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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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Ashe - #39132

November 9th 2010

Is it passion or boredom , not really sure lol

Dave Ussery - #39136

November 9th 2010

pds - #39125


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.

good grief - once again we are completely not understanding each other!  i apologise.  From MY PERSPECTIVE, I thought you’d pretty much given up, offering a weak disclaimer - but I don’t LIKE that article you say.  Fine.  I didn’t ask whether you liked it or not.  This article clearly offers a step-by-step mechanism of how another completely different part of the cell (microtubules) can be converted into a cilium, via 8 gene duplications.  But this isn’t the ONLY article that’s been published on this… How about this one?

“How did the cilium evolve”

p.s., I’d LOVE to hear from others on this - I’m curious whether everyone on this list agrees with PDS that these articles are not talking about cilium evolution.  Default is “everyone agrees” - Behe’s right, I’m wrong.  Who agrees with this???

Roger A. Sawtelle - #39142

November 9th 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?

Response: Thank you for directing me to another helpful article, particularly this statement (with typo?)

“Our findings further indicated that possibly a relatively small set of genes could confer niche specialisation allowing V. cholerae to be adopted (sic) to a unique environment, so that over time V. cholerae have become a distinct species.”

Congratulations on being a contributor to the paper.

Roger A. Sawtelle - #39144

November 9th 2010

Part 2

The point that I have been trying to make on these pages and have made in my book, DARWIN’S MYTH, is that science, philosophy, and theology are all interconnected.  Dawkins clearly makes this point by building his a-theology on flawed neoDarwinist science and realtivitist post modern philosophy. 

The problem with BioLogos is that it is committed to the effort to bring neoDarwinism with conservative theology, while ignoring the breakdown of traditional philosophy and without taking the necessary hard look at both evolutionary science and traditional theology.  The question has been as to whether conservative theology is the procrustean bed on which science is made to fit, or vice versa.  The answer is that there is no procrustean bed, but science and theology need to reconciled, not jimmied into place.

Community is central as you say, while many extreme fundamentalists on both sides overemphasize individualism.  The problem isn’t Behe, it is restoring community by reconciliation and rejecting bad theology and bad science which oppose community, such as Malthusism

pds - #39148

November 9th 2010


I am making a distinction that you just can’t seem to grasp.  Behe makes the same distinction.

Please read this:  that article is definitely on the topic of cilium evolution.

You said,

“I’m curious whether everyone on this list agrees with PDS that these articles are not talking about cilium evolution”

How can you say that when I clearly stated that it “seems to be focused on phylogenetic trees (which could support common descent).”

Did you read that?

I will make this really simple:

An article can be on the topic of “cilium evolution” without discussing the building of the cilium in a Darwinian step by step fashion with an explanation of how each step provided a survival advantage.

Two kinds of articles:

1. an article on cilium evolution.

2. an article discussing the building of the cilium in a Darwinian step by step fashion with an explanation of how each step provided a survival advantage.

Two different things.

unapologetic catholic - #39162

November 9th 2010

“I’m curious whether everyone on this list agrees with PDS that these articles are not talking about cilium evolution. “

No, of course not, PDS is well known to talking in a vaporous manner and avoiding direct questions.

His considered strategy is to avoid at all costs from makign any affirmative claim and he always respond with some version of “That’s not excatly what I said” and you don’t seem to understand what [I, Behe or ID] actually said on this subject.”

If you observe this fact, you are accused f beign uncivil.

It’s pretty straightforward strategy of obsfucation.

Pay him no attention.

The evolution of the cillium and the various forms of the flagellum has been pretty well explained for those actually interested in science.

Unfortunately, those of us who appreciate your writing don’t post “cheerleading” comments such as “You’re right! way to go!”  Naturally, you’ll get three kinds of comments-those who genuinely don’t understand but are willing to learn, those who disagree on religious grounds and no amount of science will change their positions and those who obsfucate.

Ignore the obsfucators.

Ashe - #39165

November 9th 2010

PDS, don’t you think #2 is a bit unreasonable? We don’t know every single thing that happened when the dinosaurs went extinct but we can put together a group of clues and get a decent picture of what likely happened.

hmm - #39170

November 9th 2010

pds wrote:

“Two kinds of articles:
1. an article on cilium evolution.
2. an article discussing the building of the cilium in a Darwinian step by step fashion with an explanation of how each step provided a survival advantage.
Two different things.”

