Tuesday, December 03, 2013

How do creationists interpret Lenski's long-term evolution experiment?

Lenski's long-term evolution experiment has resulted in dozens of publications in high quality journals. It has led to significant insights into evolutionary processes [e.g. Lenski's long-term evolution experiment: the evolution of bacteria that can use citrate as a carbon source]. You may be wondering how Intelligent Design Creationists react to these results since most IDiots have a natural aversion to evidence.

Denyse O'Leary wasn't impressed [The Latest From Lenski’s Lab]. She doesn't know very much about science so she has to rely on the opinions of other IDiots. In this case, she relies on Ann Gauger who published a comment on the website of The Biologic Institute [Inovation or Rennovation].

Like many other IDiots, she claims that evolution can happen but only if it breaks things or perhaps modifies an existing gene to carry out a new function. Michael Behe made a big deal of this when he published a paper in The Quarterly Review of Biology a few years back (Behe, 2010). Here's what Behe said in his abstract ...

Adaptive evolution can cause a species to gain, lose, or modify a function; therefore, it is of basic interest to determine whether any of these modes dominates the evolutionary process under particular circumstances. Because mutation occurs at the molecular level, it is necessary to examine the molecular changes produced by the underlying mutation in order to assess whether a given adaptation is best considered as a gain, loss, or modification of function. Although that was once impossible, the advance of molecular biology in the past half century has made it feasible. In this paper, I review molecular changes underlying some adaptations, with a particular emphasis on evolutionary experiments with microbes conducted over the past four decades. I show that by far the most common adaptive changes seen in those examples are due to the loss or modification of a pre-existing molecular function, and I discuss the possible reasons for the prominence of such mutations.
Behe's point is the same one that we've been hearing for decades; namely, that evolution cannot create new information or new genes. He proposed a basic rule-of-thumb that he calls The First Rule of Adaptive Evolution.
Break or blunt any functional coded element whose loss would yield a net fitness gain.
Behe "predicted" that Lenski's citrate-utilizing bacteria would simply have evolved a way of expressing the citrate transporter gene (citT). He imagined that this would be a loss-of-function mutation ...
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 [functional coded elements], 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.

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 of loss-of-FCT.
Behe was correct when he predicted that the mutation would involve the citT gene but the actual mutation(s) turned out to be "a noteworthy gain-of-FCT mutation" that did not conform to The First Rule of Adaptive Evolution [Lenski's long-term evolution experiment: the evolution of bacteria that can use citrate as a carbon source].

A few years later, Ann Gauger spins it this way in her article ...
A few years ago, though, they published a paper describing the evolution of a “new” function in E. coli: the ability to use citrate as a carbon source for growth. Citrate had always been present in their minimal medium, but it was inaccessible to E. coli under normal lab growth conditions. After about 30,000 generations, though, the bacteria evolved the ability to take up and use the abundant citrate in the medium, thus allowing them to grow and reproduce faster. This announcement was splashed across headlines as evidence for the power of evolution to produce new adaptive traits.

But how significant was this innovation? 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.
It's important to recognize what the IDiots are conceding. They admit that Lenski's long term evolution experiment does lead to evolution of a new strain of cit+ E. coli. This is a gain-of-function phenotype no matter how you try to spin it differently. The new function is the result of an entirely new gene formed from the fusion of two genes, rnk and citG. This, in turn, creates a new operon where a second copy of the citrate transporter gene (citT) is under the control of a second copy of the rnk promoter.

New genes and new information have been added to the genome while all of the old genes are still present. It's true that the new genes and new information arose from pre-existing bits of DNA that were already in the genome but that seems to be quibbling. So rather than admit that these new genes are really new information they fall back on a modified claim. The IDiots say that this is not really a "genuine innovation" (i.e. no true Scotsman). Here's how Ann Gauger puts it ...
But does this adaptation constitute a genuine innovation? That depends on the definition of innovation you use. It certainly is an example of reusing existing information in a new context, thus producing a new niche for E coli in lab cultures. But if the definition of innovation is something genuinely new, such as a new transport molecule or a new enzyme, then no, this adaptation falls short as an innovation. And no one should be surprised.
What she says is correct. Lenski's group did not witness an entirely new gene poof into existence from thin air. Nobody should be surprised at that because the gods are very clever—they would never let anyone catch them in the act. They take care to make it look like evolution is a very natural process.

