaerobic growth (when no oxygen was available). He postulated that a change in gene regulation could turn on citrate transport and permit growth on citrate under aerobic conditions.
    After an enormous amount of work, having sequenced the genomes of many clones along the lineages that led to the ability to use citrate, as well as lineages that never did, and testing the phenotypes of identified mutations, Blount et al. have now reported that Behe was largely right. The key innovation was a shift in regulation of the citrate operon, caused by a rearrangement that brought it close to a new promoter.
    http://www.biologicinstitute.o.....ation?og=1

    Rose-Colored Glasses: Lenski, Citrate, and BioLogos – Michael Behe – November 13, 2012
    Excerpt: In my own view, in retrospect, the most surprising aspect of the oxygen-tolerant citT mutation was that it proved so difficult to achieve. If, before Lenski’s work was done, someone had sketched for me a cartoon of the original duplication that produced the metabolic change, I would have assumed that would be sufficient — that a single step could achieve it. The fact that it was considerably more difficult than that goes to show that even skeptics like myself overestimate the power of the Darwinian mechanism.
    http://www.evolutionnews.org/2.....66361.html

    Bacterial ‘Evolution’ Is Actually Design in Action by Brian Thomas, M.S. – Dec. 2012
    Excerpt: At that time, the mechanism underlying the citrate-eating phenotype was unknown. Behe wrote, “If the [Cit+] phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT [Functional Coded elemenT] mutation.”2
    So, the big question is: Did E. coli evolve into a Cit+ strain by natural selection? Or did mutations construct new and functional coded elements to its DNA? If so, it would be the first in recorded biological history. If not, then it would be just another loss or modification of a pre-existing piece.
    In Lenski’s experiment, the bacteria (both Cit+ and wild-type) already possessed a gene named citT. It encodes a protein that transports a range of citrate-like chemicals. The recent results showed that the bacteria made extra copies of citT and a neighboring sequence—a process called gene amplification.
    More copies of the gene should translate to higher amounts of the transporter protein that it encodes. With enough transporters, the bacteria could access enough citrate. But oxygen deactivates citT, and having many copies of a gene that is turned off is not very useful!
    But the bacteria solved this problem when the amplification event also moved the gene sequence to a different place in the bacterial chromosome, where a different but pre-existing promoter could regulate it. Unlike the original one, it appears that the new promoter does not have an “oxygen off” switching mode. Instead, it allowed expression of citT in the presence of oxygen so that the bacteria successfully imported enough citrate to grow.
    The study authors wrote, “The structure of the cit amplification led us to propose that the Cit+ trait arose from an amplification-mediated promoter capture.”1 Further investigation confirmed the proposal.
    So, the bacteria solved the problem of accessing an alternative food source by generating extra copies of the critical gene and by placing those copies under the control of an appropriate promoter. Does any of this resemble natural, undirected Darwinian evolution? Not at all. This amazing mechanism invented no new functional coded elements. It merely modified pre-existing elements.
    Therefore, not only did the Cit+ bacteria not evolve in the molecules-to-man direction, but they showed what could only be ingenious DNA rearrangement mechanisms. What mainstream headlines portrayed as evidence for evolution is actually the opposite.3
    http://www.icr.org/article/bac.....ly-design/

  195. 195
    fifthmonarchyman says:

    PaV says,

    The supposed scientific definition, as used by wd400, is at odds with the “common sense” notion, and ends up confusing the issue. It is my impression that evolutionary biologists, otherwise known as Darwinists, like it just this way; however, the general public, and science itself, is not served by using equivocal terms.

    I say,

    exactly!!

    quote:

    “By 2050—earlier, probably—all real knowledge of Oldspeak will have disappeared. The whole literature of the past will have been destroyed. Chaucer, Shakespeare, Milton, Byron—they’ll exist only in Newspeak versions, not merely changed into something different, but actually contradictory of what they used to be……….The whole climate of thought will be different. In fact there will be no thought, as we understand it now. Orthodoxy means not thinking—not needing to think. Orthodoxy is unconsciousness.”

    end quote:

    George Orwell 1984

    peace

  196. 196
    Piotr says:

    The problem, Piotr, is that there is a common sense notion of evolution, and then there is a “scientific” understanding of evolution. The supposed scientific definition, as used by wd400, is at odds with the “common sense” notion, and ends up confusing the issue.

    When you want to discuss physics, you ought to use words like “mass”, “power”, “wave” or “potential” in their scientific sense, not colloquially. Ditto for biology. Every discipline has its technical terminology for the sake of precise communication. If you don’t use it, you confuse the issue.

    You say that worms “evolve.” That there are all kinds of phyla. wd400 says that “evolution” is changing allele frequencies (which, of course, in any given species, as in humans, can already be found, though there is no “evolution”). I don’t think anyone associated “evolution” with either of these notions.

    Well, all biologists do.

    Why not try to be clear in what we are saying: such as, “adaptation,” and “diversification.” That the chordate lineage produced such things as dinosaurs, birds, apes and humans—now that is “evolution.”

    You clearly don’t realise how much invertebrates differ from one another in terms of complexity, body plan, and even intelligence. Look at the millions of insect species, or the mollusc lineage, which has produced a variety of animals from sedentary mussles with no brain at all to octopuses with a complex brain as big as a cat’s and with ape-like intelligence.

    As I stated before, a caterpillar (I wonder the phyla) becomes a butterfly. Can you think of any greater phenotypic diversity in all of nature? No.

    No? How about spawn, tadpoles and adult frogs, an egg and a chicken, an acorn and an oak-tree? A single life cycle is not evolution, just like one rung is not a ladder and one note is not a musical piece.

    And it happens in a matter of weeks or days. And yet there are NO allelic frequencies changing because it’s the exact, same genome that produces both.

    Yep, that’s why it’s developmental biology, not evolution (micro- or macro-).

    With this simple observation, all of Darwinian theory should be thrown out.

    Non sequitur.

  197. 197
    PaV says:

    Piotr:

    When you want to discuss physics, you ought to use words like “mass”, “power”, “wave” or “potential” in their scientific sense, not colloquially. Ditto for biology. Every discipline has its technical terminology for the sake of precise communication. If you don’t use it, you confuse the issue.

    Let’s look at this two ways:
    (1) What do they mean when Darwinists say that “evolution” is a fact? They’re, of course, referring to the “fossil record.” But then when they talk about “evolution” they also mean RM+NS. So, which is it?
    (2) The “epicycles” of the Ptolomeic system were, I’m sure, “well-defined,” and, I’m sure, everyone knew what was meant by them. Did that make them correct?
    So, we have ‘equivocation,’ and we have ‘error’. If you want to avoid both of these problems, then talk about “change” and “adaptation.” And, if you should find instances of “evolution,” then call that evolution. Good luck finding them (and here I’m referring to “macroevolution,” which is the common sense understanding to the term)

    Look at the millions of insect species, or the mollusc lineage, which has produced a variety of animals from sedentary mussles with no brain at all to octopuses with a complex brain as big as a cat’s and with ape-like intelligence.

    I appreciate this insight. I think you’re right; I haven’t fully appreciated invertebrate diversity as much I should have. Good point.

    No? How about spawn, tadpoles and adult frogs, an egg and a chicken, an acorn and an oak-tree? A single life cycle is not evolution, just like one rung is not a ladder and one note is not a musical piece.