Yes. They are different things. Article #2 is also an article about #1. But an article #1. is not necessarily an article about #2. But as Ashe said, it would be very difficult to study the subject #2.

I just read an article titled “Directed enzyme evolution: climbing fitness peaks one amino acid at a time”. ( http://www.che.caltech.edu/groups/fha/cara.pdf ). Study about directed evolution is also study about evolution. It is one field, where researchers are studying some kind of designed evolution.

Rich - #39171

November 9th 2010

Dr.  Ussery:

What pds is asking for is not some vague assertion such as “8 genome duplications would do it,” but an account of *how* “8 genome duplications” would do it.  Precisely *which* sections of the genome were duplicated?  Did they occur all at once, or spread over millions of generations?  If they occurred all at once, you’ve got a “hopeful monster,” essentially a miracle, which Darwin and all the neo-Darwinists uniformly condemned, insisting firmly on gradualism.  And if spread out, how were the intermediate stages (where all of the duplications had not yet occurred) beneficial rather than useless or harmful to the organism?  And since (to the best of my knowledge) no one asserts that genome duplication in itself creates new traits, but rather, the duplicate part must itself undergo further change, what further changes do the duplicate parts undergo?  What pds is complaining about is the maddening lack of detail in typical genetic explanations.  ID is regularly bashed here for lacking detail; but “lacking detail” describes neo-Darwinism very well, from the 1930s to the present.  I have a much more detailed picture of the evolution of stars than of cilia or whales or bats.

Dave Ussery - #39174

November 9th 2010

Hi Rich (and PDS)

have a look at the abstract for the article I mentioned above - read the last sentence in the summary / abstract.  I realise that I am assuming you guys know how to read…  please take a look at this article.  From my perspective, this article does indeed exist.  Thus the argument ‘no articles exist’ would not allow this, if that argument were true…

The cilium is a characteristic organelle of eukaryotes constructed from over 600 proteins. Bacterial flagella are entirely different. 9 + 2 motile cilia evolved before the divergence of the last eukaryotic common ancestor (LECA). This chapter explores, compares, and contrasts two potential pathways of evolution: (1) via invasion of a centriolar-like virus and (2) via autogenous formation from a pre-existing microtubule-organizing center (MTOC). In either case, the intraflagellar transport (IFT) machinery that is nearly universally required for the assembly and maintenance of cilia derived from the evolving intracellular vesicular transport system. The sensory function of cilia evolved first and the ciliary axoneme evolved gradually with ciliary motility, an important selection mechanism, as one of the driving forces.

pds - #39176

November 9th 2010


Rich is right. 

Also, I am not asking for the actual pathway, but simply a plausible pathway.  I am not asking for a huge amount of detail, just enough to show that it is plausible, by showing the survival advantage of each step.  If it really happened that way, surely someone can imagine a plausible pathway.  Once someone does, then we can weigh the probability.  The fact that no one even tries is quite telling.

My main point above is to correct Dave’s misreading of Behe and me.

Rich - #39177

November 9th 2010

Ashe (39165):

No, pds is not being unreasonable.  He’s asking for the kind of detailed explanation in evolutionary theory that’s expected in every other successful science (physics, chemistry, engineering, etc.). 

If evolutionary biologists can’t provide the details that are being asked for, then they should lower the level of certainty of their claims.  They should say:  “We believe that the cilium could have evolved via a series of random mutations, each conferring selective advantage upon the creature so that all intermediate stages were viable, but we cannot yet specify what those steps might have been, except in the most general terms.”

What critics of Darwinian theory are looking for, and have been looking for since 1859, is a detailed account, not of how a finch beak gets 5% longer, but how lungs, heart, flagella, new body plans, etc. are built up out of *entirely blind* genetic changes which have *no plan* and are *uncoordinated* with each other, and thus cannot “think ahead” to produce “safety islands” of intermediate stages with selective advantage.  Comparative genomics cannot by itself answer this question.  Hypothetical steps must be proposed; otherwise, the theory is not testable.

hmm - #39178

November 9th 2010

Dave Ussery wrote:

“Thus the argument ‘no articles exist’ would not allow this, if that argument were true…”
“Behe says no articles exist”

Has Behe really said that “no articles exist” about cilium evolution? If so, where?

Dave Ussery - #39179

November 9th 2010

and MY main point is to actually read the articles!!!!