Did Ann Gauger, Michael Behe, and Denyse O'Leary really think that Lenski and his colleagues would discover evidence of god(s)' handiwork?

Behe, M. (2010) Experimental evolution, loss-of-function mutations, and "the first rule of adaptive evolution." Quart. Rev. Biol. 85:419-445. [PDF]


  1. " The First Rule of Adaptive Evolution. Break or blunt any functional coded element whose loss would yield a net fitness gain."

    All this says is that some adaptive changes correspond to loss of function. This is hardly news; ask any whale why it doesn't grow toes. It just SOUNDS like a profound attack on the notion that new function can arise naturally.

    1. Well, whales do kinda grow toes, or at least internal skeletal parts for same. So perhaps the Great Designer knows a function for internal toe bones that we poor humans can't think of, or perhaps it is just one of those instances of His antic sense of humor that seem to be constantly on display.

  2. Larry, in the text you give the year of Behe's QRB paper as 2012. It was 2010.

  3. Feh, same game they play with transitional fossils. There aren't any, until {long list starting with Archeopteryx}, oh but those don't count because {quickly moves goal-post for what counts as "transitional fossil"}. Evidence is always redefined as being not-evidence. Liars.

  4. Larry says: "The new function is the result of an entirely new gene formed from the fusion of two genes, rnk and citG. This, in turn, creates a new operon where a second copy of the citrate transporter gene (citT) is under the control of a second copy of the rnk promoter."

    Wait. What does the new gene, a fusion of rnk and citG, do? It's coding right-- what does it code for?

    It seems like all the heavy lifting is done by the rnk promoter-- but what role does the new gene play?

    1. According to the previous post, "Lenski's long-term evolution experiment: the evolution of bacteria that can use citrate as a carbon source", the new gene transports citrate into the cell under aerobic conditions. The cells couldn't do that before.

    2. That doesn't answer my question, at all. There are two genes relevant here. The new gene is a fusion of rnk and a new copy of citG. That's what I'm asking about. There is also a new copy of citT. It is the new copy of citT which is constitutively expressed, and thus which confers the ability to uptake citrate.

      But I'm asking about the new gene that is a fusion of rnk and a new copy of citG. What does that do, if anything?

    3. The new fusion gene is expressed as a small protein but it doesn't do anything.

    4. But the new protein folds, or is it unstructured?

    5. The rnk is a promoter region that binds the transcription machinary when in the aerobic environment...normally it promotes expression of another gene in E.coli. The citG is a transmembrane protein that transports citrate from outside the cell into the cell cytoplasm where it can be used as a carbon source. Normally, its promoter only functions under anaerobic conditions. By placing it adjacent to rnk, it not gets produced under aerobic conditions, allowing citrate into the cell. Having this whole operand duplicated increasing the production of citG, so more citrate gets into the cell. Note there are other mutations that were also found but as yet their functions have not be elucidated.

  5. What part of "descent with modification" do you reckon IDists don't understand?

  6. Evolutionary theory is about explaining the great complexity and diversity in nature.
    Lab controlled bacteria evolution as in this case seems to only show trivial attrition or opportunism of already existing elements in this life form. Even at a basic level of bacteria it seems it can't create new things or operating functional attributes. New traits in other words.
    In fact if life has within it the ability to rearrange traits, as I think it does, then a illusion would be made about evolution creating new traits.
    Its very clumsy even if this is seen as a case for evolving traits in a population.
    Complexity can't come from clumsy reactions surely.
    its all lines of reasoning from very raw data.
    Dog breeders do more evolving then these bacterias. And they don't do it at all. Just taking advantages of traits already floating about within types of creatures .

  7. One should note that Ann Gauger herself had to confess that she observed a beneficial mutation herself. See Daniel R. Brooks report at PT (ID: Intelligent Design as Imitatio Dei (report on the 2007 ‘Wistar Retrospective Symposium’))

    "The next presentation in this session was by Ann Gauger, a microbiologist and employee of the Biologic Institute, whose presentation was entitled, “Assessing the difficulty of pathway evolution: an experimental test.” Her presentation was remarkable in part because she performed experiments and reported original data.

