Home » Cell biology, Darwinism, News » Michael Behe on Lenski’s lambda virus: “Darwinian evolution took a little step sideways and two big steps backwards.”

Michael Behe on Lenski’s lambda virus: “Darwinian evolution took a little step sideways and two big steps backwards.”

In “More from Lenski’s Lab, Still Spinning Furiously” (Evolution News & Views, January 30, 2012), Michael Behe summarizes the real discovery from a much-heralded experiment involving a virus called lambda, that infects bacteria (and is supposed to be a fast learner when it comes to infecting):

To me, the much more significant results of the new paper, although briefly mentioned, were not stressed as they deserved to be. The virus was not the only microbe evolving in the lab. The E. coli also underwent several mutations. Unlike for lambda, these were not modification-of-function mutations — they were complete loss-of-function mutations.

The mechanism the bacterium used to turn off LamB in 99% of cells to resist initial lambda infection was to mutate to destroy its own gene locus called malT, which is normally useful to the cell. After acquiring the fourth mutation the virus could potentially invade and kill all cells. However, E. coli itself then mutated to prevent this, too. It mutated by destroying some genes involved in importing the sugar mannose into the bacterium. It turns out that this “mannose permease” is used by the virus to enter the interior of the cell. In its absence, infection cannot proceed.

So at the end of the day there was left the mutated bacteriophage lambda, still incompetent to invade most E. coli cells, plus mutated E. coli, now with broken genes which remove its ability to metabolize maltose and mannose. It seems Darwinian evolution took a little step sideways and two big steps backwards.

More. You can’t comment there, but you can comment here.

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39 Responses to Michael Behe on Lenski’s lambda virus: “Darwinian evolution took a little step sideways and two big steps backwards.”

  1. Pretty much what human computer users do in the short run to prevent importing viruses.

  2. ‘Pretty much what human computer users do’

    Yes, and how intellegent they are too!

  3. Behe: “As the authors state, however, the mutated viral J protein can still bind to the original protein, LamB, which strongly suggests the same binding site (that is, the same location on the J protein) is being used. It turns out that both LamB and OmpF have similar three-dimensional structures, so that strengthening the binding to one fortuitously led to binding to the other.

    In my review (Behe 2010) I discussed why this should be considered a “modification of function” event rather than a gain-of-function one. The bottom line is that the results are interesting and well done, but not particularly novel, nor particularly significant.

    Behe’s conclusion here seems rather counter-intuitive. It certainly seems to be a gain-of-function event to me. I guess I should go back and read his 2010 review.

  4. From Behe’s review: “It [modification of function] includes
    point mutations as well as other mutations
    that have a quantitative effect on a preexisting
    FCT, increasing or decreasing its
    strength, for instance, or shifting its activity
    somewhat (such as allowing a protein to
    bind a structurally-related ligand at the
    same site as its normal substrate), but
    without effectively eliminating it.

    But I don’t see why this shouldn’t be considered a gain of function. If the bacteriophage wasn’t able to bind to OmpF before, but now it can, that seems like a gain of function, whether it is at the same binding site for LamB or not.

  5. Considering the fact that Darwin himself emphasized the importance of change-of-function in evolution, and also how IDists regularly protest that change-of-function is just a wildly improbable chance event on which evolutionary biologists should not be allowed to rely in explaining systems, and also Behe’s previous claims that binding sites are amazingly precise and require multiple simultaneous mutations to evolve, it’s hard to see Behe’s statement can be seen as anything other than a huge concession to mainstream evolutionary theory.

  6. Yes, binding 2 molecules is presumably a gain-of-function compared to binding 1 molecule. But you are expecting rigorous, non-question-begging definitions from an ID advocate. Prepare to be disappointed!

  7. Bilbo I, does it not strike you as exceedingly queer that you are willingly squabbling of such a trifling thing as to be either a gain or modification of function (I hold it is merely modification), when the ‘gain of function’ that desperately needs to be explained by neo-Darwinists is many, many, orders of magnitude greater than this??? i.e. Why exactly are you willingly reduced to being such a pitiful beggar, for any substantiating evidence whatsoever, when in reality it would be merely a grain of sand that you need to payoff a mountain of empirical debt???

  8. Hi Nick,

    Most of the time I think Behe makes sense. This time, however, I’m tempted to disagree with him. What makes me hesitate is that this is from a peer-reviewed paper, where I would hope the reviewers read and accepted Behe’s defintion of “modification of function.”