Did either Rich or PDS actually bother to even read either of these two articles, which they so quickly dismissed as not giving any sort of plausible mechanism?

I see the gene duplications listed, first this one, then the next then this then that… etc.  in details, just like PDS is asking for.  So this is what I mean when I say not LIKING the article is not the same thing as denying its existence…

once again, they are relying on the ignorance of the readers - they can just say “oh, these articles never really said this…”, and someone who hasn’t read them themselves might agree.

But please don’t take my word for it!  Have a look yourselves… can someone else on the list who can read actually look at the articles and tell me their opinion??

Rich - #39181

November 9th 2010

Dr. Ussery:

Does the article in question provide a *narrated* hypothetical evolutionary pathway of this sort:

1.  Genetic change A, corresponding morphological/physiological change A’, selection advantage A’‘.

2.  Genetic change B, corresponding morphological/physiological change B’, selection advantage B’‘.

3.  Genetic change C, corresponding morphological/physiological change C’, selection advantage C’‘’.


4.  Genetic change Z, corresponding morphological/physiological change Z’, producing our modern creature.

I would count such an explanation as a properly set forth hypothetical evolutionary pathway, and as in principle testable.  But I have never seen a book or article in the biological literature that does this.  Is this article an exception?

Ashe - #39183

November 9th 2010

The paper suggests cilial sensory functions was the survival advantage at each step at first, then ciliary motion became the survival advantage at each step as the axoneme evolved.

Rich - #39185

November 9th 2010

Dr. Ussery:

I have not dismissed the articles you mentioned.  I have made no comment whatsoever about them.  My comment was only to indicate a general agreement with pds about the need for hypothetical evolutionary pathways if neo-Darwinism is to be testable.  And I have followed up on many articles cited in these discussions, and every time I have, I’ve discovered that no chronological hypothetical evolutionary pathway is proposed.

Evolutionary biology is a historical science.  It therefore must propose hypothetical historical sequences.  No one is demanding the actual sequence followed, just a physically possible sequence that can be assessed for its probability.

If evolutionary biologists believe that a bacterium without a flagellum evolved into a bacterium with a flagellum, then it is incumbent upon them to produce a proposed series of steps.  And not generalities such as “gene duplication” —specific steps such as “the duplication of Gene X,” with an account of what effect that would produce and what selection advantage it would give.

So do these articles contain stepwise narratives, or not?  Or are they merely suggestions for particular mechanisms that might have played a role, somewhere, somehow?

Dave Ussery - #39187

November 9th 2010

Here’s some quotes from the paper, since it is obvious reading isn’t your strength

1.) microtubule undergoes gene duplication - we see duplication all the time - like I say, there’s no cost for this - only cost in selection.  But having an extra copy around can sometimes provide more microtubules, for example, so there’s a slight selective advantage, and that’s all that is needed!

2.) These two genes underwent another duplication - as the authors state ‘This would have provided for the earliest possible motile cilium.’  This is based on some small changes which would stabilize a prototype of the IAD alpha homodimer…

3.) “The third gene duplication of ancestral IAD results in the ancestor of the IAD beta, and the OADs.  This would allow the existing IAD homodimer to evolve into an IAD heterodimer, while… (again, technical details)

4.) This initial OAD then underwent a further duplication… ‘At this point the OAD becomes a heterodimer with a final gene duplication’ … ‘The limited distribution of OAD gamma among extant eukaryotic taxa may imply that this latter gene duplication was after the eukaryotic last common ancestor…’

So how is this different from your points???

Arthur Hunt - #39189

November 9th 2010

David,  you are missing a video conference that has some subjects that are relevant to issues you and Ashe are discussing.


Dave Ussery - #39192

November 9th 2010

Right after their point-by-point, step wise narration of each gene duplication, the authors state the following:

“Assuming that the first motile system of the proto cilium was based only on the IADs, this would predict that if one mutationally inactivated the OADs, the motion could still continue. This is precisely what was found in a mutant of Chlamydomonas that lacked OADs.”

That is, they provide a TEST to see if their idea holds up or not.  It could be that they test it and it’s wrong….  This is the way much of science is done - one has an idea, proposes a model, and then proceeds to test that model by doing experiments.

But where are the ID experiments, publications?  It seems that they only want to generate perfect ideas and write books, but never bother to actually test their ideas with experiments published in the scientific literature…

saying ‘no one has ever done this…’ is not really proposing any new experiments!

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