Mapping fitness: bacteria, mutations, and Seattle

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ResearchBlogging.orgThinking about fitness landscapes can stimulate detailed discussion and consideration of the meanings and limitations of such metaphors, and my introductory comments did just that. Most notably, Joe Felsenstein pointed us to the various ways these depictions can be employed, and urged everyone to use caution in interpreting them. All too true, but the goal here is modest: I want to discuss the interesting questions that arise when considering the relationship between genotypes and phenotypes, i.e., how a particular genetic makeup influences fitness, whether the genetic makeup in question is simple or complex, and however fitness is conceived. These questions can take further discussion in all sorts of directions, but there are two that I have in mind in this series. First, I want to point to increasing capacity of scientists in their ability to examine these relationships experimentally. Second, I want to highlight the failure of design creationists to address or even to understand such matters.

If you know a little about evolution, you already know that mutation is a major source of genetic novelty. And you've probably heard (or surmised) that the mutation rate in a population or lineage is thought to contribute to something called "evolvability." No mutation means no evolvability. And maybe it's clear that too much mutation is a bad thing, too. And so, the mutation rate itself is a parameter that contributes to fitness, with fitness referring in this case to the ability of a population to adapt or compete over time. There can be, it seems, a fitness landscape for mutation rates, in which we could depict fitness as a function of the mutation rate. Perhaps we could even sketch such a landscape if we could generate genetic variants that differ solely in their mutation rate.

Experiments like this have been done, and the best-known examples come from work on bacteria. Earlier this year, a group at the University of Washington in Seattle, led by Lawrence Loeb, took the analysis a big step further, in work that sought "to characterize the fitness landscape across a broad range of mutation rates." The co-first authors of the report are Ern Loh and Jesse Salk.

Loh et al. introduce their work by noting that previous analyses of the influence of mutation rate on bacterial fitness were informative but limited in scope. These experiments tended to emphasize mutators (variants with higher-than-normal mutation rates) and tended to perform head-to-head competitions between only two variants (mutator vs. normal, for example). And modeling studies of the phenomena would benefit from further validation by experimental data. So the authors set out to measure bacterial fitness in the presence of widely-varying rates of mutation. Their experiment employed two innovations that filled these gaps in previous work:

  1. The panel of variants included not two, or ten, but 66 versions of the DNA copying enzyme (DNA polymerase I). These variants all grow normally when they live alone, but they exhibit mutation rates that span six orders of magnitude, from one thousandth of the normal rate to a thousand times the normal rate. (Because the DNA polymerase is the main copying machine, its fidelity is a major determinant of the error rate and therefore the mutation rate.) This means that unlike all or most previous work in this area, their library included antimutators - variants with a lower-than-normal mutation rate.

  2. The authors staged evolutionary competitions in which all 66 variants were put together and grown for 350 generations. Specifically, they regularly diluted the cultures so that the environment cycled between low density (leading to rapid growth) and high density (leading to nutrient depletion and stasis).

The experiment is, then, relatively simple in concept. Create a pool of variants and then see which ones (if any) will take over when they're in competition with all the others. We'll skip the details of the creation of this library of variants, though it could be fun to discuss in comments. Suffice it to say that because the variants all grow normally when living in isolation, any differences in competition outcome are likely due to the effects of mutation rate on the ability of variants to adapt in the face of competition.

In one excellent graph (from Figure 2 of the paper) shown below, the authors summarize their basic result: in the various competitions, only eight of the 66 variants emerged as winners or co-winners. Those eight variants represent a relatively small subset of what we might call mutation-rate space. Here's how the authors describe the outcome:

The recovered mutants were all moderate mutators, with mutation rates ranging from 3- to 47-fold greater than that of the wild type. Of these, 88% had at least a 10-fold elevated mutation rate. No antimutators were detected in the output population despite constituting 77% of the input population.

Loh et al Fig 2.jpgYou can see this from the graph: each colored arrow points to a mutation rate, representing a variant that was one of the winners, and the bar graph above it shows how often that particular variant won. The scale left to right is mutation rate. Variants from normal on down (going left on the scale), all of those antimutators, were losers. Ditto for the super-mutators at the other end of the scale.

Loh et al. went on to show that the winning variants had adapted by putting the winners into head-to-head competition with their ancestors. (Oh the cool things you can do when your experimental organism is E. coli!) In other words, the winning variants had evolved, becoming more "fit" than when they started, by virtue of competing in a crowded jungle of other variants. The winners were different from their ancestors, but also from each other, demonstrating that the winners had acquired new characteristics beyond their higher mutability. The authors conclude that "under conditions where organism fitness is not yet maximized for a particular environment, competitive adaptation may be facilitated by enhanced mutagenesis."