    Either the point eludes you (unlikely), or you choose to not look at it too closely (more likely).
    The question I asked was not: are there other examples of large-scale phenotypic diversity? I asked was there an example of greater diversity.
    The examples you give are examples of straight-forward developmental biology, and nothing more, except in the case, perhaps, of tadpoles; but this is probably nothing more than arrested development.
    However, the correct analogy would be for an acorn to become an oak tree, then dissolve into liquid, and then give rise to a fig tree. Even this is not so much of a huge change in phenotype as caterpillar to butterfly; but, at least it gets us a little bit closer to the reality.
    Finally, let’s note that you relied on “developmental biology” and not on a “change in allele frequency” when giving examples of phenotypic change. IOW, we do better when we leave the “gene-centric” view behind. That is, we’ll be hearing a whole lot more about “Junk-DNA” in the near future. (I’m speaking cryptically here, and hope you can follow)

    Yep, that’s why it’s developmental biology, not evolution (micro- or macro-).

    Neo-Dawinism links phenotypic change to genotypic change. I don’t think you would disagree with this.
    I gave an example of a HUGE phenotypic change with NO genotypic change at all to underlie it. Well, then, isn’t changing “beak sizes” trivial compared to a caterpillar becoming a butterfly? It would seem that this should give a thinking person pause before they taut the wonders of what “changing allelic frequencies” can bring about. Is the putative non-sequitur now a little bit less of a non-sequitur?

    IOW, “microevolution” is no more than an organism “adapting” to an environment; and “macroevolution” cannot be demonstrated. Let’s look for a better way of explaining things. And let’s look for a better lexicon.

  198. 198
    Paleysghost says:

    Apparently, the guy who responded didn’t understand his own link to the paper. The mutations in this VERY REDUCIBLE pathway do not contribute as being parts of a new “IC apparatus”, but are rather just STEPWISE contributions that contribute to a REDUCIBLE PATHWAY which leads to a specific function.

    You do not understand what the IC hypothesis means.
    You do not understand what your own links imply.

    Discussion on this article was DEAD and over a year ago when this troll first posted it to his FAKE ID group on facebook and the fact that is has 200 comments on UD is a testimony to how people really just feel a need to argue and type stuff on the internet for no produxctive reason.

  199. 199
    PaV says:

    Since this thread has served its purpose, let me just note one thing before leaving.

    To develop the Cit+ trait, somewhere between half-a-trillion and a trillion replications of the bacteria had to occur. And this was, just as in the case of the malarial parasite, an instance where the “selection pressure” for adaptation was quite large.

    What do we see happening? A gene duplication event (hence no new information) and a few SNP mutations afterwards (IOW, a few amino acids likely changed).

    Well, this is, AGAIN, the “edge of evolution.” So much replicating, and so little to show for it. How could such a process possibly account for large scale genomic changes?

    A Scientific American article said that in the 1930’s there were perhaps 5 to 10 million elephants in Africa.

    So, with a generation time of 25 years, and with the population replacing itself—that is, a male and female elephant give rise to another male and female elephant, the population replaces itself every 25 years.

    So, that’s 40 million “replications” per 100 years. So, it would take 25,000 of these “replications” to reach a trillion. This is equivalent to 2.5 million years. IOW, to get a gene duplication to end up in just the right place to help an African elephant, we need 2.5 million years. And, of course, there has been no new genomic information added.

    To me it seems like we either ought to pretend that we know nothing about coded information and its implication, or, we through out neo-Darwinism. Both can’t continue to co-exist.

  200. 200
    Paleysghost says:

    Done reading this garbage, lol.

    Send this OP claim over to a journal for peer-review and let your “peers’ over at Nature tell you how ignorant it is after tossing your paper directly into the garbage bin.

    ////

  201. 201
    Hangonasec says:

    fmm @167:

    Can you? [indicate permanent biological change that is not evolution],

    I say,

    Of course, Off the top of my head
    Things like HGT are not evolution. Combining two systems into a new third system is not evolution.

    I don’t see why one should accept that a single base change (point mutation), or some rearrangement/duplication from within a genome, are evolution, yet a change involving bases of external source is not.

    If a genetic fragment – say a retroviral insert, or a piece of Wolbachia – is incorporated into a genome, and then inherited down the main line, it is functionally contributing to the ‘RV’ part of the oversimplified ‘ID evolution equation’ RV+NS, just as much as point mutation.

    If 2 entire genomes combine, and the combination remains intact in subsequent generations, then again that is generating the ‘RV’ part.

  202. 202
    fifthmonarchyman says:

    Hangonasec

    I don’t see why one should accept that a single base change (point mutation), or some rearrangement/duplication from within a genome, are evolution, yet a change involving bases of external source is not.

    I say,

    Actually I would not automatically accept rearrangement/duplication from within a genome to be a random occurrence.

    At very least this has not been established it’s more likely they are not random at all,We know for example that duplication/rearrangement are more likely in stressful environments.

    As a rule of thumb the more complex the occurrence the less likely that it happened by chance. A fortuitous insertion of a complex vital structure from a external source is just too much to accept as luck of the draw.

    Especially given that a major priority of organisms is to keep these sorts of contaminants out.

    If traditional evolutionary mechanisms (RM/NS) were powerful HGC would not happen.

    The only way to include things like HGT in “evolution” is to equivocate the term until it means any change that is biological.

    Apparently that is just what is happening here

    peace

  203. 203
    fifthmonarchyman says:

    Hey Hangonasec

    When I was a boy I used to play a game called superheroes in which my brothers and I would play act battles using superpowers it would often go something like this

    player one— I have super speed I can catch you anywhere
    player two—-I have super strength so you can’t hold me when you catch me.
    player one—-I now have superpower absorbing powers. Whatever power you have I can absorb just when I need to use it.

    player two—-This game sucks. You are cheating you are guaranteed to win before we even start.

    That’s what HGC does it lets one organism steal the “evolutionary powers” of other organisms without going through the actual evolutionary process necessary to acquire them.

    Of course it’s beneficial for the absorbing organism but it’s not evolution as it’s understood by the public. It’s cheating.

    peace

  204. 204
    Zachriel says:

    PaV: Fine.

    So we have an example, according to Behe, of a gain of Functional Coded elemenT in a small experimental population of bacteria.

    PaV: To develop the Cit+ trait, somewhere between half-a-trillion and a trillion replications of the bacteria had to occur.

    Far fewer than happened in the typical human gut in the last few days.

    PaV: A gene duplication event (hence no new information) and a few SNP mutations afterwards (IOW, a few amino acids likely changed).

    Along with a potentiating mutation.

    PaV: How could such a process possibly account for large scale genomic changes?

    Let’s see… An ocean of microbes over a billion years compared to a few lab specimens over a couple of decades.

    PaV: So, that’s 40 million “replications” per 100 years.

    The pachyderm genome is far more complex, even including a body plan toolkit.

    fifthmonarchyman: As a rule of thumb the more complex the occurrence the less likely that it happened by chance.

    Complexity can increase through selection, even if each step is happenstance.

    fifthmonarchyman: The only way to include things like HGT in “evolution” is to equivocate the term until it means any change that is biological.

    Natural horizontal mechanisms are observed. Just because humans insert genes ‘horizontally’ doesn’t mean that all horizontal change is artificial.

    fifthmonarchyman: Of course it’s beneficial for the absorbing organism but it’s not evolution as it’s understood by the public.

    Then the public may need to be better educated, though most schools do cover sexual recombination at least.

  205. 205
    Joe says:

    ZAchriel may need to be better educated as no one can say if blind watchmaker processes produced the changes Lenski observed.

  206. 206
    fifthmonarchyman says:

    zac says,

    Natural horizontal mechanisms are observed. Just because humans insert genes ‘horizontally’ doesn’t mean that all horizontal change is artificial.

    I say,

    Who said anything about natural verses artificial? We are talking about evolutionary verses other natural processes.

    The only way your comment makes any sense is if you are assuming that all natural biological processes are evolutionary.