    She began with the repetitive attempt at a reductio ad absurdum, stating that the current complexity of metabolic pathways within cells could not have been created by gene duplication or gene recruitment (another name for co-option), and therefore they were designed. She suggested that contemporary evolutionists believe if there is not a payoff in terms of adaptive value within a few generations, any duplicated gene will be lost, and that for recruitment/co-option to work, function must change within a very few mutations. It is factually untrue that these assertions are an essential part of Darwinian theory. At most, they were initial starting points for investigations into protein evolution long ago, but today’s evolutionary biology does not adhere to any of them. Gene duplication is considered an integral part of evolutionary dynamics and one major source of the co-option that is so ubiquitous in evolution.

    She suggested that when similar proteins are “arranged by hierarchy,” the evidence suggests they arose from a common ancestor that predates the eukaryote/prokaryote split and perhaps even the Archaea. Gauger thus, like Behe, accepted not only a phylogeny of life but an ancient singular origin of life. Then she embarked on a series of experiments designed to emulate 2 billion years of microbial evolution in Petri dishes over a few bacterial generations. Specifically, she wanted to see if either of two forms of a protein would mutate directly into the other under those experimental conditions. They did not.

    Gunther Wagner congratulated Dr. Gauger on doing some great experimental work, but noted some logical inconsistencies in inference. The first is a phylogenetic comparative issue; it is necessary to know the ancestral state of the two proteins. If you are dealing with two proteins each derived separately from a common ancestor, then the experiment involves a minimum of two steps, backwards to the ancestral condition and then forwards to the alternative derived condition. It seems unlikely that you would be able to do that experimentally, especially if you have no idea of the environmental conditions under which the evolutionary diversification took place, and no idea if there were any intermediate forms that no longer survive. In response, Gauger admitted that the two proteins she studied are quite old and that studies of enzymes that are more recently diverged from each other report a lot of functional co-option, but only on a small scale.

    She was then prompted by one of her colleagues to regale us with some new experimental finds. She gave what amounted to a second presentation, during which she discussed “leaky growth,” in microbial colonies at high densities, leading to horizontal transfer of genetic information, and announced that under such conditions she had actually found a novel variant that seemed to lead to enhanced colony growth. Gunther Wagner said, “So, a beneficial mutation happened right in your lab?” at which point the moderator halted questioning. We shuffled off for a coffee break with the admission hanging in the air that natural processes could not only produce new information, they could produce beneficial new information."

  8. Later Gauger claimed that that something different had happened:

    "This is the result I reported at the private meeting. No mistake -- the mutated cells grew on medium without added biotin, but this ability was the result of increasing their ability to scavenge biotin from the medium, not because they could make biotin. They had not found a way to replace BioF function, which was the whole point of the experiment.

    I explained this to the group, and one participant, biologist Günther Wagner of Yale, said, smiling, "So, a beneficial mutation happened right in your lab?" I said "Yes," also smiling, and everyone laughed. Then the session ended.

    Günter Wagner (and most of the other participants, I assume) knew that the mutant strain I found did not solve the problem I had posed -- namely, how new enzyme functions, or the ability to make biotin, arise in the first place. It was beneficial only in the sense that the mutant cells could scavenge biotin from the medium better than before, which allowed them to grow better. In fact, he probably realized that it demonstrated just how sensitive my assay was. If the cells could find a way to make or find even a little biotin, it would have been enough for them to grow.

    In his leaked report, Dan Brooks claimed that I had found a mutant with beneficial new information. This is stretching things quite a bit. What I probably found was a mutant with an extra copy of the genes required to transport biotin from the medium, or with a higher affinity for biotin. That kind of mutation would help glean every available biotin molecule, but it would not help make biotin in the first place. There was no new genetic function generated, or sufficient information to make biotin. In the end, this adaptation would be a dead end for these cells once exogenous biotin was exhausted."

    It's not quite clear to me why the enhanced ability to take up biotin wouldn't qualify as a beneficial mutation.

    IMO her approach to bind all biotin by adding streptavidin to the medium is moving the goalposts and doesn't help her case. It's like placing a mouse in a pure nitrogen atmosphere and later claim it cannot breath.

