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Is There an Edge to Evolution? Part 4

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November 3, 2010 Tags: Design

Today's entry was written by David Ussery. Please note the views expressed here are those of the author, not necessarily of The BioLogos Foundation. You can read more about what we believe here.

In the first three parts of this series, molecular biologist, Dr. David Ussery examines, chapter by chapter, the arguments put forward in the book, The Edge of Evolution, by Michael Behe. This book, like Dr. Behe’s previous book, is written in an engagingly accessible style and has been highly acclaimed by many non-specialists who think that Behe has identified the limits of what science can explain without needing to insert an external Intelligence. David Ussery is a Christian molecular biologist who, like all of us at BioLogos, is deeply concerned that other Christians be aware that Dr. Behe has not identified biology’s edge. Furthermore, none of us are sure why anyone should expect to find an Edge—a place where nature ends and God begins. Nature after all—all of nature—is God’s. There is no aspect of creation which is not God’s. Here is David Ussery’s analysis of Chapters six and seven of Behe’s book.

Note: Title of Dawkins' book was corrected on 11/4/10.

Chapter 6 - Benchmarks

This chapter details how Behe decides whether some biological features are unlikely to have been produced by random mutation and natural selection. As an example, he chooses a quote from an article on how to evaluate proposed mechanisms for biological speciation, based on what seems “biologically reasonable.” Behe claims that the idea of whether evolution is “biologically reasonable” has not been fully tested for all of evolution, and proposes to do so in this chapter. To “judge whether random mutation hitched to natural selection is a biologically reasonable explanation for any given molecular phenomenon,” he uses two criteria: how many steps are necessary to create this?, and coherence - the ordering of steps towards a goal. Richard Dawkins goes through both of these steps in his book, Climbing Mount Improbable. I was surprised to find that, although Charles Darwin, Daniel Dennett, John Maynard Smith, Alan Orr, Jerry Coyne, and Francois Jacob are mentioned here, somehow Behe doesn't say anything about Dawkins classic book that deals specifically with the arguments in this chapter, written in 1996, around the same time as Behe’s Darwin’s Black Box. I think that Dawkins scores a valid point in his review of The Edge of Evolution, when he says that unlike Behe's first book, Darwin's Black Box, in the

…second is the book of a man who has given up. Trapped along a false path of his own rather unintelligent design, Behe has left himself no escape. Poster boy of creationists everywhere, he has cut himself adrift from the world of real science.

In this chapter, Behe concludes that evolution is a 'tinkerer', not an engineer. Fair enough. But then he concludes that “If Darwinism is just a tinkerer, then it cannot be expected to produce coherent features where a number of separate parts act together for a clear purpose, involving more than several components.” (Page 119). But what about Dawkin's Mount Improbable? What about the classic example of the eye? There are many books on this, as well as scientific articles. I encourage the interested reader to go to Amazon.com for example, and have a look at some of the books published on the evolution of eyes in animals. One can find exactly what Behe is claiming can never happen, laid out in clear detail, slow, gradual, evolution of complex systems such as the eye. And in my opinion (as a molecular biologist), there's not much difference in the evolution of the eye than the evolution of a complex biochemical system. Certainly there is a difference in scale, but the same principles apply. But please don't just take my word for it. Again, go to PubMed, type in “evolution complex systems,” and see what is there.

Chapter 7 - The Two-Binding-Sites Rule

In this chapter, Behe further explores his claims of incredulity. Now, instead of looking at single mutations within single genes, Behe examines the likelihood of evolutionary mechanisms producing two different proteins with shapes that will fit each other—that is with “binding sites” which are complementary. What are the chances, he asks, of having TWO binding sites evolve at the same time? The probability is so tiny, as to essentially be impossible, he claims. Yet once again, there are problems here with the initial assumptions. I really hate to sound like a broken record, but once again, the interested reader is invited to have a look at the vast literature in this field. I went to PubMed, typed in “evolution protein binding sites,” and got back more than 5000 articles. The title of one recent article was “Using peptide loop insertion mutagenesis for the evolution of proteins,” and another is “Beauty is in the eye of the beholder: proteins can recognize binding sites of homologous proteins in more than one way.” This brings me to one of the (many) flaws in this argument in chapter 7—there is a lot of room for change in the binding site; it does not have to be a 100% perfect match. It only has to be the right shape, and this can be achieved through many many different amino acid sequences. So the probability is not nearly as dire as one might expect from naive and bad first approximations.

