Thinking 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:
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.
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.
You 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
jkc · 27 November 2010
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?
DS · 27 November 2010
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.
Steve Matheson · 27 November 2010
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.
MichaelJ · 27 November 2010
The ID crowd will say that these experiments were done by humans and were intelligently designed, therefore Jesus.
Mike Elzinga · 27 November 2010
“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.
Steve Matheson · 27 November 2010
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."
Chris Nedin · 27 November 2010
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.
Mike Elzinga · 27 November 2010
raven · 28 November 2010
Frank J · 28 November 2010
DS · 28 November 2010
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".
Frank J · 28 November 2010
Paul Burnett · 28 November 2010
Mike Elzinga · 28 November 2010
JGB · 28 November 2010
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.
Mike Elzinga · 28 November 2010
eric · 29 November 2010
Mike Elzinga · 30 November 2010
Henry J · 30 November 2010
Kris · 1 December 2010
Kris · 1 December 2010
Henry J · 1 December 2010
Michael Behe · 7 December 2010
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."
Steve Matheson · 7 December 2010
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.
Michael Behe · 7 December 2010
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.
Stanton · 7 December 2010
Michael Behe · 8 December 2010
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.
Stanton · 8 December 2010
DS · 8 December 2010
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.
Michael Behe · 8 December 2010
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.
Michael Behe · 8 December 2010
DS, thank you for dialoguing with me in a respectful manner. The same respect I accord you, I hope to receive in return.
[quote]
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.
[/quote]
Yes, there is information on a deck of cards. The cards were built by an intelligent source. Moreover, it is intelligence that interprets the information after the hands have been dealt.
[quote]
Random mutation and natural selection produce information. That is how molecular phylogenetics works.
[/quote]
Evidence please.
[quote]
As for the mutations responsible for citrate metabolism, whole genome sequencing will definitively answer this question.
[/quote]
I predict that no new genes will be built.
[quote]
If you really wanted the answer, you would be doing this type of experiment yourself.
[/quote]
I'm too busy working on studying the bacterial flagellum.
[quote]
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.
[/quote]
Since you're speculating about possible results I won't comment. I'll wait for the results.
Stanton · 8 December 2010
Stanton · 8 December 2010
DS · 8 December 2010
DS · 9 December 2010
Information can be produced by random processes. It doesn't take intelligence to produce information, it takes intelligence to interpret information.
That's how astronomy works. There is information in the absorption spectrum of a star. There is information in the red shift of stars. There is information in the periodicity of a pulsar. There is information in the wobble of star.
That's how population genetics works. There is information in the allele frequencies in a population. From this type of data you can estimate population size, mutation rate, migration rate, selection, inbreeding, population substructure, etc.
In the end, it doesn't matter if citrate metabolism evolved due to production of a new gene or not. The adaptation evolved by random mutations which were selected on in the environment. Some of the mutations were beneficial and increased in frequency. This represents an increase in information. That is why they are doing whole genome sequencing. That's the way evolution works.
DS · 9 December 2010
I guess Mikey doesn't include responses to the answers to his questions under the category of "respect".
Michael Behe · 9 December 2010
Stanton · 9 December 2010
Mike Elzinga · 9 December 2010
There don’t appear to be any consistent definitions of “information” in any ID/creationist literature. Nor does there appear to be any definition of information that has anything to do with how Nature works.
Some of the ID/creationist uses of information that suggest it organizes matter are completely at odds with known physics and chemistry. There is no such thing as some kind of top-down “information” that pushes matter around into arrangements that some other physical system called a living organism “recognizes as significant.”
And any possible definition of information that could coordinate states of an observed system with states in an “observer” system requires that there be some correspondence and interaction between the system states and “observer” states that initiates a set of events or responses on the part of the “observer” system.
To say that any physical system contains “information” seems to imply a physical observer for which (or for whom) that particular configuration of the physical system has some “meaning”. And the meaning of “meaning” would suggest it has something to do with prior states in the observer that have predisposed it to respond to that configuration of states in the observed system in some way.