The paper is fun to read and relatively approachable. Check it out.

So back to the two points I wanted to emphasize. First, the authors briefly employ the "fitness landscape" metaphor, simply to indicate that mutation-rate variation (in this case due to engineered genetic variation in DNA polymerase I) is likely to map onto "fitness" (in this case, ability to win an evolutionary competition under a certain set of environmental conditions) in interesting and perhaps surprising ways. Their data add a layer of intriguing complexity to studies and discussions of the roles of mutation and mutability in evolution and evolvability. Second, they did their experiments at the University of Washington School of Medicine. Less than 12 miles away, in Redmond, Washington, is a research institute dedicated to intelligent design. According to Google Maps, it's a 16-minute drive from that institute to the UW School of Medicine. (Or 40 minutes in traffic. Neither of these numbers impresses me, having lived in metropolitan Boston for five years.) Now, some of the researchers at that institute are keenly interested in mutation and evolution in bacteria. Do you suppose those researchers are interacting with the Loeb lab? Attending seminars, exchanging research materials, collaborating, consulting? I would be interested to hear from scientists at either place. If, as I suspect, none of those things has happened, then maybe the folks at that institute in Redmond could, with our encouragement, expand their influence and find new opportunities by contacting their world-class colleagues, right in their own neighborhood. As curious as they claim to be about evolution and mutation, they would be crazy not to. Right?

(Cross-posted at Quintessence of Dust.)

Loh E, Salk JJ, & Loeb LA (2010). Optimization of DNA polymerase mutation rates during bacterial evolution. Proceedings of the National Academy of Sciences of the United States of America, 107 (3), 1154-9 PMID: 20080608

107 Comments

Very interesting paper and an excellent summary. Thanks for keeping us laypeople in the loop.

Just to play devil’s advocate and anticipate DI objections: how do the different variants of DNA Polymerase come to be and how did we end up with the ones that are in the medium-mutaton range? And, if the medium mutators were selected for, what caused the mutations that allowed for their to be many different variants of mutators? In other words, where does the (presumably non-infinite) regress end?

Thanks Steve. This is certainly interesting stuff.

Now I wonder why the ID crowd hasn’t done similar experiments to show that only advantageous mutations poof into existence?

But seriously, if the mutations that increase mutation rate are simple ones and no wild type ever wins such competitions, it makes one wonder why the wild type mutation rate isn’t higher? Perhaps selection is more complex in the long term that these relatively short term experiments would seem to imply.

In the future, I’m sure we can look forward to whole genome sequencing in order to determine the exact mutations that imparted the competitive edge to the winning strains. Now that is going to be cool stuff. Kind of blows the “no beneficial mutations” nonsense out of the water though - again.

jkc, if you’re asking about the real world, mutators occur normally in the population, due to genetic variation in the normal machinery. They seem to come to the fore when evolutionary pressure is applied, e.g. during adaptation to environmental changes or during competition. So the answer to your question is that the copying machinery can vary in its fidelity, and fidelity (and therefore mutation rate) can likewise vary depending on the environment.

DS, the idea is that the “wild-type mutation rate” could be the state of the system in what we might call equilibrium, but that during adaptation, mutators can be beneficial by increasing genetic diversity. As the authors mention in their summary statement, we might postulate that once the population is “maximized for a particular environment,” then the mutator phenotype is no longer an advantage, and selection can reduce the mutation rate back to “wild-type.”

Loh et al. addressed these issues in their discussion. Have a look, and note their references to the extensive literature on these subjects.

The ID crowd will say that these experiments were done by humans and were intelligently designed, therefore Jesus.

“Evolvability?” Hoo boy! How is that related to “fitness?”

If I may take the role of Simplicio here, maybe I can ask the stupid questions others may be thinking about (probably not).

Just for simplicity (because I think I get this part), let’s go back to the lattice of frequencies (actually probabilities) and talk in terms of the population for the moment. In other words suppose the following for the set of alleles Ai, ai where i is the index running over all alleles:

We let pi be the freq(Ai), and of course, qi = 1 - pi = freq(ai).

Now the set of pi traces out a set of axes, each from 0 to 1, that form a unit hypercube describing probabilities of all the alleles in the population, however many there are (and assuming for the moment they change independently).

Here is where it gets a bit murky for me. Suppose that at some location within that hypercube there is a fitness peak. Now, in the real world, that peak is not solely determined by the specific set of pi at that location. The peak is also determined by external environmental conditions (e.g., gravity, temperature, and a host of other specific properties of the environment).

If it were the case the members of the population never competed with each other, then that fitness peak would be labeled by a set of other parameters, but not the pi. As it is, it is a function of both sets.