    Oh never mind you are assuming that 😉

    I hope you see why such equivocation makes productive communication impossible

    peace

  207. 207
    Zachriel says:

    fifthmonarcnhyman: We are talking about evolutionary verses other natural processes.

    Is this another case where you are using special fmm definitions? Horizontal gene transfer results in a heritable change to an organism, so, of course, it can result in evolution.

    fifthmonarcnhyman: The only way your comment makes any sense is if you are assuming that all natural biological processes are evolutionary.

    Sex is not evolution. Development is not evolution. Metabolism is not evolution. Ambulating is not evolution. Mastication is not evolution. A flower blooming is not evolution.

  208. 208
    fifthmonarchyman says:

    Zac says

    Then the public may need to be better educated, though most schools do cover sexual recombination at least.

    I say,

    Lets see,

    The un-evolutionarily process of two organisms in the same population combining to produce a third organism in the same population is some how relevant to a population stealing vital structures from a completely unrelated population at just the right time being the result of evolution.

    You kill me Zac

    peace

  209. 209
    fifthmonarchyman says:

    Zac say,

    Horizontal gene transfer results in a heritable change to an organism, so, of course, it’s evolution.

    I say,

    eyes roll.

    Any heritable change to an organism is evolution.

    Really?

    peace

  210. 210
    Zachriel says:

    fifthmonarchyman: Any heritable change to an organism is evolution.

    Evolution refers to the population, so the change has to become part of the population. (ETA: That might be encapsulated in the term heritable.)

  211. 211
    Joe says:

    Natural selection, ie evolution, pertains to individuals…

  212. 212
    fifthmonarchyman says:

    Zac,

    Just to be super clear.

    Your position is that any heritable change to a population has to be the result of evolution whether it has any connection to RV/NS or not.

  213. 213
    Hangonasec says:

    fmm

    Any heritable change to an organism is evolution.

    Really?

    Really. Now you’re gettin’ it!

    I would differ with Zachriel somewhat in that it does not have to become widespread, although it is of little interest (like quantum particles popping into and out of existence) until it does.

  214. 214
    Hangonasec says:

    Natural selection, ie evolution, […]

    Joe, natural selection and evolution are not synonyms.

  215. 215
    Joe says:

    If you have natural selection you have evolution. Why? Because there would be a change in allele frequency, which is the very definition of evolution.

  216. 216
    Zachriel says:

    fifthmonarchyman: Your position is that any heritable change to a population has to be the result of evolution whether it has any connection to RV/NS or not.

    That’s not the same statement as before.

    fmm: Any heritable change to an organism is evolution.

    fmm: any heritable change … the result of evolution.

    Evolution is what we call the change in populations. A heritable change to an organism that enters the population is evolution.

    Hangonasec: I would differ with Zachriel somewhat in that it does not have to become widespread

    Not widespread, just not stillborn. We modified our original statement with ETA.

  217. 217
    Hangonasec says:

    fmm

    [player 1 … player 2]

    That’s what HGC does it lets one organism steal the “evolutionary powers” of other organisms without going through the actual evolutionary process necessary to acquire them.

    Of course it’s beneficial for the absorbing organism but it’s not evolution as it’s understood by the public. It’s cheating.

    ‘Cheating’ is widespread in evolution. See, for example, The Selfish Gene. A fair chunk of the public has read it, if not understood it.

    Nonetheless, this is not an accurate representation of horizontal mechanisms. If, say, a virus or a phage inserts a retroelement into a genome, or there is simply uptake of ‘naked’ DNA from the medium, this can prove beneficial, just as a transposon from within the genome, or a plain old mutation for that matter. The host is not stealing the virus’s ‘powers’ – it does not become virus-like. Its genetic sequence is simply amended in some way, heritably.

  218. 218
    Zachriel says:

    Hangonasec: like quantum particles popping into and out of existence

    We were cutting it rather fine! There seems to be a limit though …

  219. 219
    Hangonasec says:

    Joe

    If you have natural selection you have evolution. Why? Because there would be a change in allele frequency, which is the very definition of evolution.

    Which would not make them synonyms – even if the only cause of allele frequency change were natural selection (which it isn’t).

  220. 220
    Hangonasec says:

    Zachriel @216, Understood!

  221. 221
    Joe says:

    If you have natural selection you have evolution. Yes evolution can occur in the absence of NS but that has nothing to do with what I said.

  222. 222
    fifthmonarchyman says:

    Hey Hangonase,

    If you define evolution in that way Biological ID is evolution and IC structures are the result of evolution by definition.

    Obviously IC structures exist so obviously they are the result of evolution

    It’s fine if you want to define it that way but it makes discussion impossible.

    quote:

    “Don’t you see that the whole aim of Newspeak is to narrow the range of thought?”

    George Orwell

    end quote:

    peace

  223. 223
    Zachriel says:

    fifthmonarchyman: If you define evolution in that way Biological ID is evolution and IC structures are the result of evolution by definition.

    Evolution, from the Latin evolutio to unroll (as a scroll), implies incremental change.

    The IC Argument considers (falsely) that irreducible structures can’t evolve incrementally (wherein intermediates have selectable capabilities), but have to be snapped together in one piece, as it were.

  224. 224
    Hangonasec says:

    fmm

    If you define evolution in that way Biological ID is evolution and IC structures are the result of evolution by definition.

    It is not impossible for intelligent agents to produce heritable genetic changes, nor to act as selective agents, so yes, intent can be directed towards evolutionary change. Nonetheless, there are numerous other mechanisms which cannot simply be brushed aside as of minor significance.

  225. 225
    Joe says:

    Zacho chokes:

    The IC Argument considers (falsely) that irreducible structures can’t evolve incrementally

    It has been demonstrated that is so. And you don’t have anything that counters ID’s claims.

  226. 226
    CHartsil says:

    “It has been demonstrated that is so. And you don’t have anything that counters ID’s claims.”

    My OP counters it, in case you haven’t noticed. It requires multiple components to be in place to function at all, and it evolved.

  227. 227
    PaV says:

    Zachriel:

    Let’s see… An ocean of microbes over a billion years compared to a few lab specimens over a couple of decades.

    It’s not quite so simple because bacteria in natural environments are switched to other food sources and allowed to grow over and over again.

    But, certainly, yes, a billion years of bacteria mutating. Wow. And what happens? Multicellularity happens. Not a big jump, really; just individual cells now communicating and adhering.

    Yet, we know that multicellular organisms aren’t going to replicate as fast as one-celled organisms.

    So, as the rate slows down more and more, we see large-scale phenotypic changes happening faster and faster. The Cambrian Explosion.

    This does not fit into Darwinian expectations.

  228. 228
    Zachriel says:

    PaV: It’s not quite so simple because bacteria in natural environments are switched to other food sources and allowed to grow over and over again.

    That’s right. The natural environment is far more complex than Lenski’s lab! One of the surprising results is that so much evolution took place in Lenski’s lab even though the environment was largely static.

    PaV: Multicellularity happens. Not a big jump, really; just individual cells now communicating and adhering.

    Depends on what you mean by “big jump”. It’s a huge change from the point of view of microbes.

    PaV: So, as the rate slows down more and more, we see large-scale phenotypic changes happening faster and faster.

    Of course, “faster and faster” is still tens of millions of years. Several factors probably impact the Cambrian Explosion, the rise of oxygen in the atmosphere, the end of a global ice age, the evolution of the Hox body plan system. and adaptive radiation.

    PaV: This does not fit into Darwinian expectations.

    Darwin’s expection was that “the periods during which species have undergone modification, though long as measured in years, have probably been short in comparison with the periods during which they retain the same form.”

  229. 229
    fifthmonarchyman says:

    CHartsil says,

    It requires multiple components to be in place to function at all, and it evolved.