But just because some physical system “likes” some configuration in some other physical system doesn’t mean there is anything out of the ordinary going on. All that might be happening is that one system is settling into a different state that is constrained by its interaction with another system that is in some particular state.
And all that is more concisely and accurately described by the laws of chemistry and physics; laws we understand pretty well.
There is no “ghost in the machine.”
DS · 9 December 2010
Mike,
No one is claiming that any new gene was produced from "scratch". Are you? As for insults, if you aren't the "real" Micheal Behe then you cannot be insulted. If you are the "real" Micheal Behe then you made those comments under oath in a public court of law.
I'm glad that you agree on common descent. Presumably then you agree that there is information in the nested hierarchy of SINE insertion in primate genomes. This information was not produced by any intelligence. It was produced by random transposition events followed by selection. The information did not require an intelligence to produce it, only to interpret it. The information is still there whether or not any intelligence interprets it.
In the end, it doesn’t matter if citrate metabolism evolved due to production of a new gene or not. The adaptation evolved by random mutations which were selected on in the environment. Some of the mutations were beneficial and increased in frequency. This represents an increase in information. That is why they are doing whole genome sequencing. That’s the way evolution works. No intelligence produced the changes but intelligence will be required in order to understand the lessons they can teach us.
Dale Husband · 9 December 2010
Michael Behe · 9 December 2010
DS,
I recommend you to read the proceedings of the Wistar Conference 1967. It took a while for biologists to decode which DNA codes for which amino acids and how complex proteins really are. Moreover, it took a while for super computers to calculate large numbers. But finally in 1967 mathematicians were able to look at the math of evolution and they found out that the numbers didn't add up. Mathematicians essentially told biologists in 1967 that there theory was wrong but biologists are too stubborn to listen to their advice and they did this at the Wistar Conference. See Marcel Schutzenberger for quick information. Do the math, 20 different amino acids in a chain of 150, that's 10^138 different combinations. And there are only 10^80 atoms in our universe and 10^17 seconds in our history. "This information was not produced by any intelligence. It was produced by random transposition events followed by selection." Information is immaterial and you need intelligence to interpret it. I have already stated why and you have refused to accept my argument. You will continue to confuse data with information, I will do the opposite. I'm sure you will also continue to deny the mathematics of DNA and amino acids. Darwinism was construed in an era when information theory was not known. It will be information which will lead to the downfall of Darwinism. And I, as the leader of the ID movement, will go down in history as a sort of Galileo and you will go down in history as an oppressive Catholic Church that clung to an old idea and refused to let it go in spite of evidence.
Michael Behe · 9 December 2010
DS · 9 December 2010
DS · 9 December 2010
Mikey,
I recommend that you read the following link:
http://www.talkorigins.org/faqs/abioprob/abioprob.html
Seems that mathematicians didn't really disprove evolution after all. I guess that kind of explains why no real scientist has bought their argument in the last fifty years. But then again, the "Galileo" of modern biology would have already known that now wouldn't he? As for the Catholic Church, I'm not the one threatening people with anything as a punishment for what they believe, are you?
Dale Husband · 9 December 2010
Stanton · 9 December 2010
Michael Behe · 9 December 2010
Michael Behe · 9 December 2010
Stanton,
The only thing you have proven to me is the exorbitant amount of hatred you Darwinists have been attacking with me ever since my book came out in 1996
DS · 9 December 2010
Mikey;
Here it is from me personally:
It's pure crap.
If you want to know why, the link I provided gives several very good reasons. I have already provided you with one. The calculation has nothing whatsoever to do with the way that evolution is known to work. It's nothing but a red herring. Why do you think that no real biologist has been convinced in fifty years? Are they all stupid? Are they all biased? Are they all anti religion?
Hers is how a real creationist thinks:
I won't be bothered to learn about the evidence or the real mechanisms proposed for evolution, I'll just ridicule my own contrived caricatures, that should fool everyone.
Pointing out that you have been duped is not an insult. Since you refuse to deal with the real theory of evolution, what else is left but to point out that you are sadly mistaken?