Towards the end of this chapter, Behe brings up the work of Richard Lenski, at Michigan State University. Behe claims that, despite having grown E. coli in the test-tube for more than 40,000 generations, “nothing fundamentally new has been produced.” I've known Rich Lenski for many years, and recently he was here as an opponent for a Ph.D. thesis exam. Rich gave a wonderful talk, demonstrating that early on in his experiments, there was a clear, measurable increase in fitness from the [random] mutations generated in his evolution experiments. For example, a set of mutations which altered DNA topology (three dimensional structure) occurred in many of the strains, thereby increasing fitness. (DNA topology is the expertise of both Behe and myself—it is a real shame that Behe no longer works in the lab with DNA structures and evolution!) In some of Lenski’s later experiments, after the cells had been growing for more than fifteen years (!), a strain arose with an increased mutation rate. Following that, the frequency of newly generated mutations and diversity went through the roof. Early on, for the first 20,000 generations (ten years growing in the laboratory), the number of fixed genetic changes was, on average, just a small handful (usually less than ten). After this “mutator” strain arose, however, the number of fixed mutations (new genetic varieties which came to be present in all cells) rose to more than 250, and the number of single changes altogether rose to more than a thousand.

For me, this in a nutshell is what we see from the genome sequences. Lab stains don’t have much diversity compared to what we see in the natural world. On the one hand, we know that outside of the lab, there is an incredible amount of diversity within an organism (like E. coli). On the other hand, when we sequence a genome of a strain that's been grown in the laboratory for awhile, there are often just a small number of changes (a few hundred) associated with property differences. In nature, it is a whole different story. We have a paper that just came out a few weeks ago, comparing the genomes of sixty-one naturally occurring isolates of E. coli. Although some of the E. coli genomes are quite similar, others are VERY different - having more than a MILLION “extra” bases (DNA letters) in one genome, not found in another. The fraction of shared proteins between two strains ranges from nearly all (99.7%) to less than half (48%). Most E. coli genomes contain around 5000 genes, but if we look for all the different genes in all the genomes analyzed so far, we find more than 15,000 different gene families (or more than 3 times the size of any one E. coli genome!). Less than a thousand genes are conserved across all the E. coli genomes sequenced so far. What does this mean? As an example, pick an E. coli genome, and sequence it. Out of those 5000 genes, less than 20% will be found in nearly all other E. coli genomes, and for every one gene in this genome, there are perhaps another nine or ten E. coli genes that are found in other E. coli genomes, but not present in that particular E. coli genome. In addition to the 15,000 gene families discovered so far, we estimate there are probably around 30,000 more E. coli gene families in the intestinal tract of just a single person. This represents a tremendous diversity of genetic information. Since these many E.coli strains can readily exchange genes and parts of genes, there is an absolutely enormous potential to build new varieties of proteins. Behe’s naïve (to be frank) calculations don’t even scratch the surface in calculating this potential to generate new proteins and new protein interactions. He was not aware of any of this.

Take a look at the above figure. Note that the common lab strain of E.coli has 960 families of genes and from that it can build 4144 proteins. But there are other genes, found in some E. coli genomes, missing in others. How many other gene families are available, in nature to add to its protein repertoire? We estimate around 44,000 gene families are out there, in some E. coli genomes, but missing in others, in addition to the 960 present in the above strain.

So my point is, when Behe claims that in the E. coli evolution experiments 'Nothing fundamentally new has been produced.' (page 142), he is ignoring parts of the story which are extremely important. Since most people will not be familiar with the literature, we consider this to be misleading. There is a vast literature which shows just what can be done! Obviously evolution can happen in E. coli, on large scales, and it can be seen to happen under our very eyes, in the laboratory, under the right circumstances. With regard to the Lenski experiments, in my opinion, it is not being honest to only look at the first half of Rich Lenski’s experiments, where he saw little change, and to conclude that evolution does not happen in E. coli. The mutator (which arose halfway through) changed things dramatically.

The Figure above is a comparison of 61 E. coli genomes (each of the concentric circles is one strain of E. coli), showing the conservation of genes; for more details see Figure 5 in Oksana’s Microbial Ecology paper mentioned previously. The point I want to show here is that there are many large gaps (lighter-colored– regions of genes that are missing in many genomes, but present in others. Some of these regions encode novel ‘molecular machines’ – or what I think many (but not Behe) might call ‘fundamentally new’ complexes.


