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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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David Ussery - #38973

November 8th 2010

Hi Mike,

Thanks for the link to your page on synthetic biology.  I liked what you had to say there.

You clearly have a good understanding of biochemistry / molecular biology.

So what I am curious about is if you do this as a hobby?  In my case, I love to read about the history of science but this is kind of a hobby for me - it is not what I am getting paid to do.

My comment about terraforming was a question about applying some of these design principles.

Do you think that I’D can be useful for science?  If so, what has hindered I’D so far?

So I think your comments about ID are great - but is this just a aide hobby for you or do you plan on making some creative, useful predictionsto be tested??

Or maybe I have missed it (which is entirely possible as I have not been following the field)

David Ussery - #38974

November 8th 2010

I meant ‘side hobby’

Am typing this on my phone whilst on a train…

beaglelady - #38984

November 8th 2010

Evolutionists are actually doing the research for ID theorists when do these long term evolution experiments. ID theorists couldn’t ask for more.

If that is true then why do they complain about lack of funding for their own research?

Roger A. Sawtelle - #38989

November 8th 2010

Dave Ussery #38776

Thank you so much for this reference to the study of how e. coli evolve.


The title clearly states the findings of the study. 

“RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media”

The study found that when e. coli were placed in environments, where they were not expected to thrive (minimal media,) genetic mutations developed that allowed some of these e. coli to adapt to these new environments.  These mutants reprogramed the organisms to make better use of the resources available for optimal growth.

This study indicates that evolutionary change is triggered primarily by ecological change, not by genetic change.  Genetic mutation appears as a response to a change in the environment or medium.  This is contrary to neoDarwinistic understanding of evolution.  The study shows that natural selection is best seen as ecological and “fitness” is ecological adaption.

Roger A. Sawtelle - #38990

November 8th 2010

Part 2

Darwin saw that evolution was based on two factors, variation and natural selection.  NeoDarwinism has the variation aspect about right, but natural selection is not right.  The ecological view is much better.

Lest you think that I am off topic, IMO Behe observes that genetic change alone cannot explain evolution, and so there must be another factor in this process.  I agree with this as far as it goes.  The difference is that ecological natural selection is the other factor for me, such as this study supports.

As for the cosmological and theological aspects of the issue, evolution is the interplay of the physical environment and the genetic structures of life.  Both are rationally structured and both are created by God.  It is not by chance that the biosphere flourishes with life, beauty, purpose, and harmony.

Ashe - #39008

November 8th 2010


And in fact, when I examine all the genomes available, I find just this - not a single protein (including cytochrome oxidases) are conserved across all phyla

Actually cytochrome c oxidase is encoded within the mitochondrial genome. It is found all throughout mitochondrion bearing taxa…from mammals to protozoans,therefore it’s probably rather ancient.

pds - #39027

November 8th 2010

Dave #38891

I did see that study and already commented on it briefly.  From the Abstract and the other paragraph you quoted, it does not appear to discuss the building of the cilium in a Darwinian step by step fashion with an explanation of how each step provided a survival advantage.  It seems to be focused on phylogenetic trees (which could support common descent), but not a purely Darwinian historical narrative of random mutations and natural selection.

John - #39033

November 8th 2010


Why on earth would anyone present the explanation in exactly the way that Behe petulantly specifies and you parrot?

Why would it fit in a single manuscript?

Do you think the silly game you’re playing isn’t obvious?

Dave Ussery - #39054

November 8th 2010


I should have made myself more clear.  When I say “phyla”, I am referring to bacterial phyla.

Yes, I’m sure it’s found in most eukaryotes - but the mitochondria is from an alphaproteobacteria - my point is that aerobic organisms were quite rare before about 2 billion years ago, and likely did not exist at all 3 billion years ago, and it seems difficult to imagine how they could have been around when the early cyanobacterial communities first started building up, more than 4 billion years ago.  So ‘ancient’ by animal terms is only a ‘mere’ 0.45 billion years ago, compared to 4.5 billion years for bacteria.  My point is that these proteins are not conserved across bacterial phyla - in particular in anaerobes, which is what would be expected, based on what we know of the conditions then (very little oxygen to breathe!).

Dave Ussery - #39055

November 8th 2010

Roger A. Sawtelle - I agree absolutely with you, the ecological view is much better - in my opinion it is all about communities!  And I think this goes both for theology as well - rather than emphasizing individuals, for me our purpose is being integrated and helping and serving the community.  From my perspective, Christianity is teaching that it is not about ‘me’, but about helping others - and this is indeed what I think we see in biology as well!

Have you seen Tammi’s paper on Vibrio genomes?