  9. B77: “Bilbo I, does it not strike you as exceedingly queer that you are willingly squabbling of such a trifling thing as to be either a gain or modification of function….

    I squabble over it because Behe squabbled over it. I’m trying to understand why he did so.

  10. Not that I am in any way qualified to speak for Dr. Behe, but I would guess that it has something to do with his previous work in “The Edge Of Evolution” looking for gains in novel protein-protein binding site complexity;

    notes to that effect:

    “The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 protein-protein binding sites being generated by accident) in the history of life. It is biologically unreasonable.”
    Michael J. Behe PhD. (from page 146 of his book “Edge of Evolution”)

    Nature Paper,, Finds Darwinian Processes Lacking – Michael Behe – Oct. 2009
    Excerpt: Now, thanks to the work of Bridgham et al (2009), even such apparently minor switches in structure and function (of a protein to its supposed ancestral form) are shown to be quite problematic. It seems Darwinian processes can’t manage to do even as much as I had thought. (which was 1 in 10^40 for just 2 protein-protein binding sites)
    http://www.evolutionnews.org/2.....hes_t.html

    A review of The Edge of Evolution: The Search for the Limits of Darwinism
    The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155).
    http://creation.com/review-mic.....-evolution

    Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution
    “Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.”
    http://www.evolutionnews.org/2.....20071.html

    Following the Evidence Where It Leads: Observations on Dembski’s Exchange with Shapiro – Ann Gauger – January 2012
    Excerpt: So far, our research indicates that genuine innovation, a change to a function not already pre-existent in a protein, is beyond the reach of natural processes, even when the starting proteins are very similar in structure.
    http://www.evolutionnews.org/2.....55171.html

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://biologicinstitute.org/2.....t-collide/

  11. Bilbo, to give a little more background on just how far apart 2 novel protein-protein binding sites in gain of functional complexity is from what is required to be explained by neo-Darwinian processes, I offer these references;

    So, how many protein-protein binding sites are found in life?

    Dr. Behe, on the important Table 7.1 on page 143 of Edge Of Evolution, finds that a typical cell might have some 10,000 protein-binding sites. Whereas a conservative estimate for a multicellular creature is,,,

    Largest-Ever Map of Plant Protein Interactions – July 2011
    Excerpt: The new map of 6,205 protein partnerings represents only about two percent of the full protein- protein “interactome” for Arabidopsis, since the screening test covered only a third of all Arabidopsis proteins, and wasn’t sensitive enough to detect many weaker protein interactions. “There will be larger maps after this one,” says Ecker.
    http://www.sciencedaily.com/re.....144936.htm

    So taking into account that they only covered 2%, of the full protein-protein “interactome”, then that gives us a number, for different protein-protein interactions, of 310,000. Thus, from my very rough ‘back of the envelope’ calculations, we find that this is at least 30 times higher than Dr. Behe’s estimate of 10,000 different protein-protein binding sites for a typical single cell (Page 143; Edge of Evolution; Behe). Therefore, at least at first glance from my rough calculations, it certainly seems to be a gargantuan step that evolution must somehow make, by purely unguided processes, to go from a single cell to a multi-cellular creature.

    Even though the evidence of novel protein-protein binding site generation by neo-Darwinian processes is severely lacking (1 in 10^40 for only 2 sites; Behe) this following study indicates that there is very dramatic restructuring of entire protein-protein interaction networks among different kinds of species;

    A Top-Down Approach to Infer and Compare Domain-Domain Interactions across Eight Model Organisms
    Excerpt: Knowledge of specific domain-domain interactions (DDIs) is essential to understand the functional significance of protein interaction networks. Despite the availability of an enormous amount of data on protein-protein interactions (PPIs), very little is known about specific DDIs occurring in them.,,, Our results show that only 23% of these DDIs are conserved in at least two species and only 3.8% in at least 4 species, indicating a rather low conservation across species.,,,
    http://www.plosone.org/article.....ne.0005096

    further note:

    Viral-Binding Protein Design Makes the Case for Intelligent Design Sick! (as in cool) – Fazale Rana – June 2011
    Excerpt: When considering this study, it is remarkable to note how much effort it took to design a protein that binds to a specific location on the hemagglutinin molecule. As biochemists Bryan Der and Brian Kuhlman point out while commenting on this work, the design of these proteins required:
    “…cutting-edge software developed by ~20 groups worldwide and 100,000 hours of highly parallel computing time. It also involved using a technique known as yeast display to screen candidate proteins and select those with high binding affinities, as well as x-ray crystallography to validate designs.2″
    If it takes this much work and intellectual input to create a single protein from scratch, is it really reasonable to think that undirected evolutionary processes could accomplish this task routinely?
    In other words, the researchers from the University of Washington and The Scripps Institute have unwittingly provided empirical evidence that the high-precision interactions required for PPIs requires intelligent agency to arise. Sick!
    http://www.reasons.org/viral-b.....-sick-cool