Well now that you have admitted that random process can produce information, there is nothing left to discuss. You have admitted that there is no theoretical reason why evolution could not occur. Thanks for playing.
As for repetitive sequences, they can definitely be produced by chance. That's the way DNA replication works, or are you ignorant of that as well? (See that was a deliberate insult). Ever hear of DNA fingerprinting? Ever been to the desert?
DS · 9 December 2010
Hey Mikey, have you read those references on the evolution of the immune system yet? You might be back in court any day now, It would look really bad if you still hadn't read them. You know there are thousands more to catch up on now don't you? Better get busy.
DS · 10 December 2010
Hey MIkey,
If you think your calculations are so great, then you won't mind enlightening everyone as to exactly which evolutionary process they are being used to model. You know, what proposed mechanism is being tested? See, the thing is, I think that calculation had nothing whatsoever to do with evolution. I think it conclusively proves that god cannot exist cause the calculations prove that she couldn't pop out of nothing spontaneously. Unless of course you think that god is less complex than a protein!
Stanton · 10 December 2010
Stanton · 10 December 2010
Michael Behe · 10 December 2010
Mike Elzinga · 10 December 2010
Michael Behe · 10 December 2010
raven · 10 December 2010
raven · 10 December 2010
Stanton · 10 December 2010
DS · 10 December 2010
Mikey wrote:
"translation and transcription requires about a 100 proteins. They all have to be there at once in order for translation and transcription to work. You need to build those proteins with the foresight that they will eventually work together. NS can’t do that."
Evidence please.
Foresight is not what what is required for the production of complex systems. Random mutations and neutral variation, combined with cumulative selection is sufficient. In fact, the evidence shows that this is exactly how the transcription and translation machinery evolved, as well as the intron splicing mechanism, etc. There was a recent article in Science that addressed this very issue. I'm sure you subscribe to Science, right? I'm sure you read the scientific literature, right?
"There is evidence, namely, NS can not construct with foresight. There is clear evidence of foresight in the cell. Intelligence is the only thing in our cosmos that has foresight. See above for evidence."
But you presented no evidence whatsoever, only baseless assertions assuming your conclusion. Look dude, as long as you define "information" as only being produced by intelligence, you aren't going to get anywhere. No real biologist buys your crap. Calling it "data" doesn't magically remove the information.
Now how about answering my question about your probability calculation? Do you still claim that this is a valid argument?
DS · 10 December 2010
Here you go Dr. Behe. I found that article for you.
Gray et. al. (2010) Irremediable Complexity? Science 380(6006):920-921.
From the article:
"Complex cellular machines may have evolved through a rachet-like process called constructive neutral evolution."
Perhaps you should publish a rebuttal article, since you claim to have evidence that this could not possibly be true. I would suggest that you at least read the article, otherwise your next court appearance might be even more embarrassing than the last one.
Mike Elzinga · 10 December 2010
Michael Behe · 10 December 2010
DS,
As for Gray, did you mean Terry Gray with this paper:
http://www.asa3.org/evolution/irred_compl.html
He wrote
I am not going to claim that I know how complex biochemical systems originated. My opponent is absolutely correct in his claim that little is known for certain and in much detail and that there is very little in the professional literature on this subject. What I will be presenting are broad outlines and hints of an explanation. They are most certainly wrong in the details, but they have convinced me that the "intelligent design" inference from "irreducible complexity" is fundamentally wrong-headed.
I really like his argument: I don't know how biochemical arose, therefore they are not designed. A classic argument from ignorance.
Michael Behe · 10 December 2010
Elzinga,
It is you who makes unsupported assertions not me. I already stated my reason for supporting intelligent design, so I was just restating my thesis. I will state it one more time. 64 DNA codons code for 20 different amino acids. These amino acids have specific properties. These properties are information, just as it is information that water boils at 100 C. When you sequence amino acids into strings of about 400 (in the human) you get proteins which have new properties. The properties of these proteins are information. An intelligent source had to know the content of this information as well as the content of the information of the elements and the molecules because these proteins have been constructed such that their properties have been exploited to form cells, working in conjunction with other proteins.