David Ussery is an associate professor of comparative microbial genomics at the Center for Biological Sequence Analysis at the Technical University of Denmark and on the faculty at the University in Oslo, Norway. Ussery is the co-author of Computing for Comparative Microbial Genomics and has authored or co-authored 130 articles for science and professional journals. He is also a frequent public speaker on the topic of bacterial genomics.

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Rich - #40903

November 20th 2010

(concluding confirmation of John’s excellent point)

Creationist Nicholas Hotton III, Curator of Fossil Amphibians and Reptiles at the Smithsonian:

“... genes ... are subject to spontaneous changes, called mutations, that take place randomly at measurable rates ... “

*The Evidence of Evolution*, p. 22.


And note that this is just a tiny fraction of the internet hits and book references which prove beyond doubt that only creationists, not real evolutionary theorists, speak about “random mutations.”

John, you’ve outdone yourself.  You haven’t been this “right” since you said that no scientist anywhere had ever spoken of a 94% similarity between chimpanzee and human genomes.  That was another great moment where you established your authority here as an expert on evolutionary biology.  Good thing we have you around, to keep us informed.


John - #41030

November 21st 2010

Rich,

Remember that when pressed under oath, Behe’s definition of “looking high and low” for papers about the evolution of the immune system consisted of a PubMed search for “random mutation.”

I find it predictable that not a single one of the instances of use of the term “random mutation” comes from the primary literature, which you and Behe seem to avoid whenever possible.

When we do Behe’s lame search on PubMed, we get:

“random mutation” - 168 citations
“mutation” - 568,121
“evolution” - 277,951
“evolution” “mutation” - 26469

So my point stands. “Random mutation” is an oversimplification, because mutation is random in only one respect: fitness.


John - #41031

November 21st 2010

Rich, in how many of the quotes you mined did the real scientists make it clear that they were referring to randomness WITH RESPECT TO FITNESS?

Now, if we Google and include “intelligent design,” because ID promoters don’t bother to do any ID science that would show up in a PubMed search, we find that the term “random mutation” is used very differently:

“intelligent design” “random mutation” - 70,100 hits
“intelligent design” “mutation” - 1,150,000
“intelligent design” “evolution” - 1,790,000
“intelligent design” “evolution” “mutation” - 1,150,000

So, Rich, quantitative analysis indicates that ID promoters use the term 100-fold more often than real scientists do. Behe is a prime offender, as he ignores the polymorphism that already exists and has been measured.


John - #41035

November 21st 2010

I wrote:
”... random mutation, a creationist term.”

Rich went with the straw man fallacy:
“Of course.  That’s why it’s never found in writings by serious scientists,…”

Nope, I never said that, so your effort only suggests a desperate need to deceive others.

Don’t serious scientists routinely define the respect in which mutation is random in the cases you offered?

Aren’t serious writings by serious scientists found in the primary scientific literature, from which zero of your cases were taken?

Don’t you and your fellow IDCreationists fail to define the only respect in which mutation is random when you use the term?


James - #41051

November 21st 2010

John,

yes my comments are terse and poorly explained, which is more than Mr. Ussery’s article deserves.

Look, I haven’t read through your previous posts so I’m not sure of your angle, but if you haven’t read The Edge of Evolution I recommend you do so and engage the arguments, not the author.  There are things in TEOE that I disagree with or am skeptical about - but I do at least understand the arguments.  Ussery doesn’t.

Defend evolution if that’s your position, but don’t defend Ussery - his review is a disaster.


Rich - #41071

November 21st 2010

Re: 41035

It’s odd, you know.  If someone said “baraminology, a creationist term,” any educated English speaker would understand that to mean that creationists coined the term, or that creationists are the only people who use it, or that hardly anyone other than creationists ever uses it.

Similarly, when someone says, “random mutation, a creationist term,” an educated English speaker would understand that to mean that creationists invented the term “random mutation,” or that creationists are the only people who use “random mutation,” or that hardly anyone other than creationists speaks about “random mutation.”  Yet, lo and behold, we find that mutations are referred to as “random” thousands upon thousands of times, in both published technical literature and in general books and articles on evolution written by scientists.  So one would think that someone who made such a claim would retract it.  But when one is motivated by testosterone rather than by a love of truth, one does not retract.  One instead presents lawyer-like arguments, claiming that the the original statement meant something other than what it plainly said.  Very sad that a (purported) Ph.D. in biology is incapable of simply retracting an error.