    Further notes:

    Falsification Of Neo-Darwinism by Quantum Entanglement/Information
    https://docs.google.com/document/d/1p8AQgqFqiRQwyaF8t1_CKTPQ9duN8FHU9-pV4oBDOVs/edit?hl=en_US

    Does Quantum Biology Support A Quantum Soul? – Stuart Hameroff – video (notes in description)
    http://vimeo.com/29895068

    Verse and Music

    Psalm 100:3
    Know that the LORD Himself is God; It is He who has made us, and not we ourselves;

    Steven Curtis Chapman – God is God (Original Version) -
    http://www.youtube.com/watch?v=qz94NQ5HRyk

  12. Hi Nick,

    All we get from you is question-begging scenarios.

    So what is your posint?

  13. Considering the fact that Darwin himself emphasized the importance of change-of-function in evolution,

    Darwin? The guy who didn’t know what he was talking about?

    and also how IDists regularly protest that change-of-function is just a wildly improbable chance event on which evolutionary biologists should not be allowed to rely in explaining systems

    reference please- we all know how you like to make things up wrt IDists.

    and also Behe’s previous claims that binding sites are amazingly precise and require multiple simultaneous mutations to evolve

    Reference please. He puts the limit on two new protein to protein binding sites.

  14. It is a modification of function because it can still bind to the original protein, which means the other protein it can now bind to is very similar in shape to that original protein. And it is still doing basically the same thing- using it to get inside the cell.

  15. Clarification, please, Joe.
    If you believe Nick “made up” that ID proponents protest that function change is a wildly improbable event, does that mean that you yourself think such events are NOT so improbable? Or are you asking for a reference because you like asking for references?

  16. I doubt IDists make the claim that Nick says we make. So I need a reference.

  17. And might evolution proceed (in part) by successive modification upon modification until the end result is unequivocally a change rather than a mere modification? These modifications you speak of do seem to happen in a rather facile fashion.

  18. Do you have any examples?

  19. Not offhand, no, although J. Mol. Biol. (2001) 307, 1113±1143 is relevant

    Do you then think it infeasible? Why should such a modification not be further and further modified?

  20. Could you please make your point?

    Do I think it is feasible that the paper is relevant?

    If you have a protein that is doing some function- an essential function- if modifying it stops it from doing that function before it does some other function that will replace that lost essential function, then that would be a problem.

    That is why gene duplications are called upon- you keep the original function and are then free to hammer away to find something new.

  21. Some people would rather “hash things out” rather than just acepting them.

    Accepting Intteligent Design is one thing. Just accepting whatever all leading proponents of ID say, is another.

    Here we have a loss of specificity leading to an ability to bind to another, albeit very similar, protein.

    To me it is like putting a metric socket on a US nut- the metric socket fits its corresponding metric nut perfectly. But if the metric nut “mutates” into a US nut of similar (slightly smaller) dimensions the fit isn’t so good but it will still work.

  22. Sorry, being too indirect. I was trying to suss out your particular flavour of ID. I think possibly the only major point of issue between you and I is that you have said that you think both stochastic and directed processes are at work in producing mutations; and I don’t see how you can possibly know that, or tell which mutation was due to which type of mechanism.
    My point in citing that paper was that it shows just how closely related molecules having different functions can be – just for general information, really

  23. The only way I would infer all mutations are stochastic in nature is if living organisms arose from non-living matter via stochastic processes, that is living organisms are reducible to matter, energy, necessity and chance.

    That said even with design not all mutations need to be directed, meaning stochastic processes still exist.

    Dr. Behe’s caveat:

    “Intelligent design is a good explanation for a number of biochemical systems, but I should insert a word of caution. Intelligent design theory has to be seen in context: it does not try to explain everything. We live in a complex world where lots of different things can happen. When deciding how various rocks came to be shaped the way they are a geologist might consider a whole range of factors: rain, wind, the movement of glaciers, the activity of moss and lichens, volcanic action, nuclear explosions, asteroid impact, or the hand of a sculptor.
    The shape of one rock might have been determined primarily by one mechanism, the shape of another rock by another mechanism.