DS, you asked for evidence that the cell needs about 100 genes to perform translation and transcription. It's here
http://mmbr.asm.org/cgi/content/full/68/3/518#%28i%29_Basic_transcription_machinery. Let me quote from it:
RNA metabolism. RNA metabolism refers to all processes that involve RNA, including transcription, processing, and modification of transcripts; translation; and RNA degradation and its regulation. It is the central and most evolutionarily conserved part of cell physiology. The genes involved in these pathways represent more than 50% of the total number of genes included in our proposed minimal set (107 of 206 genes).
Basic transcription machinery. Five genes that encode components of the basic transcription machinery
Translation. The largest category of preserved genes corresponds to those involved in protein synthesis (78 genes), represented mainly by aminoacyl-tRNA synthases and ribosomal proteins.
we assume that the minimal number of ribosomal proteins required for proper functioning of the ribosome corresponds to the gene set present in M. genitalium, which includes 31 proteins for the large ribosomal subunit and 19 proteins for the small one.
WOW!!! all those genes working together!! what amazing foresight! This is what I tried to tell Ken Miller at Dover but he wouldn't listen to me. The judge made the wrong decision.
William Dembski · 10 December 2010
Great point, Michael. You really know how to show up the Darwinists!
stevaroni · 10 December 2010
Flint · 10 December 2010
Ichthyic · 10 December 2010
Great point, Michael. You really know how to show up the Darwinists!
maybe you could make some sort of flash-based fart animation out of it, Bill?
I mean, that would really show up all the "darwinists", right?
the irony you guys generate is scrumptious, but I can't indulge too much for all the high fat and cholesterol.
DS · 10 December 2010
DS · 10 December 2010
Mikey wrote:
":DS, you asked for evidence that the cell needs about 100 genes to perform translation and transcription. It’s here"
That's not what i asked for evidence for and you know it. You have provided absolutely no evidence whatsoever that complex systems cannot evolve. All you have done is make the assumption. It is unjustified. Since you have made no attempt to justify it, everyone can see that it is unjustified.
DS · 10 December 2010
Mikey wrote:
"WOW!!! all those genes working together!! what amazing foresight! This is what I tried to tell Ken Miller at Dover but he wouldn’t listen to me. The judge made the wrong decision."
Well Mikey, that should tell you something. An expert was not convinced by your hand waving. An impartial observer was not impressed by your bullshit. Man, either you got nothin, or you really suck at communication. or both. I guess they had the data but not the information, right?
Ichthyic · 10 December 2010
This is what I tried to tell Ken Miller at Dover but he wouldn’t listen to me. The judge made the wrong decision.”
well, maybe you should have told it to the judge instead?
oh, wait, you did.
and he LAUGHED IN YOUR FACE.
much like we are doing now.
Say, do you and Bill have some new predictive dates for the demise of the ToE?
WATERLOOOOOO!!!!
Stanton · 10 December 2010
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]
Steve P. · 10 December 2010
DS · 10 December 2010
Dr. Behe,
It is indeed a pleasure to have such an extinguished individual gracing the pages of this humble blog. Since you are a real scientist, I am sure that you are well aware of the relevant literature pertaining to your field. However, I realize that you may be too busy to keep up with all of the literature, given your ambitious speaking schedule. Therefore, please allow me to bring your attention to the following references. They show conclusively that the ribosomal protein genes have arisen through a process of gene duplication and mutational divergence. Furthermore, they document the mechanisms whereby new functions are acquired and the mechanisms responsible for the evolution of the regulatory mechanisms affecting the coordinated expression of these genes . As you no doubt are aware, this is a very active field of research. I hope that this short list will aid you in your efforts to address these issues in an intellectually honest fashion, rather than simply denying that any evidence exists. I thank you in advance for your willingness to review these references.
Golden et. al. (1993) Ribosomal protein L6: structural evidence of gene duplication from a primitive RNA binding protein, EMBO Journal 12(13):4901-4908.