    I say,

    Using the definition that has been proffered here. We can grant your point and Joe’s at the same time and in the same relation.

    In fact we could hold that the system was created from scratch all at once and at the same time that it evolved.

    See what happens when you equivocate. Communication becomes impossible

    peace

  230. 230
    CHartsil says:

    “In fact we could hold that the system was created from scratch all at once and at the same time that it evolved.”

    Except that we know it evolved.

  231. 231
    Joe says:

    CHartsil- you have no idea if it was unguided evolution

  232. 232
    CHartsil says:

    “CHartsil- you have no idea if it was unguided evolution”

    If you’re claiming it was designed, the onus is on you to show how and how you determined that.

  233. 233
    Joe says:

    LoL! If you’re claiming is was accidental the onus is on you to show how and how you determined that.

  234. 234
    Joe says:

    How- “built-in responses to environmental cues”

    How that was determined- in part because “it just happened” is a pathetic explanation

  235. 235
    CHartsil says:

    “How- “built-in responses to environmental cues””

    If you’re claiming it was designed, the onus is on you to show how and how you determined that.

  236. 236
    fifthmonarchyman says:

    CHartsil says.

    Except that we know it evolved.

    I say,

    Apparently that just means there was a “heritable change to the organism”.

    If that is your only claim it is completely vacuous. The equivalent of observing any change whatsoever. It simply means the population is different now than it was before.

    You can thank your co-travelers for turning your argument into something like

    “stuff happens and we call that evolution”

    talk about boring

    peace

  237. 237
    Hangonasec says:

    See what happens when you equivocate. Communication becomes impossible

    No, communication becomes impossible when people clarify their viewpoint and yet their interlocutors resort to silly word-gaming off the back of that clarification. Creation of an entire fully-functioning genome is not evolution. Tinkering with a current genome would be, if heritable. The essence is of change in descent – some mechanism (there are several) that changes the heritable material passed down a series of generations, such that, instead of exact copies, there are variations.

  238. 238
    Zachriel says:

    fifthmonarchyman: You can thank your co-travelers for turning your argument into something like “stuff happens and we call that evolution”

    Evolution, from the Latin evolutio to unroll (as a scroll), implies incremental change. Whether a particular instance is consider incremental depends on the level of analysis, but generally, if a cat conceives and gives birth to a dog, or God forms a man from the dust of the ground, then it is not evolution.

  239. 239
    Hangonasec says:

    OK, fifthmonarchyman, what definition of evolution should we be using? Bearing in mind that LGT, heritable transpositional rearrangements, genome unions, permanent heritable changes caused by intelligent agents etc must be something – you can’t simply define them out of existence because you have decided that evolutionary change only occurs through point mutation.

    And bear in mind that, whatever definition you choose, you may well be the only one using it.

  240. 240
    fifthmonarchyman says:

    Hangonasec says,

    Creation of an entire fully-functioning genome is not evolution.

    I say

    What?

    before you specifically agreed to this definition.

    “Any heritable change to an organism is evolution.”

    Creation is change is it not? How much creation can we have before it’s not evolution 20% 80%.

    Zac says,

    if a cat conceives and gives birth to a dog, or God forms a man from the dust of the ground, then it is not evolution

    I say,

    I’m confused

    A cat giving birth to a dog would require a change in the genome would it not?? So would the morphing of Actinobacteria into homo sapien.

    It seems to me that you guys need to get your heads together and come up with a specific definition that you are happy with and get back to me.

    I can’t discuss this with you if the meanings of words keep changing.

    Is the instantaneous combination of multiple integrated parts into a new functioning system evolution? Apparently it is.

    On the other hand Zac seems to now offer the condition that such a change must be incremental but that qualification was not on the table before.

    How much change is allowed at any one step before we are beyond the scope of evolution. 80% 20%.

    How do we quantify what one step is is it one generation 4 generations?

    Is the endosymbiotic absorption of an entire organism all at once an incremental change?

    The questions just keep coming.Not only is the definition of species extremely fuzzy in your worldview apparently evolution is as well

    I hope you see the communicational difficulty that results from equivocation.

    Peace

  241. 241
    fifthmonarchyman says:

    Hangonasec

    OK, fifthmonarchyman, what definition of evolution should we be using?

    I say

    How about the dictionary one offered by PAV in comment 186

    Quote:

    1. the process by which different kinds of living organisms are thought to have developed and diversified from earlier forms during the history of the earth.

    [synonyms: Darwinism, natural selection
    “his interest in evolution”]
    2. the gradual development of something, especially from a simple to a more complex form.

    Webster

    end quote:

    That would work for me

    Of course it would require us to ascribe the kinds of instantaneous jumps we see in HGC and the origins of IC systems to something other than evolution. Happy coincidence maybe, sympathetic Magic maybe

    It would also eliminate the kind of mischaracterizations we see in the OP and allow for some actual fruitful discussion of the IC argument.

    peace

  242. 242
    Hangonasec says:

    Creation is change is it not? How much creation can we have before it’s not evolution 20% 80%

    Well, it’s pretty obvious that creation from scratch, ie 0% inheritance, is not evolutionary, as defined. The essence, to repeat, is generational replication/reproduction with variation. The bulk of the genome is copied as is in an evolutionary scenario, with comparatively little coming from anywhere other than the parent(s). Of course ‘the bulk’ is imprecise, but only those with a degree in advanced word-gaming would struggle with the concept.

    “the process by which different kinds of living organisms are thought to have developed and diversified from earlier forms during the history of the earth.”

    That’s not very good, TBH. It’s also the one Google gives you, indicating a lack of depth in research! Still, that vague ‘the process’ allows much latitude, and certainly includes all the things I have indicated – ‘conventional’ mutation plus rearrangements, whole-genome duplications, LGT, genome merger, etc.

    You reject my definition because ‘it can be anything’ and replace it with one that … well, can be anything!

  243. 243
    fifthmonarchyman says:

    Hangonasec says

    The essence, to repeat, is generational replication/reproduction with variation.

    I say,

    Why not just let the “essence” be the definition. That would be the simple and clear thing to do.

    I would argue that the reason you need to go beyond the essence is because you want to subsume all the epicycles that keep being added with out acknowledging that you have moved the goalposts .

    you say,

    Still, that vague ‘the process’ allows much latitude, and certainly includes all the things I have indicated –

    I say,

    Did you catch the term “gradual” in the second definition and “Darwinism” as a synonym. Surely the addition of those terms would exclude the processes we are now discussing. Don’t you agree?

    You say,

    Of course ‘the bulk’ is imprecise, but only those with a degree in advanced word-gaming would struggle with the concept.

    I say,

    I understand the concept. My problem is with processes that directly contradict the concept being included in the term so the term looses it’s original common sense meaning.

    That is equivocation and it is a discussion killer.

    As witnessed by the OP

    peace

  244. 244
    fifthmonarchyman says:

    Hey Hangonasec

    Maybe this will help.

    Right now in another thread Reciprocating Bill is arguing that the theory of evolution would be falsified if a large change like one species evolving into another was ever directly observed however according to your definition such a change is well with in the range of the definition.

    It’s heads you win tails we loose

    When a term can mean anything it means nothing.

    peace

  245. 245
    wd400 says:

    What a waste or words.

    Biological evolution has a simple definition. It’s change in hertible properties of populations over generations. That’s just what evolution means in biology. If you want to argue about specific kinds of evolution go for it, but you can’t invent your own meanings of words.

    The modern theory of evolutionary biology (as opposed to the fact that evolution has happened) is the explanatory framework we have developed to explain how life has evolved. There used to be others, but they didn’t work as well (and of course the modern theory of evolution has kept pace with new findings, so is quite different from the “Darwinism” of the turn of the 20th Century).