Furthermore, is it reasonable to take an entire specific set of pi and use it as a label for a phenotype? Presumably phenotype depends on environmental factors as well (gravity, chemicals in the environment, conditions in the womb or egg, the state of “switches” determining growth, etc.).

So it appears to me that fitness plots are not plots in quite the same sense as plots in mathematics and physics. There is a “backwards” way in which they can be interpreted in which the location of fitness peak “selects” both a set of environmental factors and a set of alleles in the population as “special.”

It is almost like the “volume” of intersection of a couple of hyper-cubes or hyper-spheres.

Mike: In this case, fitness refers roughly to reproductive success. The variants that experienced the highest reproductive success have, in this conception, the highest fitness. Their higher fitness seems to result from their ability to accumulate genetic variation, and that’s one way to understand “evolvability.”

SM: we might postulate that once the population is “maximized for a particular environment,” then the mutator phenotype is no longer an advantage, and selection can reduce the mutation rate back to “wild-type.”

Where do such marked differences in mutation rate leave molecular clocks? If mutation rates can cycle between short periods of significantly increased intensity, and then (presumably) longer periods at reduced intensity, you end up with a Gould/Eldredge pattern of ‘punctuated’ rates, rendering elapsed time calculation rather difficult.

Steve Matheson said:

Mike: In this case, fitness refers roughly to reproductive success. The variants that experienced the highest reproductive success have, in this conception, the highest fitness. Their higher fitness seems to result from their ability to accumulate genetic variation, and that’s one way to understand “evolvability.”

Yeah, I think I have the fitness part.

It is perfectly reasonable - and, in fact, necessary – to find descriptions of complex systems that acknowledge the emergent properties that may dominate the system behavior. If biological systems are not to appear to violate the laws of physics and chemistry, it would be hoped that such terms used to describe biological systems aren’t “built in the air” so to speak.

One would hope that such terms would be ultimately expressible in terms of more fundamental concepts as linkages among various levels of complexity become understood. This has been very much the history of chemistry and physics; and there is no reason to think biological systems, despite their complexity, should not be simply a continuation of this evolution in understanding.

So in the case of mutations rates contributing to “evolvability,” by allowing organisms to have enough variants to take advantage of a wider range of environments makes sense, provided the proliferation of words doesn’t cloud the issues.

In the case of physical/chemical systems in general, binding energies have a lot to do with the way a system responds to external forces. If a system, such as a complex of molecules, exists at temperatures comparable to its binding energy potentials, relatively small perturbations can rearrange bonds (cause mutations?). If the system exists in a bath of other molecules that provide a sort of catalytic background that also assists in rearranging bonds, we would expect to see the same effects as we do with increases in temperature.

My own suspicions are that the distances between the descriptions of biological systems and the fundamentals of chemistry and physics are not as great as they might appear at the moment. It’s more a matter of finding the right descriptions and the right relationships.

As I think I have mentioned before, the replicating part of biological systems may not be as big a gap as it appears. This process simply replaces a system with surrogates having the requisite variations to adapt to whatever environmental changes occur (provided such changes don’t destroy the system). In a sense, such systems “melt” or “deform” to match changes. But the melting and deformations depend on such systems being near their melting temperatures. Being near melting temperatures or in the presence of catalytic agents simply increases the rates of change and the ranges of opportunities.

jkc:

how do the different variants of DNA Polymerase come to be and how did we end up with the ones that are in the medium-mutaton range?

SM:

(in this case due to engineered genetic variation in DNA polymerase I)

For this paper, the various mutators were engineered into DNA polymerase 1 so the strains only differ by one mutation in one gene.

You can select for and find mutator phenotypes in the wild. If one selects for rare mutations such as streptomycin resistance, some of those will also be mutators.

IIRC, Lenski in his citrate evolution experiments also picked up a few mutators as well.

High levels of selection pressure are all that is needed to select for mutator phenotypes.

Selection of a Mutant of Escherichia coli Which Has High Mutation … by RB Helling - 1968 - Cited by 24 - Related articles [PubMed]; Newcombe HB, Hawirko R. SPONTANEOUS MUTATION TO STREPTOMYCIN RESISTANCE AND DEPENDENCE IN ESCHERICHIA COLI. J Bacteriol. 1949 May;57(5):565–572. … www.ncbi.nlm.nih.gov › Journal List › J Bacteriol › v.96(4); Oct 1968

MichaelJ said:

The ID crowd will say that these experiments were done by humans and were intelligently designed, therefore Jesus.

I don’t think that the DI’s Klinghoffer or Medved would go with that. And none of them publicly objected to Behe’s admission (at the Dover trial) that the designer might no longer exist. One might expect their Biblical literalist fans to collectively pass out from that, but they’re good at tuning out anything inconvenient as long as it comes from someone willing to tell them other things that feed their cravings.