James - #41079

November 21st 2010

Briefly, I’ll make the following ellaboration on my initial comment…

Regarding the relevant ‘literature in the field’ on the time for two mutations, Ussery might want to add the names Koonin, Durrett & Schmidt into his PubMed search - he’s in for a nasty suprise, especially if he then views Durrett & Schmidt’s ammendments to the paper “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution” (Durrett, R & Schmidt, D. 2008. Genetics 180: 1501-1509), which reluctantly confirms TEOE (See part 1 - 5 of Behe’s comment on this paper, starting at http://behe.uncommondescent.com/2009/03/waiting-longer-for-two-mutations-part-1/)

As for Lenski’s work, I’m too lazy to summarise but see http://behe.uncommondescent.com/2009/10/new-work-by-richard-lenski/ .  All of Lenski’s work confirms Behe’s calculations (see “Simulating evolution by gene duplication of protein features that require multiple amino acid residues”, Behe & Snoke 2009, well summarised at http://www.evolutionnews.org/2009/10/richard_dawkins_the_greatest_s026651.html).

Lastly, John, don’t re-copy my typing errors with [sic] next to them - I don’t like it.


James - #41080

November 21st 2010

If empirical data were to emerge which falsifies Behe’s ‘edge’ of evolution - the requirements are simple - then trust me, you won’t here about it because some bright spark at BioLogos has been dredging the PubMed archives.  It would be trumpeted from the roof of the Smithsonian, accompanied by a triple book release and commemorative t-shirt from Richard Dawkins.

As things stand, the rare appearances of chloroquine resistence in malaria populations over the last 50 years retrodictively confirms Behe’s work.  At the moment any dissent does not have an empirical basis.  End of. (http://www.evolutionnews.org/2007/11/rebuttal_to_paul_gross_review004428.html)


John - #41084

November 22nd 2010

James wrote:
“Look, I haven’t read through your previous posts so I’m not sure of your angle, but if you haven’t read The Edge of Evolution I recommend you do so and engage the arguments, not the author. “

I have read it. I’ve also read the primary literature, which Behe doesn’t do and I predict that you will be afraid to do.

“There are things in TEOE that I disagree with or am skeptical about - but I do at least understand the arguments.  Ussery doesn’t.”

He does, as do I. Let me illustrate with Behe’s greatest deception here:

“Toward the end of the article they criticize my observation of the rarity of two amino acid substitutions…from the viewpoint of their model. Citing malaria literature sources (WHITE 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20.”

So, James, please answer a simple question for me:

Does that probability have anything to do with the frequency of the occurrence of those mutations?

If so, when was the frequency of those mutant alleles measured in a population that later became chloroquine resistant?


John - #41085

November 22nd 2010

James, Behe continues, either cluelessly or dishonestly:
“I then wrote that “for humans to achieve a mutation like this by chance,…”

What does “achieve a mutation” mean in this context?


James - #41338

November 24th 2010

Hi John…

my answers to your three questions:

1 - The point mutation rate would be a key factor in modeling the probability of chloroquine resistence arrising in Plasmodium falciparum.  However the figure of 1 in 10^20 is not based on point mutation rates.  It is derived from data on malaria population size and appearances of chloroquine resistance.

2-  as far as I know, never

3 - I imagine he is referring to a beneficial mutation that requires two specific amino acid substitutions, where one of these substitutions by itself would either be invisible to natural selection, or be deleted by natural selection.

So what is the great deception?


John - #41414

November 24th 2010

James, my responses:

1) Why? We already know the point mutation rate. What’s the relative fitness of the two substitutions in the parts of the life cycle in which no chloroquine is present? Wouldn’t that be far more important for modeling, something Behe couldn’t be bothered to do?

2) So why is Behe talking about substitutions and mutations instead of fixation of alleles?

3) Does Behe have any data to suggest that either of the substitutions by themselves would have a lower fitness? Why would it be a problem if one was “invisible” to natural selection?