    Perhaps you think HGT is not compatabile with our theory of evolution. If so, I think you are wrong, but when claim changes wrought by HGT are not evolution you are not even wrong.

  246. 246
    fifthmonarchyman says:

    wd400 says,

    Biological evolution has a simple definition

    I say,

    Apparently it’s not simple enough to be included in the dictionary.

    You say.

    It’s change in hertible properties of populations over generations.

    I say,

    According to that definition Biological ID and even Creationism is evolution.

    It’s fine if you want to go with that but you need to realize you have destroyed language the only means we have for communication.

    If the very same word can describe the sudden purposeful addition of entirely new features and gradual random point mutations words really have no meaning.

    You say,

    If you want to argue about specific kinds of evolution go for it, but you can’t invent your own meanings of words.

    I say

    Once again I’m simply using Webster’s definition. It’s not my own definition it’s the standard English definition.

    English is my point of contact. If you choose to deviate from that standard in a way that makes a term mean the opposite of the dictionary definition I’m just not sure how productive discussion is possible.

    Oh well in the end it’s up to you guys.

    peace

  247. 247
    Mung says:

    wd400:

    Biological evolution has a simple definition. It’s change in hertible properties of populations over generations. That’s just what evolution means in biology.

    And the heritable property of populations over generations is what, exactly? How is it identified? How is it quantified? What is it named?

    wd400:

    Perhaps you think HGT is not compatabile with our theory of evolution. If so, I think you are wrong, but when claim changes wrought by HGT are not evolution you are not even wrong.

    Let’s pretend that the ‘G’ in HGT stands for “gene.” Let’s call it a “non-inherited property”

    Let’s pretend that your “heritable property” of your population is also called a “gene.”

    So “genes” may be both inherited and not inherited (acquired by non inheritance methods – HGT).

    HGT is not evolution unless the “gene” so acquired is heritable.

    So your own claim is not even wrong.

    What a waste or words indeed.

  248. 248
    wd400 says:

    Mung,

    DO you seriously not know what “heritable” means? Measuring the heritability of traits has a long history in evolutionary genetics.

    Let’s pretend that the ‘G’ in HGT stands for “gene.” Let’s call it a “non-inherited property”

    H’uh? Genes are inherited. HGT can only change a population over time if those genes are passed on. As I said, changes wrought through HGT are evolution.

  249. 249
    wd400 says:

    Have you read the Webster’s definition you keep referring to?

    Tthe process by which different kinds of living organisms are thought to have developed and diversified from earlier forms during the history of the earth.

    That’s just change. Indeed, to take HGT as an example, horizontal transfer of gene is absolutely part of the mainstream theory ofhow organisms “are thought to have developed and diversified”.

  250. 250
    Mung says:

    wd400:

    Genes are inherited. HGT can only change a population over time if those genes are passed on.

    So there is no such thing as HGT. Got it!

    Genes are inherited. HGT can only change a population over time if those genes are passed on.

    Don’t be silly. If they are not passed on they are not genes.

  251. 251
    fifthmonarchyman says:

    WD400 says,

    Have you read the Webster’s definition you keep referring to?

    I say,

    Indeed I have, All of it, Apparently you have not got past the first sentence.

    you say,

    That’s just change.

    I say,

    Definition 2 uses the term “gradual” and “Darwinism” is listed as a synonym. When I go here

    http://www.merriam-webster.com...../evolution

    I see phrases like “over a very long time” and “a process of slow change and development”

    HGC is none of these things.

    to recap:

    When the average Joe reads a OP that claims that an Irreducibly Complex System in Lenski’s E. Coli is the result of evolution he thinks it arrived via slow gradual Darwinian means.

    But all the OP is really claiming is that an IC system exists in a state that it did not always exist in.

    The proper response to such a claim is “Well Duh change happens”

    Don’t you see how equivocation is a discussion killer?

    peace

  252. 252
    Hangonasec says:

    fmm

    Did you catch the term “gradual” in the second definition and “Darwinism” as a synonym. Surely the addition of those terms would exclude the processes we are now discussing. Don’t you agree?

    Heh heh. I love all this argumentum ad Websterium! Let’s get Webster to define Quantum Field Theory for us! We’re just humble speakers of English an’ all. If it’s not in Webster, it’s not science! But you can’t dismantle a theory by defining it badly.

    Here we go:

    1.the process by which different kinds of living organism are believed to have developed from earlier forms during the history of the earth.
    2.the gradual development of something.
    3.the giving off of a gaseous product, or of heat.
    4.a pattern of movements or manoeuvres.
    5.the extraction of a root from a given quantity.

    You’ll note that the word ‘gradual’ appears in the second definition, not the first. So do we add gas from the 3rd as well? Movements and manoeuvres? You can’t create an amalgamated definition of a multiple-meaning word.

    Gradualism aside, the first definition is poor. It might pass muster with ‘the public’, but it is hopelessly inaccurate. It includes ultra-rapid post-ark modifications. In the form you quoted it synonymises evolution with Natural Selection – no Drift, no mechanisms of variation – and with ‘Darwinism’ – no evolutionary processes other than those described by his Bearded Saintliness, and therefore again no Drift or genetic mutation, and nothing but minor change, given that he favoured strict gradualism.

    But it’s not 1859. The mechanisms occur, and they change genomes heritably, and so within the actual academic definition of evolution, rendered briefly as “descent with modification”, they are evolutionary. Whether a change of a given size or complexity can non-fatally occur or not is entirely a different point. If it does, within a background dominated by inheritance, it’s evolution. The natural change processes tend to cluster at the ‘minor’ end of the change scale, but are not definitionally disbarred from doing more, just mechanistically limited. Still, there comes a point, well beyond that accessible to generational mechanisms, where the very word ‘change’ becomes a misnomer. “I’ve changed your program”. “But it’s entirely different”. “I kept the title!”.

  253. 253
    Hangonasec says:

    Mung – if a retrovirus inserts its RNA into a genome, how does that avoid being inherited (ie ‘passed on’)?

  254. 254
    fifthmonarchyman says:

    Hey Hangonasac,

    you say

    Let’s get Webster to define Quantum Field Theory for us! We’re just humble speakers of English an’ all.

    I say,

    In internal conversations of our respective fields we often use specialized definitions and short hand. It’s the same for every field.

    But in public conversations it is important to be clear so you are not misunderstood.

    It’s obvious that when nonspecialists hear the term “Evolution” they picture something radically different than what you apparently mean by the term.

    This should not even be controversial.

    If you want to continue to use a term in public discourse in a way contrary to it’s accepted standard definition you will continue to be misunderstood and honest level headed discussion with the public will continue to elude you.

    It’s what happens when you equivocate.

    Maybe that is what you want

    peace

  255. 255
    Hangonasec says:

    But in public conversations it is important to be clear so you are not misunderstood.

    ]

    And so I type many words in clarification, specifically to avoid being misunderstood … and what comes back?

    It’s obvious that when nonspecialists hear the term “Evolution” they picture something radically different than what you apparently mean by the term.

    This should not even be controversial.

    It’s not controversial. It’s what ‘evolution’ means within the field of evolutionary biology. If the public thinks it means something different, surely they are capable of learning? If this hypothetical member of the public were new to the discussion, it would be more understandable, but you have had it explained, yet still you cling to Webster over a textbook of evolutionary biology.

    Nonspecialists who attempt to critique a field should perhaps understand the terms as the field uses them, not waft dictionaries in their faces and tell them they are wrong, wrong, wrong! They can learn. If someone thinks that evolution is the same as Natural Selection and the same as ‘Darwinism’, I simply can’t adopt that teeth-gratingly incorrect and simplistic viewpoint, just to patronise ‘the public’. How would you go about talking to someone who insisted that and ‘fruit’ and ‘banana’ were synonyms? Simply adopt their usage?