It’s open access, so if you follow the link, you can download the whole article.

Ashe - #39056

November 8th 2010

I should have made myself more clear.  When I say “phyla”, I am referring to bacterial phyla.

Oops, sorry about that. Unless I’m mistaken, there is a super-family of about 8 related families of haem-copper oxidoreductases, 5 of which are found exclusively in Archaea. I would take this to mean that there was an ancestral haem-copper oxidoreductase in LUCA, which subsequently diverged independently in archaea and bacteria (giving cytochrome oxidase as we know it in the bacteria only).

Dave Ussery - #39061

November 8th 2010

HI Ashe,

maybe you missed this conversation with Mike Gene - just because these genes are in some Archaea TODAY does not mean that they’ve been around since the LUCA - in particular, since they are not in all archaea, and they could have been horizontally transferred - scroll up a bit for the previous conversation…

It’s a wonderful idea, that bacteria could use oxygen to ‘breathe’ 4 billion years ago - but also a bit of an extraordinary claim - hence strong proof is necessary - and I just don’t see it, based on looking at modern day genomes only.

Ashe - #39062

November 8th 2010

Hi Dave,

Not sure what that conversation has to do with what I wrote. heme-copper oxidoreductases are found in both archaea and bacteria, and some members are in fact, found in all archaea and all bacteria.

Ashe - #39063

November 8th 2010

I should say, nearly all bacteria.

Ashe - #39064

November 8th 2010

Oh sorry David, I see which convervation you mean now.

Ashe - #39096

November 9th 2010

Hi David,

I just read through your previous conversation here. However, aren’t all archaea, don’t they all and share an A-type ATP synthase? They must therefore have had an ancestral mechanism for coupling electron flow to proton pumping, and that would seem to be an ancestral version of a haem-copper oxidoreductase. These are widespread if not universal, and conceptually something of the sort had to be present in the ancestor for chemiosmosis to work at all. I agree with you that horizontal gene transfer was probably responsible for the bacterial-type cytochrome oxidase, which is indeed found in only a few Archaea,  But the more general ability to couple electron flow to proton pumping and ATP synthesis (chemiosmotic coupling) is universal and ancestral to both Eubacteria and Archaea.

Ashe - #39097

November 9th 2010

Sorry “don’t they all and share” should read “aren’t they all chemiosmotic”

Dave Ussery - #39108

November 9th 2010

Hi Ashe,

Yes, I think they are.  You make a good point! 

To be honest, now that I think about this some more, OF COURSE proton pumping would be important to generate a gradient across the membrane, for energy.  I mean, in a sense, this is kind of setting up what life is all about, right?  That’s how a lot of toxins work, is by poking holes in membranes, destroying that gradient, hence the cell can no longer has any energy to tap, and essentially becomes like any other material - with no difference between inside and out.

But I thought this type of system in the mitochondria evolved more recently [a ‘mere’ billion years ago or so - long time after Archaea and Bacteria split]. I thought for example the early cyanobacteria photosynthesis was quite inefficient, and slowly became slightly better (still not that great, from an efficiency point of view!).  This article in Science magazine about the mitochondria giving the cell all that extra energy from a better way of doing things, seems to me to indicate the previous cells could NOT do this.

But this seems something you are both passionate and knowledgable about - so can you think of any way to probe this idea, to see if what you are proposing can be tested?

Dave Ussery - #39116

November 9th 2010

johan - #38966

The Lenski experiment with E.coli or the long-term evolution experiment with Drosophila turned out to be very supportive of ID expectations, despite the fact that these were done within an evolutionary framework. In fact, it makes for a stronger case for ID when the evidence for ID comes from evolutionary experiments done by evolutionists themselves.

ummm, I’m not sure I understand this - where did really ID predict Lenski’s results?  HOW are they consistent with ID?  Now, if you were talking about Isaac Asimov, I think he hinted at the mutator strain in his famous Foundation Series - ‘the mule’.  It’s a great piece of fiction, written by a great biochemist.  He had a lot of insight here.  But I don’t see anything like this coming from the ID community.  But then again, since I don’t really read all of their popular science writings - it’s entirely possible the ID people HAVE predicted something like this, and they have just never bothered to publish it in the scientific literature.

So, johan, please enlighten me here! where have the ID people predicted the type of evolution the Lenski sees, and how did the non-ID scientists miss it?

pds - #39125

November 9th 2010


Based on your lack of response, I will assume that you agree that your study does not, in fact, discuss the building of the cilium in a Darwinian step by step fashion with an explanation of how each step provided a survival advantage.

Lots of great minds have tried to envision a Darwinian pathway and have been unable.

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