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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 BioLogos. 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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John - #39299

November 10th 2010

pds wrote:
“It does seem that the article has some discussion of Darwinian pathways.  Thank you.  So at least you are now on the same dialogue page with what Behe is talking about. “

And pds will never engage Dave Ussery on the content of Ussery’s post on which pds is commenting.

“...I am not the best person to evaluate how many steps are discussed and whether the survival advantages are plausible at each stage.”

Yet this is what you were demanding. Now that it has been produced, you run away.

“I would like to see Pez and Sal or others respond to your article. “

Won’t happen.

“Looks like DBB is already addressing the content.”

DBB is falsely claiming, “Not once in the entire article was any mathematical or probability analysis attempted.” That’s your idea of addressing content? Denying the content’s existence?

“BTW, I did read everything you posted here about your article.  You are really in no position to condescend about reading abilities.”

I’d say that he is, since you are now agreeing that you are unable to understand the very article you demanded.

John - #39306

November 10th 2010

pds wrote:
“As I said before, I don’t read your comments.  Too many personal insults and bad logic.”

How would you know if you hadn’t read them?

“Biologos, How many personal insults from John will you allow?”

I’m pointing out that you and Rich are afraid to engage Dave Ussery on the subject of his post—you’re adding comments to it.

If you want to demonstrate that I’m using insults and bad logic, simply engage Dave on the evidence and the articles he’s graciously produced.

John - #39314

November 10th 2010

Rich wrote:
“It sounds as if this article (for which I did read the abstract, by the way) provides more than the usual number of detailed steps. I praise the authors for attempting to do this.  However, do we have any time constraints within which all these mutations are supposed to have happened?  For example…”

For example, you can address your questions by reading the papers.

pds wrote:
“I don’t have access to the entire article. “

Problem solved!

1) Get yourselves a disposable address at mailinator.com.
2) Send an anonymous email to me at .(JavaScript must be enabled to view this email address).
3) Notify everyone here that you have done so.
4) I will reply with links to both papers.
5) Then you can either engage Dave Ussery on the subject of the post on which you are commenting or continue to make irrational excuses for your failure to read the papers that you claimed to be seeking.

Is this contributing something useful to the discussion, troy?

Ashe - #39320

November 10th 2010

How rather gracious of you of John.

Arthur Hunt - #39321

November 10th 2010

David, Ashe, (others),

Rumor has it that there will be a Q&A for the NASA conference on The Panda’s Thumb.  You should check into the latter site every so often after the meeting ends (around 5PM Eastern Time today).

Ashe - #39328

November 10th 2010


Arthur Hunt - #39329

November 10th 2010

Loren Williams, at least, said he will stop by Panda’s Thumb.

troy - #39337

November 10th 2010


“Is this contributing something useful to the discussion, troy?”

Yes, thank you. Since I have access to most scientific journals, I’ll add that an email to troyuller at gmail dot com with a request for a specific paper will land you that paper in your inbox no questions asked.

troy - #39338

November 10th 2010

Oh, and that offer goes for anyone, and troy uller isn’t my real name so don’t bother googling,,,

pds - #39372

November 11th 2010


You are forgetting the context.  You said,

“Yet this is what you were demanding.”

I didn’t demand anything.  I pointed out how Dave was misrepresenting (and then ridiculing) Behe, by not stating accurately what Behe said was lacking.

If you want to be constructive, post a comment at Telic Thoughts with your article and what you think it shows.  My guess is that someone there would be happy to comment.  Unless you are a “afraid” to, of course.

John - #39388

November 11th 2010

pds read my comment, which he/she claimed not to, and wrote:
“I didn’t demand anything. I pointed out how Dave was misrepresenting (and then ridiculing) Behe, by not stating accurately what Behe said was lacking.”

Ah, but you did much more than that:

“If you quote Behe accurately, everyone could see that he is looking for “a Darwinian explanation for the step-by-step origin of the cilium.”  p. 95.  Surely you can summarize a study that does this? Perhaps just the first three to five steps of the step by step sequence, and the survival advantage of each?”

So you directly asked for it, Dave directly produced it, and you’ll use any excuse to avoid addressing real evidence without a pseudoauthority filtering it for you. You have no faith that the evidence will support what you wish to be true.

“If you want to be constructive, post a comment at Telic Thoughts with your article and what you think it shows. “

Are you kidding? When did this become *my* article? What’s preventing you from being constructive and discussing it right here, in the comment thread to Dave’s post?

pds - #39390

November 11th 2010


From the article:

“The proteins of the IFTD systme are related to the transport of vesicles from the Golgi.  This fact inspired Jekely and Arendt [Jekley and Arendt, 2006] to conjecture that the cilium began from a system that transported coated vesicles to the membrane.”

Conjecture that it started from a “system”?  That does not sound like a description of the step by step pathway from the very beginning with the survival advantage of each.

You said,

“Are you kidding?”