    If you want to continue to use a term in public discourse in a way contrary to it’s accepted standard definition you will continue to be misunderstood and honest level headed discussion with the public will continue to elude you.

    The accepted standard definition is the scientific one, for the purpose of science. If a member of the public has a different understanding, the kinds of clarification we have been giving should suffice to address that matter. The member of the public continuing to insist “No, it means X!! It really does!!” eventually comes across as a bit obtuse.

    It’s what happens when you equivocate.

    Maybe that is what you want

    Yes, of course that’s what I want! That’s why I’ve spent considerable time attempting to clarify, and explain why I think the Webster definition is inadequate. [Rolls eyes].

  256. 256
    Zachriel says:

    fifthmonarchyman: I’m confused

    No, you’re not. A simple definition of biological evolution will always be incomplete. You are making a semantic argument rather than a substantive one.

  257. 257
    fifthmonarchyman says:

    Hangonasec says

    That’s why I’ve spent considerable time attempting to clarify, and explain why I think the Webster definition is inadequate

    I say,

    I do appreciate the clarification but it’s pointed in entirely the wrong direction.

    Ive already pointed out that in another thread on this website your fellow traveler is claiming that the theory of “evolution” would be falsified if a large change in the genome was directly observed and in this very thread the OP is pointing to the “evolution” of an an IC structure as a falsification of Behe’s IC argument.

    According to the definition you are using both of these posters are to use WD400’s phase “not even wrong”.

    Apparently it’s your side that you need to educate. That is if you really want clarity.

    peace

  258. 258
    fifthmonarchyman says:

    ZAc says,

    You are making a semantic argument rather than a substantive one.

    I say,

    Why is it always about debate with you Zac?

    I’m not making any argument I’m only pointing out the obvious equivocation of terms.

    It’s not necessary to make an argument in this case. The claim made in the OP fails simply on definitional grounds. as has been repeatedly demonstrated by yourself and others.

    quote:

    It is by definition irreducibly complex and it was observed to evolve.

    end quote:

    I just wish I did not have to be the one to point out the vacuousness of this statement.

    peace

  259. 259
    Zachriel says:

    fifthmonarchyman: I’m not making any argument I’m only pointing out the obvious equivocation of terms.

    There is natural and incremental change in the heritable composition of populations, a process called evolution. However, short definitions are necessarily incomplete, so if you have a question, feel free to ask, but don’t then pretend you haven’t been provided answers.

    fifthmonarchyman (quote): “It is by definition irreducibly complex and it was observed to evolve.

    The statement is not hard to parse. The ID claim is that irreducible structures can’t evolve, that is, they can’t assemble through incremental change where each step of the process is functional. In other words, all the components have to be in place before there is any function. However, irreducible structures can evolve, a process for which we have provided two plausible scenarios, one of which was proposed by the Nobel prize-winning geneticist H. J. Muller in 1918.

  260. 260
    Eric Anderson says:

    Zachriel, that is an incorrect understanding of irreducible complexity:

    The ID claim is that irreducible structures can’t evolve, that is, they can’t assemble through incremental change where each step of the process is functional.

    No-one, certainly not Behe, claims that a complex functional structure cannot evolve if: (i) each step of the process is functional, (ii) there is an adequate population, and (iii) there is adequate time.

    However, when we see a complex functional structure, if we are to be objective, we must ask: (i) is it realistic to believe (indeed, do we have any observational evidence for the claim) that each step of the process would have been functional, (ii) was there an adequate population, and (iii) has there been adequate time.

  261. 261
    Zachriel says:

    Eric Anderson: However, when we see a complex functional structure, if we are to be objective, we must ask: (i) is it realistic to believe (indeed, do we have any observational evidence for the claim) that each step of the process would have been functional, (ii) was there an adequate population, and (iii) has there been adequate time.

    Sigh.

    The ID claim is that irreducible structures can’t {plausibly} evolve, that is, they can’t assemble through incremental change where each step of the process is functional. In other words, all the components have to be in place before there is any function. However, irreducible structures can evolve, a process for which we have provided two plausible scenarios, one of which was proposed by the Nobel prize-winning geneticist H. J. Muller in 1918.

  262. 262
    Joe says:

    Zachriel:

    The ID claim is that irreducible structures can’t {plausibly} evolve,…

    That is incorrect. The ID claim is that blind and undirected chemical processes cannot produce IC. And Muller did not even address IC at the molecular level.

    Zachriel is just confused, as usual.

    ID is OK with IC evolving by design. Your position has an issue if it requires more than two specific genetic changes.

  263. 263
    Hangonasec says:

    fmm @257,

    Ive already pointed out that in another thread on this website your fellow traveler is claiming that the theory of “evolution” would be falsified if a large change in the genome was directly observed and in this very thread the OP is pointing to the “evolution” of an an IC structure as a falsification of Behe’s IC argument.

    There is absolutely no conflict between the definition of evolution as ‘descent with modification’ and the mechanistic restriction on the possible modifications available to a process of descent.

    Local leaps are more likely to succeed than larger ones, whose probability of success declines towards a limit. One-step recapitulation of a form that has independently arisen stepwise would be even less likely. It would be entirely outside the expectations of evolutionary biology (more specifically, genetics), even if, technically, a ‘descent with modification’.

    I think you are confusing definition with the predictions available to a framework. Definitions can’t be falsified; expectations can. A cat giving birth to a dog, or the yet-to-be-demonstrated ‘true’ IC would not falsify the definition of evolution, but it would falsify current theory.

    According to the definition you are using both of these posters are to use WD400?s phase “not even wrong”.

    I hope the above helps to address why that is not the case.

    Apparently it’s your side that you need to educate.

    No … no, I’m pretty sure they get it.

    That is if you really want clarity.

    You seem genuinely to doubt that. I’m wounded!

  264. 264
    Joe says:

    True IC has been demonstrated.

  265. 265
    Hangonasec says:

    No it hasn’t. It has been asserted. There are rational paths by which incremental change can produce apparent IC (that is, a structure that cannot now be subject to subunit knockouts non-fatally). Unless these paths are eliminated, you cannot distinguish ‘true’ IC from ‘apparent’ IC.

  266. 266
    Joe says:

    True IC has been demonstrated. That is a fact of science.

    There are rational paths by which incremental change can produce apparent IC

    That is only an opinion.

  267. 267
    Eric Anderson says:

    Zachriel:

    The ID claim is that irreducible structures . . . can’t assemble through incremental change where each step of the process is functional.

    No. You are still misstating it. This is a critical nuance. Read carefully what I wrote and the difference with what you are writing.

    I’ll try to put up a post on this later this week if I get a chance, as this may be an issue that a number of people are confused about.

  268. 268
    Zachriel says:

    Eric Anderson: No-one, certainly not Behe, claims that a complex functional structure cannot evolve if: (i) each step of the process is functional, (ii) there is an adequate population, and (iii) there is adequate time.

    Evolutionary theory claims that complex structures evolve incrementally. The ID claim is that there are no such pathways, so they throw a bunch of exponents around as if saying unlikely events are unlikely is an argument.

  269. 269
    fifthmonarchyman says:

    Hey Eric,

    Thank you in advance for the upcoming post.

    The failure of the critics to address the actual IC argument is frustrating to me. They seem instead to be content to continually battle straw-men.

    It’s as if we are talking past each other. As witnessed by the OP.

    I hope you will be able to break through the communication barrier where others have failed.

    peace

  270. 270
    Joe says:

    Zachriel:

    Evolutionary theory claims that complex structures evolve incrementally.