But you’re right that they often object that any experiment conducted by humans “smuggles in” design. They may be terrible at research - they know better than to even try any experiment that could shed light on what the designer did, when or how - but they are good at playing “heads I win, tails you lose” word games.

Well the mutator variants were definitely designed. However, they can and do occur spontaneously in nature, so eventually this experiment would be carried out in nature. Perhaps more importantly, the environment, and hence the selection pressure, was designed. Apparently this type of selection is not very common in nature, or the wild type mutation rate would probably be higher. However, once again, this type of selection will inevitably occur in nature, so this experiment would occur spontaneously as well.

Experiments, by their very nature, are designed. That’s the way science works. Laboratory experiments usually don’t tell us much about what has actually occurred in nature, but they usually tell us a great deal about what could occur in nature. In this case it has been demonstrated that variation in polymerase fidelity will produce variation in mutation rates and that some of these variants will more quickly produce adaptive mutations in certain types of environments than the wild type. This alone is sufficient to falsify several common creationist claims. If sequencing reveals that any of these adaptations are the result of multiple mutations, then another creationist claim will be falsified. This would not be at all surprising, since this is essentially the result that Lenski got under different environmental conditions.

No wonder these guys never bother to do any research. Closing gaps doesn’t appear to be in their “research agenda”.

DS Wrote:

No wonder these guys never bother to do any research. Closing gaps doesn’t appear to be in their “research agenda”.

As you probably know, some of them do some research. But it either supports evolution or at best can be used to spin misleading incredulity arguments. The Behe and Snoke paper apparently qualifies as both.

At the risk of giving them too much credit as skilled verbal strategists I see them exploiting both lay people whose who are sympathetic to “underdogs” (especially if they share one’s “worldview”) and critics. The former generally extrapolate any perceived incredulity of evolution as validating their childhood fairy tale. The latter are forced to defend evolution in greater detail, giving the scammers more evidence and quotes to take out of context to spin more incredulity to the uninformed/misinformed. And if those critics tangent onto religion and politics, it further lets the scammers off the hook from providing any detail about their “theory.” But that would involve closing “gaps,” or at least trying to. And as you note, they have no intention of doing anything of the sort.

If we say that none of them do research, they trot out Behe and Snoke. If we say they avoid peer-review they trot out Meyer’s paper. If we object that it was not properly peer-reviewed they whine about being “expelled.” If I may repeat one of the best descriptors of their antics that I have ever heard, they like to play “heads I win, tails you lose.”

Mike Elzinga said: It is almost like the “volume” of intersection of a couple of hyper-cubes or hyper-spheres.

Is the fitness map restricted to two dimensions (x,y)? They look like topographic maps - three dimensions represented on a two-dimensional map (x,y,z). Four dimensions doesn’t seem out of hte question.

Paul Burnett said:

Mike Elzinga said: It is almost like the “volume” of intersection of a couple of hyper-cubes or hyper-spheres.

Is the fitness map restricted to two dimensions (x,y)? They look like topographic maps - three dimensions represented on a two-dimensional map (x,y,z). Four dimensions doesn’t seem out of hte question.

No, it isn’t. The x-y plane, if you like, is a simplified picture involving, say, the frequencies (actually probabilities) of two different alleles. That’s what Joe referred to as the lattice on the other thread. The axis perpendicular to this is fitness.

This kind of plotting is also encountered in physics in which a 2-D plane is used as a simplified picture for visualization purposes. In relativity, for example, only two spatial dimensions are shown in a horizontal plane while time is shown on a separate axis passing through that plane (it’s a little difficult to visualize more than three dimensions projected onto a two-dimensional piece of paper or chalkboard). From the mathematical perspective, one just adds more numbers to the array of numbers representing a specific point in a higher dimensional space. There are other issues to consider, such as orthogonality; but as far as the plotting is concerned, it is meant to be a representative slice through a higher dimensional space.

In statistical mechanics, phase-space diagrams are shown in two dimensions with a position axis and a momentum axis. But these are a slice through something like 1023 dimensions representing the positions and momenta of all the particles making up a system.

I know the discussion cropped up on a different thread in regards to the vector or scalar nature of fitness. And I think some of the fuzziness in the landscape model points back to that question. If you model genotypes as vectors and the environment as a vector. Fitness naturally comes out as the scalar result of multiplying two vectors. One could then do as Mike suggests and picture the landscape as a slice of the genotype space against the fitness (assuming a constant environment) or alternatively perhaps a slice of the environment space against fitness at a constant genotype.