Behe’s great deception here is that he is falsely portraying the fixation of an allele in a population as a mutation frequency. The deceptive title “Waiting Longer for Two Mutations” is an explicit case of that. Behe’s quote mine was about waiting for an allele to become fixed in a population, not waiting for mutations to happen. Note that in the beginning of the book, Behe makes it very clear that he doesn’t dispute natural selection.


James - #41870

November 29th 2010

The thing is, to the extent that your point has any relevance, it lacks substance.  Behe has set an epic problem for Darwinnian evolution - it requires a proportionate solution,, and picking at the details doesn’t cut it.

By the way, in his book and letter responses Behe does provide some data in answer to points 1 & 3 which you raise, and where he lacks data he explains the basis for his assumptions.  The onus is on his challengers to demonstrate why his assumptions are unreasonable, rather than simply to point out that they are assumptions.

A mutation invisible to natural selection does not spread quickly through the population, and may even be ‘un-done’.  This greatly limits the population in which the second required mutation would confer a benefit


John - #41963

November 29th 2010

James wrote:
“Behe has set an epic problem for Darwinnian evolution - it requires a proportionate solution,, and picking at the details doesn’t cut it.”

So you say, but the data say the opposite.

“By the way, in his book and letter responses Behe does provide some data in answer to points 1 & 3 which you raise, …”

James, he does nothing of the sort. If you believe he does, point to the data instead of making empty assertions. Behe is simply deceiving his audience.

“...and where he lacks data he explains the basis for his assumptions. “

Then point me to Behe’s explanation of the relative fitness of the two substitutions in the parts of the life cycle in which no chloroquine is present.

You won’t, because it doesn’t exist.


John - #41964

November 29th 2010

James:
“The onus is on his challengers to demonstrate why his assumptions are unreasonable, rather than simply to point out that they are assumptions.”

What a cowardly thing to say! Behe is the challenger. Either way, it’s Behe’s responsibility to perform empirical tests of his own hypothesis, but we both know that he will never do so because he has no faith in it.

“A mutation invisible to natural selection does not spread quickly through the population,…”

Yes, it does quite often. Two examples: drift and linkage to an allele that confers higher fitness.

Neither you nor Behe has done anything to demonstrate that a mutation has to occur de novo, so calling it a “mutation” instead of an allele constitutes circular reasoning.

“... and may even be ‘un-done’.  This greatly limits the population in which the second required mutation would confer a benefit”

Hilarious! Neither you nor Behe has shown that any mutations are required, you claim that Behe addressed this, yet immediately afterward, you revert to claiming that the resistant alleles aren’t already present in the population.


Rich - #41995

November 29th 2010

James:

Pleased to have you aboard.  Your comments are pertinent and useful.

I predicted that when you dared to say something even fair or moderate about Behe (never mind supporting Behe), sooner or later, John’s replies would turn to the personal, as his replies to ID supporters generally do.  And sure enough, up in 41964, in answer to your polite point, “John” responds to you:  “What a cowardly thing to say!”  And then of course he goes on to imply intellectual dishonesty in Behe, by saying that Behe has no faith in his own hypothesis.

I’ve found the best thing to do with people who resort to insults and/or accusations of low motives is not to engage them at all, until they have learned civilized manners.


John - #42006

November 29th 2010

Rich wrote:
“And sure enough, up in 41964, in answer to your polite point, “John” responds to you:  “What a cowardly thing to say!””

In what way is it polite to claim that Behe can make all sorts of claims without support, while the onus is on real, working scientists to demonstrate why they are unreasonable? James himself demonstrated this when he admitted that neither he nor Behe knows whether the mutations Behe claims are being waited for are already there.

“And then of course he goes on to imply intellectual dishonesty in Behe, by saying that Behe has no faith in his own hypothesis.”

Behe’s actions show zero faith in his own hypothesis, as do his words. Are you claiming that a PubMed search for “random mutation” constitutes searching “high and low” for science’s answers on evolution of the immune system?


John - #42013

November 30th 2010

Oh, and Rich,

How many times have you commented on Dave Ussery’s six posts here at Biologos, and in how many of those did you engage Dave or any of the evidence he has presented?


Trevor K. - #42272

December 2nd 2010

The edge to evolution [molecules-to-man] is where it meets a straight forward reading of the bible in Genesis 1. Then it falls to pieces.
Read here:http://creation.com/lennox-design-and-suffering


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