    1. What she means by it not qualifying as a "beneficial mutation", is that it is not the precisely specific kind of beneficial mutation that she thinks would confirm that evolutionary processes can produce novel, beneficial traits.

      Of course, don't ask her to specify exactly what that would be. All she knows is that God says evolution is false. So if any mechanism is shown to produce beneficial mutations, that mechanism can't be evolutionary in nature, because that would mean God lied to her. And then she'll have a sad.

    2. Ann Gauger writes: "In his [Daniel Brooks'] leaked report"

      What a liar Ann Gauger is! Brooks report was not "leaked"; he attended their ID witches' coven and wrote up, for publication on the internet, an honest, accurate description of what the IDers said and did; and then he published it. Gauger did not catch him writing anything inaccurate.

      So Gauger engages in a lying dishonest ad hominem attack: "All participants [at the ID conference] were asked to keep the proceedings confidential -- and all did. One participant, however, Daniel Brooks of the University of Toronto, later violated that agreement, and published his version of events on-line."

      What a lying little snot Gauger is! Daniel Brooks never "agreed" to anything, as Gauger falsely states! The IDiots did not issue their gag order-- not an agreement, but a gag order to censor ID claims-- until after the conference was over. Daniel Brooks had nothing to do with their gag order and never promised to self-censor as IDiots do.

      But the IDiots were furious that they couldn't order people into silence, so they libelled Daniel Brooks.

      If I were him, I'd sue her lying ass for libel.

    3. And, of course, that's how scientific conferences are always run, right? You make all attendees sign a confidentiality agreement. Because the last thing you want is for all those new scientific findings to be publicized and communicated to the larger public.

      This is how creationists actually think science works.

      To coin a phrase, "And you wonder why they're called "IDiots"?

    4. They had at least two other super secret conferences both in 2011. The first was so secret that Berlinski's daughter had to publish videos of interviews with the attendees (see J. Shallit's post on his Recursivity blog). The second was so secret that it gained its own thread on AtBC and has been discussed in several Pandasthumb posts. I doubt that they've met since then because otherwise some of them would have trumpeted this.

  9. I admit to being a grunt in the health care world (licensed practical nurse) and the text describing Dr. Lenski's work made my poor brain hurt. However, creationists are the same folk who stated that the t-rex was a peaceful plant eater and therefore the other animals on the ark would have been safe from its monstrous teeth. Thus, I will assume that Dr. Lenski is onto something of importance, and I will continue to allow the creationists to make me laugh.

    1. We're sorry you had trouble understanding the text. It's not our desire to confuse or intimidate anybody. We're trying to make this stuff understandable to non-scientists... not always successful.

    2. Hi Wanda, and since I don't recall seeing your name here before I'll say welcome aboard. :)

  10. As usual, the IDiots are decades behind the times as far as evolutionary biology is concerned. The idea that "co-option" of existing genes into new functions (including loss-of-function as change-of-function) is essentially what Gould and Vrba described as exaptation, which they proposed as an important form of evolutionary change. I would go further than this: exaptation (and its close cousin, neutral/random change) is ALL there is in evolution. To assert that adaptation (i.e. changing "towards" a more perfect fit with the environment) is how evolution works is to resurrect teleology in evolutionary biology, which we all (except the IDiots) have categorically rejected.

  11. "Dog breeders do more evolving then these bacterias. And they don't do it at all. Just taking advantages of traits already floating about within types of creatures."

    Right. Now think about all the wonderful traits that were floating around in the monkeys. They probably have floated down the drain by now, and I am thankful we got them before too late.

  12. Just few quotes Larry missed:

    "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"

    "And the end result is a better adapted e-coli bacterium. These adaptations appear to be conservative."

    Yeah, Idiots can't read and they don't understand anything.

    1. Uh huh. And exactly how does that change anything, LouiseG?

    2. Louise, what you prove is in fact the dishonesty of IDologues. You copy two quotes, without citing either-- the first is from the Abstract of the Lenski paper, and sounds scientific because it is.