JGB said:

I know the discussion cropped up on a different thread in regards to the vector or scalar nature of fitness. And I think some of the fuzziness in the landscape model points back to that question. If you model genotypes as vectors and the environment as a vector. Fitness naturally comes out as the scalar result of multiplying two vectors. One could then do as Mike suggests and picture the landscape as a slice of the genotype space against the fitness (assuming a constant environment) or alternatively perhaps a slice of the environment space against fitness at a constant genotype.

There are a number of ways to “multiply” vectors, including inner (or dot) product, vector (or cross) product, and various kinds of tensor products.

The dot product is a scalar, and it requires that the vectors have the same dimensions.

In the case you suggest, it is not necessarily the case that the two spaces would have the same dimensions.

And, even if they did, the norm of such a product would not necessarily have anything to do with fitness.

In fact, the significance of the volume of intersection of two such sets would be a property determined independently, namely, the reproductive success of the organisms possessing the set of alleles in that intersection.

If people are interested in this subject they might also like this Op-ed: Evolving the Single Daddy by Olivia Judson (New York Times, 2008). Its not about mutation per se, but it comes to the same conclusion as the Loeb et al. article: while evolution can produce species with very low variability, they get outcompeted. The money quote from the op-ed:

The evolution of traditional, female-only asexuality typically leads to a swift extinction. We know this because although such species frequently evolve, they don’t stay around for long. If you look at the tree of life, female-only asexual groups are all out on the twigs: there are no great asexual lineages equivalent to fish or birds. Instead, the asexual groups are a few species of snail here, a dandelion there.

Male-only asexuality is likely to lead to extinction too, but faster.

This is consistent with the results of the Loeb et al. research. Low variability = swift extinction.

eric said:

This is consistent with the results of the Loeb et al. research. Low variability = swift extinction.

I gather that this does not have to be the case, however.

Aren’t there some species (coelacanth, for example; and some sharks) that have maintained pretty much the same phenotype for unusually long periods of time?

Of course, that doesn’t necessarily indicate the genotype has remained as constant.

Aren’t there some species (coelacanth, for example; and some sharks) that have maintained pretty much the same phenotype for unusually long periods of time?

Of course, that doesn’t necessarily indicate the genotype has remained as constant.

Also, having the hard parts stay fairly constant for a long period doesn’t necessarily mean that all the soft parts did. Or the proteins and other biochemistry, either.

Henry J

eric said:

If people are interested in this subject they might also like this Op-ed: Evolving the Single Daddy by Olivia Judson (New York Times, 2008). Its not about mutation per se, but it comes to the same conclusion as the Loeb et al. article: while evolution can produce species with very low variability, they get outcompeted. The money quote from the op-ed:

The evolution of traditional, female-only asexuality typically leads to a swift extinction. We know this because although such species frequently evolve, they don’t stay around for long. If you look at the tree of life, female-only asexual groups are all out on the twigs: there are no great asexual lineages equivalent to fish or birds. Instead, the asexual groups are a few species of snail here, a dandelion there.

Male-only asexuality is likely to lead to extinction too, but faster.

This is consistent with the results of the Loeb et al. research. Low variability = swift extinction.

http://biology.about.com/od/genetic[…]oduction.htm

http://www.cosmosmagazine.com/news/[…]100000-years

http://en.wikipedia.org/wiki/Parthenogenesis

http://onlinelibrary.wiley.com/doi/[…]9.x/abstract

http://www.sciencedaily.com/release[…]03111210.htm

http://www.sciencedaily.com/release[…]23072254.htm

Henry J said:

Aren’t there some species (coelacanth, for example; and some sharks) that have maintained pretty much the same phenotype for unusually long periods of time?

Of course, that doesn’t necessarily indicate the genotype has remained as constant.

Also, having the hard parts stay fairly constant for a long period doesn’t necessarily mean that all the soft parts did. Or the proteins and other biochemistry, either.

Henry J

I think it should also be mentioned that the genotype, soft parts, proteins, and biochemistry could have remained as constant. It’s something that would have to be determined for each species, if possible.

I think it should also be mentioned that the genotype, soft parts, proteins, and biochemistry could have remained as constant. It’s something that would have to be determined for each species, if possible.

In general, I’d think one would need living (or at least recently living) close relatives of the species in question, in order to check aspects that don’t generally leave traces in fossils.

Henry J

Steve, whatever happened to: “Second, I want to highlight the failure of design creationists to address or even to understand such matters.” You sort of left that part out. Try reading what they wrote, here I’ll make it easy for you: “Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken. This finding has particular significance for models of gene recruitment, since weak new functions are likely to require costly over-expression in order to improve fitness. If reductive, cost-cutting mutations are more abundant than mutations that convert or improve function, recruitment may be unlikely even in cases where a short adaptive path to a new function exists.”