    That is not a complete statement Evolutionism claims those steps are via blind and undirected chemical processes.

    The ID claim is that there are no such pathways,

    That is also incorrect.

  271. 271
    Hangonasec says:

    Joe,

    True IC has been demonstrated. That is a fact of science.

    If it were a fact of science, you would be able to point to a reputable source. So far, we only have ‘apparent IC’ – no more convincing than “the heart needs blood and blood needs the heart – IC!”. 😀

    Me: There are rational paths by which incremental change can produce apparent IC

    Joe: That is only an opinion.

    A devastating critique, Professor!

  272. 272
    Joe says:

    Peer-reviewed papers are a reputable source and they demonstrate there are many IC systems and subsystems. Also there are plenty of evos trying to refute the premise. Why would they be doing that if IC didn’t exist?

    As for my devastating critique- well look at what I was responding to- your evidence-free drivel.

  273. 273
    Hangonasec says:

    Peer-reviewed papers are a reputable source and they demonstrate there are many IC systems and subsystems.

    I think you pressed ‘send’ before your post was complete. Generally, following such a claim, there would be a citation of such a peer-reviewed paper in support of it. The claim that ‘true’ IC has been demonstrated, that is (rather than the well-known fact that organisms have bits you just can’t chop out nonfatally).

  274. 274
    Joe says:

    Read any paper on ATP synthase- or any bacterial flagellum- or any blood clotting system- asexual reproduction- sexual reproduction- the list is long.

  275. 275
    CHartsil says:

    “Read any paper on ATP synthase- or any bacterial flagellum- or any blood clotting system- asexual reproduction- sexual reproduction- the list is long.”

    The do a search on the evolution of said systems.

  276. 276
    CHartsil says:

    We have observation that a system which cannot be deconstructed can evolve.

    You have inference that it can’t.

    We win

  277. 277
    Eric Anderson says:

    CHartsil, re-read #260. You misunderstand irreducible complexity. As well as fundamental lesson of Lenski’s experiments.

  278. 278
    Eric Anderson says:

    CHartsil @275:

    The[n] do a search on the evolution of said systems.

    This is a great suggestion.

    What you will find are speculations, hypotheticals, “what-if’s”, wild guesses, question-begging assumptions and the like.

    What you will not find is any empirical evidence that such systems can arise via blind, undirected processes.

  279. 279
    Box says:

    // irreducible complexity //

    By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning.
    An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution. Since natural selection can only choose systems that are already working, then if a biological system cannot be produced gradually it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act on.
    Even if a system is irreducibly complex (and thus cannot have been produced directly), however, one can not definitively rule out the possibility of an indirect, circuitous route. As the complexity of an interacting system increases, though, the likelihood of such an indirect route drops precipitously. And as the number of unexplained, irreducibly complex biological systems increases, our confidence that Darwin’s criterion of failure has been met skyrockets toward the maximum that science allows.
    In the abstract, it might be tempting to imagine that irreducible complexity simply requires multiple simultaneous mutations—that evolution might be far chancier than we thought, but still possible. Such an appeal to brute luck can never be refuted. Yet it is an empty argument.
    One may as well say that the world luckily popped into existence yesterday with all the features it now has. Luck is metaphysical speculation; scientific explanations invoke causes. It is almost universally conceded that such sudden events would be irreconcilable with the gradualism Darwin envisioned. Richard Dawkins explains the problem well:

    Evolution is very possibly not, in actual fact, always gradual. But it must be gradual when it is being used to explain the coming into existence of complicated, apparently designed objects, like eyes. For if it is not gradual in these cases, it ceases to have any explanatory power at all. Without gradualness in these cases, we are back to miracle, which is simply a synonym for the total absence of explanation.

    [Behe, Darwin’s Black Box, p. 39/40]

  280. 280
    Box says:

    //follow up #279//

    CHartsil’s “aerobic citrate metabolizing system” is not a single systemsee Behe’s definition of irreducible complexity #279. It goes without saying that it’s a small part of a much larger system.

  281. 281
    Zachriel says:

    Behe: An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional.

    Such systems can be produced; for example, by the addition of helpers that become essential through optimization; or through duplication followed by functional migration.

  282. 282
    Collin says:

    Zachriel,

    Helpers to what? A system that is already functional? An already irreducably complex system?

  283. 283
    Collin says:

    Box,

    But couldn’t you say that EVERYTHING is part of a larger system?

  284. 284
    Hangonasec says:

    Joe

    Read any paper on ATP synthase- or any bacterial flagellum- or any blood clotting system- asexual reproduction- sexual reproduction- the list is long.

    And I seriously doubt that any of those papers has one word to say about IC, so unless you can give a cite, I’d say you are blowing hot air. It’s no good just naming things in biology. Biological organisms and their systems are known to be integrated, and parts non-optional now. But that does not prove their non-optional relations the day the system came into being. Demonstration of ‘true’ IC is not a trivial matter. There are probably more bits that can’t be chopped out now than can, so that is obviously not the way to do it. It has to be separated from apparent IC, of which there are several potential mechanisms of formation. And no, I don’t have to demonstrate their formation by incremental change in order to prove they are not IC. You have to demonstrate they are IC. That’s what you said has been done. Not just asserted to be, shown to be. So back it up.

  285. 285
    franklin says:

    box

    CHartsil’s “aerobic citrate metabolizing system” is not a single system

    except that the IC system that was documented to have evolved in the Lenski long-term expt is the aerobic transporter system for citrate across the cell membrane.

    If you think that system is not IC tell us which part can be removed and have the function of aerobic transport of citrate into the cell maintain function……in leui of that you can just acknowledge that the Lenski expt. did document the evolution of a IC system as per Behe requirements that you posted above.

  286. 286
    Box says:

    Franklin:
    except that the IC system that was documented to have evolved in the Lenski long-term expt is the aerobic transporter system for citrate across the cell membrane.

    Nonsense. Of course, there is no newly evolved “transporter system for citrate across the cell membrane” – don’t be silly. This transporter system, which normally transports citrate in the absence of oxygen, was already in place. In post #82 Joe gives the perfect summation of what happened.

    Joe:
    It is a duplicate of an existing gene that was placed under the control of an existing regulatory system.

  287. 287
    Box says:

    Collin: But couldn’t you say that EVERYTHING is part of a larger system?

    You have a point. However it’s obvious to anyone that a flagellum is more a “single system” than a piece of DNA-code.

  288. 288
    franklin says:

    box

    Nonsense. Of course, there is no newly evolved “transporter system for citrate across the cell membrane” – don’t be silly.

    If that was the case why were the E coli unable to transport oxygen across the cell membrane in the presence of oxygen?

    box

    This transporter system, which normally transports citrate in the absence of oxygen, was already in place.

    Of course we are discussing the transport of citrate across the cell membrane in the presence of oxygen. Did the E. coli have the ability to transport citrate across the cell membrane, in the presence of oxygen, at the start of the expt? If it did not how did this ability arise? Evolution perhaps? If not that could you outline the steps that led to the ability to transport citrate across the cell membrane in the presence of oxygen?

    What Joe describes is the evolution of a new and novel pathway to transport citrate across the cell membrane in the presence of oxygen. A decidedly advantageous development to the E coli. If you think this is not a IC system which parts may be removed and have the E coli maintain the ability to transport citrate across the cell membrane in the presence of oxygen.

    List the evolutionary steps which were documented and led to this ability and we can compare them to your Behe requirements and see how they match up. OK?

  289. 289
    Box says:

    Franklin, if you happen to find a car key by pure chance, which happens to fit the Lamborghini in front of your house, are you claiming that chance brought about an “entire new car”?