    Similarly, evolutionary biologists have recognized that a number of factors might have affected the development of life: common descent, natural selection, migration, population size, founder effects (effects that may be due to the limited number of organisms that begin a new species), genetic drift (spread of “neutral,” nonselective mutations), gene flow (the incorporation of genes into a population from a separate population), linkage (occurrence of two genes on the same chromosome), and much more. The fact that some biochemical systems were designed by an intelligent agent does not mean that any of the other factors are not operative, common, or important.”

    Dr Spetner attempted to address that- what mutations are stochastic- and came up with point mutations being stochastic. For example he said wrt transposons which contain within their sequence the coding for two of the enzymes required to “cut-n-paste”-

    ”The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism random before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.”

  24. So you find Spetner’s argument from incredulity persuasive?
    I don’t, I’m afraid. Not without empirical evidence. He can’t tell a stochastic event from a directed event either.

  25. It’s not from incredulity- what he says he says from observations and experiments.

    OTOH all evos have is their personal incredulity. Go figure…

  26. I guess it would help if we compared and contrasted Behe’s definition of “gain-of-FCT” with “modification of function:”

    2) A “gain-of-FCT [functional coded elemenT]” adaptive mutation is a mutation that produces a specific, new, functional coded element while adapting an organism to its environment. The construction by mutation of a new promoter, intron/exon splice site, or protein processing site are gain-of-FCT mutations. Also included in this category is the divergence by mutation of the activity of a previously duplicated coded element.”

    3) A “modification-of-function” adaptive mutation is a mutation whose defining property is negative—while adapting an organism to an environment, it does not lead to the loss or gain of a specific FCT. This definition is intended to be broad enough to act as a “catch-all” for anything that falls outside the first two modes. It includes point mutations as well as other mutations that have a quantitative effect on a preexisting FCT, increasing or decreasing its strength, for instance, or shifting its activity somewhat (such as allowing a protein to bind a structurally-related ligand at the same site as its normal substrate), but without effectively eliminating it….this process does not by itself produce a new functional element, although it may, like other events classified here as “modification-offunction,” be a step to future gain-of-FCT events.

    So unless there is a new functional coded element (FCT) it falls into the “catch-all” category of “modification of function.” I guess I would suggest that had the reviewers thought that something like the current bacteriophage case would come up, they might have insisted on perhaps a fourth category, instead of just throwing it into the “catch-all” category of “modification of function”; and that this fourth category would be closer to the “gain-of-FCT” category.

    But perhaps I’m just being too nitpicky.

  27. “when the ‘gain of function’ that desperately needs to be explained by neo-Darwinists is many, many, orders of magnitude greater than this???”

    And there are many, many orders of magnitude more time and organisms involved in this experiment.

    So where is the “impossible”..so much so that we must invoke design? Behe and everyone here seems to want to gloss over that the virus repeatedly fixed four or more mutations to bind a new receptor.

    Your calculations might say “the chance of all four mutations arising at once is roughly one in a thousand trillion trillion.” Therefore design? Or some horribly misguided, and now empirically denied calculations?

    http://www.nytimes.com/2012/01......html?_r=1

  28. Joe, I really would like to see the experiments that tested the hypothesis that some mutations are directed, and the data produced therefrom – I must have missed them.
    Would you be kind enough to post a link?
    Thanks in advance

  29. Binding to a similar receptor and doing the same thing- no we don’t need to invoke design for something this trivial.

  30. Plenty of experiments that elucidate transposons, gene duplications, inversions, recombinations, etc.

    As I said transposons carry withing their sequence the coding for two of the enzymes it needs to get cut-n-pasted.

  31. OmpF and LamB aren’t very similar at all.

    “for something this trivial”

    Funny, your “trivial” has “one in a thousand trillion trillion” odds by some metrics. Perhaps we should plug it into KF’s reduced chi-metric or whatever.

    Behe argued 2 simultaneous mutations were past the edge of evolution-here we have 4+ required, that repeatedly emerged.

  32. From DrREC:

    OmpF and LamB aren’t very similar at all.

    From Dr Behe:

    It turns out that both LamB and OmpF have similar three-dimensional structures, so that strengthening the binding to one fortuitously led to binding to the other.

    From DrREC:

    Behe argued 2 simultaneous mutations were past the edge of evolution

    Behe argued more than two new protein-to-protein binding sites were beyond the edge.