Uh, hi “Michael Behe.” Not sure who you’re quoting there, but if your goal was to illustrate the failure of design creationists to address or even to understand fitness landscapes and evolutionary trajectories, that silly quote will do very nicely.

what you’re failing to understand about the Lenski experiment, Steve, is that the mutations of the E Coli have been shown to be incoherent and disordered, which is exactly what we would expect from NS. Since Lenski started his experiment no new molecular machinations have been built and this, in spite of the fact that it has tracked I forget how many generations, maybe 10^12. 10^12 generations and still nothing of any significance. The only thing that has evolved is just a few broken genes.

Michael Behe said:

what you’re failing to understand about the Lenski experiment, Steve, is that the mutations of the E Coli have been shown to be incoherent and disordered, which is exactly what we would expect from NS. Since Lenski started his experiment no new molecular machinations have been built and this, in spite of the fact that it has tracked I forget how many generations, maybe 10^12. 10^12 generations and still nothing of any significance. The only thing that has evolved is just a few broken genes.

Yet, that still doesn’t explain why we should assume that Natural Selection doesn’t exist, and it still doesn’t explain why we should assume that Intelligent Design is supposed to have explanatory power.

Also, if the only things that evolved are “a few broken genes,” then how does that explain the fact that Lenski directly observed the evolution of citrate-metabolizing Escherichia coli bacteria from Escherichia coli bacteria that could not metabolize citrate?

Or does this question raise a “pathetic level of detail” that you, as an Intelligent Design proponent, are hypocritically not obligated to explain?

I started this thread because I wanted to highlight the fact that you failed this promise: “I want to highlight the failure of design creationists to address or even to understand such matters.” Why don’t you read the article you posted, quote from it, and show where it’s wrong? Do you read any ID literature or does cognitive dissonance prevent you from doing that?

“why we should assume that Intelligent Design is supposed to have explanatory power.” Dna is information. Chance cannot produce information, intelligence can.

“if the only things that evolved are “a few broken genes,” then how does that explain the fact that Lenski directly observed the evolution of citrate-metabolizing Escherichia coli bacteria from Escherichia coli bacteria that could not metabolize citrate?” Was this new citrate-metabolization just a case of epigenetics? Was the gene already there and the environment turned it on? Was a completely new gene built that would metabolize citrate? Or was one already-built gene mutated with the result on one amino acid changing? Which gene was it? Which amino acids changed places? I want direct quotes, not hearsay evidence.

Michael Behe said:

I started this thread because I wanted to highlight the fact that you failed this promise:

I want to highlight the failure of design creationists to address or even to understand such matters.

Why don’t you read the article you posted, quote from it, and show where it’s wrong? Do you read any ID literature or does cognitive dissonance prevent you from doing that?

All “ID literature” ever says is “Evolution is wrong and can’t happen because we’re too lazy to understand it, therefore GODDIDIT”

If you’re that concerned, why not quote from the relevant papers, yourself? On the other hand, it’s been my personal experience that the sole reason why no Intelligent Design proponent ever quotes the relevant papers is because such things do not exist. And such things will never exist because Intelligent Design proponents are totally incapable and unmotivated to do research.

why we should assume that Intelligent Design is supposed to have explanatory power.

Dna is information. Chance cannot produce information, intelligence can.

And yet, you still have not demonstrate how Intelligent Design allegedly has explanatory power with this non sequitor. So it is experience, not cognitive dissonance like you falsely accuse, that tells me Intelligent Design proponents are incapable of saying anything beyond “GODDIDIT” In fact, from the way you misspell “DNA,” it strongly suggests you’re an impostor who probably never taken a high school science class.

if the only things that evolved are “a few broken genes,” then how does that explain the fact that Lenski directly observed the evolution of citrate-metabolizing Escherichia coli bacteria from Escherichia coli bacteria that could not metabolize citrate?

Was this new citrate-metabolization just a case of epigenetics? Was the gene already there and the environment turned it on? Was a completely new gene built that would metabolize citrate? Or was one already-built gene mutated with the result on one amino acid changing? Which gene was it? Which amino acids changed places? I want direct quotes, not hearsay evidence.

This rant of yours strongly suggests that you lack the rudimentary brain and will power needed to look up the Wikipedia article about Lenski’s experiment, as well as the fact that the only “science” you’ve ever learned is from mindlessly parroting pro-Creationist sites.

Of course, even if I do quote directly, you’re just going to pull some inane, nonsensical excuse to simultaneously magically invalidate what I say while magically excusing yourself from providing any actual explanations or even coherent refutations.

You have to be aware that the onus is on you and other Intelligent Design proponents to explain exactly how and why Lenski’s experiments really show the magical Hand of God magically diddling with the bacteria within, and not Random Mutation + Natural Selection.