      Your second quote, "And the end result is a better adapted e-coli bacterium. These adaptations appear to be conservative," originated in a comment by Arkady967 at the ID website Uncommon Descent, where most of us cannot dispute this claim, because most evolutionists are banned at UD, including myself. They do not let me comment there.

      That second quote is typical ID creationist equivocation, not cited anywhere to the scientific literature.

      By putting the two quotes next to each other, you make it appear as though both are from the scientific literature. They are not. ALL anti-evolution arguments either depend on redefinitions of the scientific method, or on factually false claims. The phrase "These adaptations appear to be conservative" could not appear in the scientific literature because it's bullshit; IDers will always equivocate about their definition(s) of "conservative."

      I would ask you for an equation to discriminate between a "conservative" vs. a "non-conservative" mutation, but there's no point-- creationists need their claims to be non-falsifiable, so they won't give us an equation.

    3. Even if you are right (doubt that) this is still not impressive in view of all the claims people like you make. If you deleted all the genes necessary to build something like a flagellum and then put bacteria under selective pressure and than it would build something resembling a flagellum, that would be a breakthrough. What you are arguing about here is minuscule details of interpretation. It has nothing to do with macroevolution or even close to it. Its bullshit, as you would put it.

    4. Boy, LouiseG. You really are stupider than a sack full of doorknobs, aren't you?

      Lenski's study is not attempting to demonstrate "macroevolution." And not even the IDiots are saying it does. So, congratulations. You have now achieved the level of "sub-IDiot."

    5. Where did I say it did? I was referring to lousy attempts of evolutionists to show that minor changes lead to major. You didn't get it because you are what? I wrote "If" you imbecile! I guess it was Freudian slip.

    6. If minor changes don't lead to major, where is the cut-off? Where is the magic barrier. When does the hand of god come down through the clouds and stop mutations from accumulating and creating novel functions for duplicated genes and shuffled protein fragments?

      Where? Give references.

    7. Minor change? If I could suddenly digest something that all other humans could not, that would not be a minor change.

    8. Would that in the long term lead to an emergence of new and properly defined species?-(that is the cut-off Mike). I'm not talking about bigger or smaller beaks or longer or shorter hair, fur or legs. I'm talking new species.

    9. Would that in the long term lead to an emergence of new and properly defined species?


    10. Would that in the long term lead to an emergence of new and properly defined species?

      Have you ever heard of the East African cichlids (with a few dozen genera and a few hundred "properly defined" species produced by an adaptive radiation over some 100,000 years)? Feeding habits and the ability to digest something you cousins can't eat played an important role in the process:


      Will you now play the "no true Scotsman" card and argue that those species are not well defined (according to your unwritten standards)?

    11. Oops, my memory didn't serve me well. A few million years and well over 1000 species.

    12. """Would that in the long term lead to an emergence of new and properly defined species?-(that is the cut-off Mike). I'm not talking about bigger or smaller beaks or longer or shorter hair, fur or legs. I'm talking new species."""

      LouiseG, could you tell me what is the proper definition of a species for bacteria? When would you consider a new bacterial species to have arised from an E. coli ancestor?

    13. At any rate we know that an E. coli strain with smaller beaks, shaggier hair and longer legs doesn't count ;)

  13. The point is, Behe said that new functional elements (genes, promoters etc.) could not evolve, but they did, so Behe is proven wrong. As always.

    ID creationists often describe genetic control as a "wiring diagram" and they say that any "wiring diagram" must be produced by "Intelligence", which is their word for conflating real things (human designers) and imaginary things (invisible spooks).

    But here is an evolved increase in the complexity of a genetic "wiring diagram" produced by natural processes of evolution, while we have never observed an invisible spook increasing the complexity of a wiring diagram. So when we observe complex "wiring diagrams" in genetics, we should assume they are the product of natural processes, not spooks.

  14. So if I've got the general drift of the ID angle on this correct: There is never a new house built because all the wood, etc., is just repurposed existing material?

  15. When precisely did Lenski add some "God" agent to his flasks for this ID element to come to be? Please tell as I'd like to reproduce the results. He didn't seem to list that detail in his M&M section of the published work.

  16. "But does this adaptation constitute a genuine innovation? That depends on the definition of innovation you use...."

    "We, of course, prefer the ones that try to make all science look like a waste of time when you could be in church..."