  33. as to:

    repeatedly fixed four or more mutations to bind a new receptor.,,, “the chance of all four mutations arising at once is roughly one in a thousand trillion trillion.”

    Thus, happening purely by ‘random’ chance the probability is still to be taken as ‘a thousand trillion trillion’, thus random Darwinian evolution is ruled out as the cause of the change, and the internal programming of the cell, i.e. the ‘natural genetic engineering’ (Shapiro), obviously calculated a proper response in he right area of the genome.,,, This finding is in no way helpful for someone (DrREC) who would wish to demonstrate what purely neo-Darwinian processes can do. And to claim that this response is purely neo-Darwinian in its nature is to be thoroughly disingenuous to the evidence.

  34. “It turns out that both LamB and OmpF have similar three-dimensional structures, so that strengthening the binding to one fortuitously led to binding to the other.”

    Weak-this statement has no criteria What is their percent identity Joe? To what RMSD do their structures align?

    Hint-not very identical, not very well aligned. Somewhat similar fold and topology.

    From DrREC:

    “Behe argued 2 simultaneous mutations were past the edge of evolution

    Behe argued more than two new protein-to-protein binding sites were beyond the edge.”

    I’m referring to the two base-pair mutations in the “chloroquine-complexity clusters” in malarial resistance. Pegged at a probability of something like 1 in 10-40? What is the likelihood of four bases mutating?

    Please, do the math. What is the increase in fscio? Why didn’t it require design, where a two-base mutation in malaria apparently did?

  35. DrREC you are simply completely disingenuous to the math!

  36. Prove me wrong. Please show your calculations.

  37. They are their calculation. They themselves said that the event

    ‘repeatedly fixed four or more mutations to bind a new receptor.,,, “the chance of all four mutations arising at once is roughly one in a thousand trillion trillion.”

    Thus, happening purely by ‘random’ chance, as neo-Darwinism is absolutely required to use in its premise, the probability is still to be taken as ‘a thousand trillion trillion’, thus random Darwinian evolution is ruled out, by their very own calculations, as the primary cause of the change,,, and the internal programming of the cell, i.e. the ‘natural genetic engineering’ (as Shapiro puts it), obviously calculated a proper response in the right area of the genome.,,, This finding is certainly in no way helpful for someone (you DrREC) who would wish to demonstrate what purely neo-Darwinian processes can do. And to claim that this response is purely neo-Darwinian in its nature is to be thoroughly disingenuous to the evidence. Moreover Dr. Behe stated:

    ‘So at the end of the day there was left the mutated bacteriophage lambda, still incompetent to invade most E. coli cells, plus mutated E. coli, now with broken genes which remove its ability to metabolize maltose and mannose. It seems Darwinian evolution took a little step sideways and two big steps backwards.’

    And here you sit DrREC trying, for God knows whatever delusional reason, trying to tout this as ‘cutting edge’ proof of what the full glory of Darwinian Evolution can do and how it shows ID to be false!!! All I can say is, when everything is considered in the experiment, you got to be out of your ever loving mind if you think this clearly degenerative process, multiplied over millions of years, built the unimagined, staggering, levels of massively integrated complexity we see in the cell;

    Systems biology: Untangling the protein web – July 2009
    Excerpt: Vidal thinks that technological improvements — especially in nanotechnology, to generate more data, and microscopy, to explore interaction inside cells, along with increased computer power — are required to push systems biology forward. “Combine all this and you can start to think that maybe some of the information flow can be captured,” he says. But when it comes to figuring out the best way to explore information flow in cells, Tyers jokes that it is like comparing different degrees of infinity. “The interesting point coming out of all these studies is how complex these systems are — the different feedback loops and how they cross-regulate each other and adapt to perturbations are only just becoming apparent,” he says. “The simple pathway models are a gross oversimplification of what is actually happening.”
    http://www.nature.com/nature/j.....0415a.html

  38. correction ” their OWN calculation. They themselves said that the event ,,,

  39. “It turns out that both LamB and OmpF have similar three-dimensional structures, so that strengthening the binding to one fortuitously led to binding to the other.”

    Weak-this statement has no criteria What is their percent identity Joe? To what RMSD do their structures align?

    Very weak- your questions have no merit.

    Show me your data. Ya see it has already been demonsttrated that you don’t know what you are talking about so you have to do more than post- you need evidence.

    And BTW can you demonstrate that all four mutations were random in any respect of teh word?

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