So you are afraid to post it at Telic Thoughts?  OK.

John - #39395

November 11th 2010

pds wrote:
“That does not sound like a description of the step by step pathway…”

Quote-mining is no way to say anything about the whole paper, but it’s all you can do. Maybe you can explain to DBB that bootstrapping represents statistical analysis.

“...from the very beginning with the survival advantage of each.”

The survival advantage at the beginning would be that their ancestors functioned in Golgi-mediated transport, which is very important to survival but in no way appears to be intelligently designed. This plumbing system of the individual cell would be like transporting both water and sewage in lipid balloons, having them often collide and fuse, mixing the sewage with the fresh water, and calling it good.

“So you are afraid to post it at Telic Thoughts?”

No. When did I say that? When has the content of a manuscipt ever been discussed there? Why do most of TT’s denizens appear to be unable to distinguish between a manuscript and a press release about the manuscript?

John - #39396

November 11th 2010

“Conjecture that it started from a “system”?”

Yes. Massive evidence for co-option of entire systems is very common. Perhaps you should read some of the relevant secondary literature, and then some of the relevant primary literature, before pretending that Behe makes any sense?

James - #40421

November 17th 2010

Terrible review.

If I were going to review a book in print, I’d read it all first before embarking on the chapter-by-chapter discussion.  I assume failing to do that is why you’ve made an ass of yourself regarding the ‘two-binding-sites rule’.

And what on earth was that ‘PubMed’ part supposed to demonstrate??  Weird.

Behe is correct regarding Lenski’s work - changes to e-coli populations in the face of heavy selective pressure (fitness, enzyme pruduction) have resulted from a loss of genomic function, not from new genomic material - therefore ‘nothing fundamentally new’.

Rich - #40432

November 17th 2010

For those interested, Michael Behe has announced that he is planning to write a response to the pieces so far published here by Dr. Ussery.  See:


John - #40796

November 19th 2010

James wrote:
“If I were going to review a book in print, I’d read it all first before embarking on the chapter-by-chapter discussion.”

You just broke my irony meter. The point of David Ussery’s essays here is to point out that Behe is ignoring the primary scientific literature in the subjects that he claims to understand better than those actually working in those subjects.

“I assume failing to do that is why you’ve made an ass of yourself regarding the ‘two-binding-sites rule’.”

Why don’t you explain your assertion, James?

“And what on earth was that ‘PubMed’ part supposed to demonstrate??  Weird.”

You might want to read Behe’s disastrous testimony in the Dover trial, when he walked back his phony claim from his first book by claiming that “looking high and looking low” really meant that he did a PubMed search for “random mutation,” a creationist term.

John - #40797

November 19th 2010

“Behe is correct regarding Lenski’s work - “

How would you know? If I were going to review a scientist’s work in print, I’d read it all first before embarking on such a global claim.

“...changes to e-coli populations in the face of heavy selective pressure (fitness, enzyme pruduction)…”

I can’t figure out what you mean. Are you claiming that fitness and enzyme pruduction [sic] are selective pressures or changes?

“... have resulted from a loss of genomic function, not from new genomic material - therefore ‘nothing fundamentally new’.”

What genomic functions were lost, specifically?

Rich - #40901

November 20th 2010

John wrote:

“... random mutation, a creationist term.”

Of course.  That’s why it’s never found in writings by serious scientists, but only in the works of creationists, such as the following:

Creationist Larry Moran:

“... mutation is, to all intents and purposes, random.  This is what Jacques Monod means when he refers to evolution as a combination of chance and necessity. The “chance” is the randomness of mutation and mutations supply the raw material for evolution…. As you can see, Jacques Monod is a strong supporter of evolution by accident…. He ... comes down on the side of “pure chance, absolutely free but blind.” He’s not the only one who takes this position; the mutationists also favor a prime role for random mutation.”


Creationist Richard Dawkins:

“The Oxford evolutionary biologist Richard Dawkins succinctly defined evolution as “random mutation plus non-random cumulative selection.” [reference: The Selfish Gene]


Creationist Carl Sagan:

” ... the majority of mutations are random ... ” 

*Intelligent Life in the Universe*, p. 99.


Rich - #40902

November 20th 2010

(continuing the confirmation of John’s excellent point)

Creationist R. Nieuwenhuys, in *The Central Nervous System of Vertebrates*, Vol. I, p. 307:

“According to the current neo-Darwinian theory, an intricate web of the following factors is considered to be involved in the process of speciation and in evolution in general ... (c) the continuous production of new variations through random mutation ...”


Creationists Lenski and Mittler (in that Creationist rag, “Science”):

“According to neo-Darwinian theory, random mutation produces genetic differences among organisms ...”


Creationist George Gaylord Simpson:

“... it suffices to point out that rates of random mutation in a moderate or large population do not set any minimum effective rate of evolution, although they do theoretically set a maximum.”

*Tempo and Mode in Evolution*, p. 47



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