Zhang (2003) Evolution by gene duplication: an update. Trends in Ecology and Evolution 18(8):293-299.
Komill et. a;. (2007) Functional specificity among ribosomal proteins regulates gene expression. Cell 131:557-571.
Wapinski et. al. (2010) Gene duplication and the evolution of ribosomal protein gene regulation in yeast. PNAS 107(12):5505-5510.
I can also provide references for the evolution of the genetic code and the evolution of intron splicing. It seems you have some catching up to do.
Michael Behe · 10 December 2010
DS, what happened to all of the insults? I kind of liked it better when you threw mud at me, that way I could rest assured that Darwinists had no arguments.
In any case, duplicating an already-built gene is not the same as build a new gene from scratch. Come on, DS, you know better than that.
stevaroni · 10 December 2010
DS · 10 December 2010
Are you some kind of retarded idiot? No one ever claimed that you had to build a "new gene from scratch". In fact, you were specifically told many times exactly what the mechanism was. Now I have provided you with references, they show exactly where new genes come from, it ain't from scratch. I can provide many more references if you demonstrate that you are willing to learn. Are you gong to read them or not? Are you going to become educated or not? Are you just going to continue to attack a hackneyed caricature of evolution or are you going to actually try to learn something? If you want to know why you can't convince anybody of anything, that is exactly the reason. I would advise you to increase your knowledge.
By the way, you made the same ignorant mistake with your bullshit probability calculation. Since you refuse to admit it, I have no choice but to conclude that you are as disingenuous as you are dishonest.
You know man, part of your job as a professor is to read the literature. How else are you going to remain current in the field? How else are you going to teach your students the latest discoveries? You do want to be a good teacher don't you? Given the disposition of your department towards your shenanigans, you wouldn't want to provide them with any excuse to fire your sorry ass now would you?
If you reread nay last post, I think you will discover a few insults in there as well. See the arguments are still valid whether I include the insults or not. Get a clue.
Flint · 10 December 2010
Stanton · 10 December 2010
Ichthyic · 10 December 2010
what happened to all of the insults?
good thing you're too dimwitted to notice he called you "extinguished".
John Kwok · 10 December 2010
John Kwok · 10 December 2010
Michael -
Thanks for stopping by. When we read your book, "The Edge of Evolution" both graduate student Dave Wisker and I independently arrived at the conclusion that you don't understand at all the concept of coevolution. How can you claim that the interaction between the malarial parasite Plasmodium and humanity can be seen as a "failure" of "Darwinism", when instead, it is a superb example of a pharmaceutically driven coevolutionary arms race between this parasite and humanity?
P. S. Ken Miller and I still eagerly await your textbook on Klingon Biochemistry. Since your American publisher, Simon and Schuster, also publishes the "Star Trek" books, I am sure that they would greet a proposal for such a textbook from you with considerable interest.
John Kwok · 10 December 2010
Michael -
Can you explain to us here at Panda's Thumb how Intelligent Design is a superior alternative to the Modern Synthesis Theory of Evolution in accounting for the origins, history and present composition (and structure) of Planet Earth's biodiversity? What testable hypotheses would you propose as suitable tests to demonstrate Intelligent Design's superiority over modern evolutionary theory in this regard?
Stanton · 10 December 2010
Stanton · 10 December 2010
John Kwok · 10 December 2010
John Kwok · 10 December 2010
Stanton · 10 December 2010
386sx · 11 December 2010
John Kwok · 11 December 2010
John Kwok · 11 December 2010
John Kwok · 11 December 2010
John Kwok · 11 December 2010
DS · 11 December 2010
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?
fnxtr · 11 December 2010
Dollars to donuts, "Michael Behe" and "William Dembski" have the same ISP.
DS · 11 December 2010
Henry J · 11 December 2010
Mike Elzinga · 12 December 2010
mrg · 12 December 2010
Flint · 12 December 2010
mrg · 12 December 2010
Dale Husband · 12 December 2010
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!
Stanton · 12 December 2010
Steve Matheson · 12 December 2010
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.
John Kwok · 13 December 2010