Going on and on with “Nuhuh nuhuh, not true ‘cuz GODDIDIT” is not a viable argument.

MB wrote:

“why we should assume that Intelligent Design is supposed to have explanatory power.” Dna is information. Chance cannot produce information, intelligence can.

Ever played poker? The cards are shuffled and dealt randomly. There is information in the combination of cards that you are dealt. That is how they decide who wins.

Random mutation and natural selection produce information. That is how molecular phylogenetics works.

As for the mutations responsible for citrate metabolism, whole genome sequencing will definitively answer this question. If you really wanted the answer, you would be doing this type of experiment yourself. It seems most likely that some type of gene duplication was involved, followed by divergence due to point mutations. That might not turn out to be the exact mechanism involved, but it would explain why the experiment showed a significant effect of historical contingency. It would also conclusively falsify several creationist claims. But then again, we already have plenty of examples of this kind of thing in nature. This would just be a good laboratory demonstration.

Stanton,

I’m afraid dialogue between us is not possible. If one side refuses to answer the other’s questions than the two sides cannot learn from each other. I asked you questions about Lenski’s experiment which you refused to answer.

William Dembski said:

Great point, Michael. You really know how to show up the Darwinists!

Loved your debate with Hitchens and your point about how all the other creation myths except for the Christian one are natural forces just like Darwinism. Those darn naturalistic creation myths. Lol, I had to get a new computer screen. That is classic comedy gold.

I was half awake, newly returned from a chamber music recital and post-concert reception, when I saw “Behe” and “Dembski” stop by. I missed your earlier comment:

Stanton said:

I noticed Michael Behe’s impostor posted again, and also neglected to provide any coherent explanation how and why Intelligent Design is supposed to be a better explanation than Evolutionary Biology.

I wonder why [/facetiousness]

386sx said:

William Dembski said:

Great point, Michael. You really know how to show up the Darwinists!

I think it is utterly fascinating that a dying Christopher Hitchens is still able to make a lot more sense than my “dear” pal Bill Dembski. Think that says a lot about the intellectual caliber of both gentlemen, don’t you think?

Loved your debate with Hitchens and your point about how all the other creation myths except for the Christian one are natural forces just like Darwinism. Those darn naturalistic creation myths. Lol, I had to get a new computer screen. That is classic comedy gold.

Sorry I goofed a bit earlier this morning, so here’s the correction:

386sx said:

William Dembski said:

Great point, Michael. You really know how to show up the Darwinists!

Loved your debate with Hitchens and your point about how all the other creation myths except for the Christian one are natural forces just like Darwinism. Those darn naturalistic creation myths. Lol, I had to get a new computer screen. That is classic comedy gold.

I think it is utterly fascinating that a dying Christopher Hitchens is still able to make a lot more sense than my “dear” pal Bill Dembski. Think that says a lot about the intellectual caliber of both gentlemen, don’t you think?

Hey Bill,

I forgot to ask you four questions last night:

William Dembski said:

Great point, Michael. You really know how to show up the Darwinists!

Here they are:

1) When are you going to return to the Dover Area School District board the $20,000 you stole from them in agreeing to serve as their lead witness for their defense at the 2005 Kitzmiller vs. Dover Area School Distict trial?

2) When will you apologize to eminent University of Texas ecologist Eric Pianka for falsely accusing him of being a potential bioterrorist to the Federal Department of Homeland Security in 2006?

3) When will you apologize to both Harvard University and to David Bolinsky, President, XVIVO, for “borrowing” the XVIVO-produced cell animation video in 2007, in which you all but admitted that it wasn’t merely an act of “borrowing”, but rather, larceny?

4) For the fourth time (twice in person after the AMNH Intelligent Design debate back in the Spring of 2002; the third when we corresponded via e-mail back in December 2007; no answers from you were ever forthcoming) can you explain how you would calculate confidence limits for the Explanatory Filter? Since I’m not nearly as smart as you are with regards to statistics, then I would imagine that it should be a trivial exercise for someone such as yourself with a Ph. D. in Mathematics from the University of Chicago and a M. S. in Statistics from the University of Illinois, Chicago.

I guess all the insults scared “Dr. Behe” away. I guess he really does use that as his excuse to ignore the substance of the arguments, just like he said.

So, let’s recap shall we?

1) Random processes can produce information, it takes intelligence to interpret the information, not to produce it.

2) New genes can be produced by random processes such as gene duplications and mutational divergence. This is a major mechanism by which new structures and functions can evolve, often through a process involving fixation of v=initially neutral variation.

3) New genes do not poof out of nowhere from scratch. That is a creationist misconception and the basis of their irrelevant and inappropriate probability calculations.