  290. 290
    franklin says:

    Box

    Franklin, if you happen to find a car key by pure chance, which happens to fit the Lamborghini in front of your house, are you claiming that chance brought about an “entire new car”?

    Huh? In your tortured analogy which part corresponds to which part of the evolution of the aerobic transport of citrate in the Lenski expt.? You’ll need to flesh this out a bit since it makes no sense in its present form.

    Alternately, you can outline the documented steps in the evolution of the aerobic citrate transporter system in E. Coli and we can compare that to the Behe requirements you posted earlier.. OK?

    If the aerobic transport of citrate in E coli is not IC which part(s) can be removed and have E. coli retain this ability? If no parts can be removed then would you agree this is a IC system that evolved in E coli?

  291. 291
    Box says:

    Franklin,

    the simple point is that the citrate transporter is a pre-existing mechanism and not something newly evolved. All the machinery for citrate metabolism is already in place. IOW we are talking about modification of pre-existing elements.

    WRT the IC claim. I think it’s not an “single system”; see #279, #280.

  292. 292
    Joe says:

    Hangonasec:

    And I seriously doubt that any of those papers has one word to say about IC,

    They don’t have anything to say about unguided evolution. The IC part can be gleaned by the details of the structure.

  293. 293
    Joe says:

    CHartsil:

    The do a search on the evolution of said systems.

    Been there, done that and there isn’t any evidence that unguided evolution can produce any of those. Did you have a point?

  294. 294
    franklin says:

    box

    the simple point is that the citrate transporter is a pre-existing mechanism and not something newly evolved.

    E. coli, at the start of the Lenski expt., did not posses the ability to transport citrate across the cell membrane in the presence of oxygen. In fact the very commonly used citrate test is a test used to differentiate between E. coli and other pathogenic bacteria because of the well known inability of E coli to transport citrate across the cell membrane in the presence of oxygen. There is absolutely no question that this is a new, novel, ability for E coli to possess and the mutational path leading to this ability, i.e., evolution, has been clearly delineated by Lenski’s group.

    As I have suggested several times (which for some reason you appear to be ignoring) is that you list each step of the evolutionary pathway that led to this ability and then we can compare it to your Behe requirements for IC evolution and see how it matches up. That seems like a straight forward way to settle this issue. How about it, Box, does that sound OK to you?

    box

    IOW we are talking about modification of pre-existing elements.

    If you think that is the case which elements of the anaerobic citrate transporter was modified and how?

    Also if the aerobic citrate transport system ( a new and novel trait for this species of bacteria) is not IC which parts can be removed and still have the aerobic transport function retained?

  295. 295
    Box says:

    Franklin,

    Franklin: E. coli, at the start of the Lenski expt., did not posses the ability to transport citrate across the cell membrane in the presence of oxygen.

    True. However there is a transport system for citrate across the cell in place, it just lacks a promoter that works in the presence of oxygen. This pre-existing ready-made transport system is being utilized in the end. IOW we are not talking about a newly evolved transport system. Are we in agreement so far? And BTW we are also not talking about a newly evolved promoter; this also pre-exists.

    Franklin: As I have suggested several times (which for some reason you appear to be ignoring) is that you list each step of the evolutionary pathway that led to this ability and then we can compare it to your Behe requirements for IC evolution and see how it matches up. That seems like a straight forward way to settle this issue. How about it, Box, does that sound OK to you?

    I more or less did all that in post #16. Let me know if you find anything missing.
    On the IC-issue, why do you keep ignoring my argument that a piece of DNA is not a “single system” – which is part of Behe’s definition of IC?

  296. 296
    franklin says:

    box

    However there is a transport system for citrate across the cell in place, it just lacks a promoter that works in the presence of oxygen

    That is a significant absence of function. IN fact it is so significant it is used as a diagnostic test to differentiate between E coli and other pathogenic bacteria.

    box

    This pre-existing ready-made transport system is being utilized in the end

    No, the preexisting system is not being utilized. The anaerobic citrate transport system remains intact and is a separate system than the aerobic citrate system.

    box

    IOW we are not talking about a newly evolved transport system

    Of course we are talking about a newly evolved transport system. You’ve already acknowledged that the aerobic transport system did not exist at the start of the expt. If it did not exist previously and now it does it is a new transport system.

    box

    Are we in agreement so far?

    No.

    box

    I more or less did all that in post #16. Let me know if you find anything missing.

    There appears to be a great deal missing in your #16 partial summary. I don’t see any mention of potentiating mutations nor activating mutations. They are part of the evolutionary details of the evolution of this new and novel transport system in E coli.

    box

    On the IC-issue, why do you keep ignoring my argument that a piece of DNA is not a “single system” – which is part of Behe’s definition of IC?

    What components, in your mind, constitute the aerobic citrate transport system?

  297. 297
    Box says:

    Okay Franklin, you insist on calling it a “newly evolved transport system”. I find that utterly ridiculous.

    Therefor I see no point in discussing this any further. Let’s agree to disagree.

  298. 298
    Joe says:

    How was it determined that gene duplication is a blind watchmaker process?

  299. 299
    franklin says:

    box

    Okay Franklin, you insist on calling it a “newly evolved transport system”. I find that utterly ridiculous.

    I call it a newly evolved citrate transport system because that is what it is. Are you suggesting that the E coli strain used in the Lenski expt. had the ability to aerobically transport citrate across the cell membrane? Previously, you acknowledged that the strain did not possess this ability. Are you now retracting that acknowledgment?

    If it did not exist in this strain previously and arose, through mutation mechanisms, then how is it NOT a new transport system? Your apparent denial of this basic result of the expt. is truly absurd.

    box

    Therefor I see no point in discussing this any further. Let’s agree to disagree.

    The results of the expt. are clear cut and fit the definition of a newly evolved IC system as per Behe which you regard so highly.

  300. 300
    Joe says:

    If this is an example of IC, and I doubt that it is, it is minimal IC at best. And no one can say if unguided evolution did it so it doesn’t do anything to Behe’s argument.

  301. 301
    CHartsil says:

    “If this is an example of IC, and I doubt that it is, it is minimal IC at best.”

    No true Scotsman

    “And no one can say if unguided evolution did it so it doesn’t do anything to Behe’s argument.”

    Argument from ignorance. If you’re claiming that it was guided, the onus is on you to show that.

  302. 302
    CHartsil says:

    “If this is an example of IC, and I doubt that it is, it is minimal IC at best.”

    No true Scotsman

    “And no one can say if unguided evolution did it so it doesn’t do anything to Behe’s argument”

    Argument from ignorance. If you’re claiming that it was guided, the onus is on you to show that.

  303. 303
    Collin says:

    If I knew more about molecular biology I could engage more. But let me ask this question:

    Is it true that what happened is that there was a system that transported oxygen and a system that metabolized citrate and that the oxygen transport got duplicated and mashed together with the citrate metabolism system?

    I figure that this issue is important enough that Behe needs to address it himself if he wants to defend his idea. I certainly can’t do it for him.

  304. 304
    franklin says:

    Collin

    Is it true that what happened is that there was a system that transported oxygen and a system that metabolized citrate and that the oxygen transport got duplicated and mashed together with the citrate metabolism system?

    No, that is not what occurred in the Lenski long-term expt. Perhaps have a go at reading the published literature from Lenski’s lab to see what the expt. was/is all about.

    Argument from ignorance. If you’re claiming that it was guided, the onus is on you to show that.

    Not only that is estimated that every nucleotide in the bacteria strain used in this expt was mutated at least once and that the total single point mutations were on the magnitude of billion…….doesn’t really sound like a directed process at all….at least not that could be differentiated from chance alone.

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