Now “Dr. Behe” is free to reject these conclusions, but until he demonstrates that he has read and understood the relevant scientific literature his opinion is essentially worthless. Those of us who are familiar with the scientific evidence, respectfully (or disrespectfully) disagree with “Dr. Behe”. SInce he has provided absolutely no evidence, I cannot think of a single reason why anyone should be convinced by his blustering. How does this guy continue to sell books anyway?

Dollars to donuts, “Michael Behe” and “William Dembski” have the same ISP.

fnxtr said:

Dollars to donuts, “Michael Behe” and “William Dembski” have the same ISP.

What’s the difference, neither one of him has a clue. Hell, I insulted the guy three times and he thanked me for not insulting him! That was after he proved mathematically that “poof” don’t happen. Oh well, if they are the same guy, that should make it easier for him to read the papers. He can just split them up and read two each.

How does this guy continue to sell books anyway?

Maybe something like this: “BUY MY BOOK!!111!!one!!” ?

DS said:

fnxtr said:

Dollars to donuts, “Michael Behe” and “William Dembski” have the same ISP.

What’s the difference, neither one of him has a clue. Hell, I insulted the guy three times and he thanked me for not insulting him! That was after he proved mathematically that “poof” don’t happen. Oh well, if they are the same guy, that should make it easier for him to read the papers. He can just split them up and read two each.

I have never been impressed with any of the ID/creationist “scientists.” Every one of them from ICR, to AiG, to the DI has extremely distorted conceptual understandings of science.

And Behe simply showed to the entire world – with his airy dismissal in Dover of piles of research - that he doesn’t even understand what is going on in what is supposed to be his own area of expertise.

So it is not surprising that trolls, who show up attempting to pose as Behe or Dembski, would have no clue when they just got nailed.

But it really is funny to watch. Troll gets whacked between the eyes, blinks dopily, and says, “Duh, I won!”

Mike Elzinga said:

I have never been impressed with any of the ID/creationist “scientists.”

I have. No matter how low I set my expectations, they keep surprising me.

mrg said:

Mike Elzinga said:

I have never been impressed with any of the ID/creationist “scientists.”

I have. No matter how low I set my expectations, they keep surprising me.

How so? Put your self in the shoes of a creationist scientist. On the one hand, creationism HAS to be true, since that was indoctinated into you in early childhood and those neural pathways can no longer be altered.

But on the other hand, the scientist in you wants to understand how things really work, what the principles are that reality operates by. You’re curious to understand your god’s methods and handiwork. And one thing you understanding intuitively is, if it requires magic, then it ain’t science. So your god had to have used principles science can explain.

But subconsciously, you’re aware that it’s not going to happen. Your theological requirements are flat antithetical to your scientific requirements. Your only possible strategy is to atomize science into a set of tiny, unrelated and disparate claims. And then find some rationalization for rejecting each one individually, without allowing yourself to notice that your rationalizations are themselves mutually exclusive.

So what’s impressive about creationist scientists, beyond their limitless ability to kid themselves, is the imaginative way they can whitewash sheer idiocy with a sheen of plausibility (if you don’t look too closely) while never losing sight of the theological constraints.

I actually admire them the way I admire a circus contortionist. They know that what absolutely must be true, absolutely can’t be true. They have to find some way to enable themselves to THINK it’s true, without shorting out their whole brains.

Flint said:

I actually admire them the way I admire a circus contortionist.

Precisely. “I couldn’t possibly do such things. It is beyong my imagining how anyone else can do such things themselves.”

Hmm, I heard the Cirque du Soleil roadshow is coming to town next month, I’ll have to check. This time I get the first-class seats.

What the hell are Michael Bee the non-stinger and William Dumbski doing here, anyway? Do we at PT often invade their stupid blog Uncommon Descent (into madness)? If we have done that lately, I do apologize, since we have better things to do with our time.….and so do they!

Dale Husband said:

What the hell are Michael Bee the non-stinger and William Dumbski doing here, anyway? Do we at PT often invade their stupid blog Uncommon Descent (into madness)? If we have done that lately, I do apologize, since we have better things to do with our time.….and so do they!

Quite frankly, if the two idiots’ idiot impostors are through humiliating themselves, then we should have this thread put out of its misery.

Stanton, that’s a great idea. Let’s all stop feeding the trolls. If you need that kind of entertainment, take Dale’s hint and head to UD.

Yours is a sentiment I endorse with ample enthusiasm. Kudos to you and Stanton, and to Dale for suggesting Uncommonly Dense:

Steve Matheson said:

Stanton, that’s a great idea. Let’s all stop feeding the trolls. If you need that kind of entertainment, take Dale’s hint and head to UD.

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This page contains a single entry by Steve Matheson published on November 27, 2010 11:24 AM.

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