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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beaglelady - #38835

November 6th 2010

We have discussed whale evolution and Richard Sternberg here.  You can find the Sternberg whale video here.


John - #38837

November 6th 2010

troy wrote:
“What I meant to say was that Behe et al. can submit their critical papers to science journals (the “primary literature” if you like)”

Troy, do you not understand the difference between the primary and secondary literature?

Journals usually publish a mix of the two. IDCreationists have only published in the latter category, never in the former. The former is almost always peer reviewed, while much of the latter is not.

“... and have them peer-reviewed, as usual. If the peers and the editors are happy, they get published. Do you have a problem with that?”

The point I’m trying to make is that much of the secondary literature is not peer reviewed, and peer review has its problems.

Do you understand now?

”What kind of data do we need? My guess, at a minimum: number of beneficial mutations to go from A to B,”

Which would necessarily be less than the number of differences between pairs of orthologous genes. Are there any pairs that have more differences than the mutation rate could cause in 18M years?

Do you realize why we multiply the 9M by 2?


John - #38839

November 6th 2010

troy:
“... rate of beneficial mutations, selection coefficients, population sizes, generation times. Agreed?”

Nope. Let’s start with the most basic test of Behe’s hypothesis that he is too cowardly to test himself. Behe is claiming that there is insufficient genetic variation for natural selection to act upon. So do the differences we observe today exceed known mutation rates? That would strongly support divine intervention, would it not?

Rich claimed that there would be many of Behe’s silly “CCCs” needed, but can’t be bothered to name a single one. Given what we know about developmental biology and the differences that have already been studied (which Rich is too cowardly to examine for himself), there’s no need for even one.


Mike Gene - #38847

November 7th 2010

Dave,

Thanks for pointing me to Caladine and Drew’s book.  I’ll definitely go looking for it.  As for Conway Morris, yes indeed he’s making predictions.  He’s making a stronger and stronger case that evolution itself is more predictable than many have previously believed.  It’s a shame his work is not discussed more on BioLogos.


John - #38852

November 7th 2010

hmm:
“As far as I know, Yes.”

Meaning you don’t know. You never looked, right?

Me: “I don’t see any criticism in there.”

“You replied so quickly, that it looks like you didn’t even read the paper. Did you?”

Yes. You didn’t, though, did you?

Me: “Why doesn’t Sternberg publish data any more?”

“The last studies he has published are from 2008:”

No, hmm. Neither of those are studies. Neither one contains data that haven’t been published before. So, why doesn’t he publish data?

“There was workplace bullying in Sternberg’s earlier job place and he resigned.”

At his place of employment?

“Now he hasn’t so good research resources as earlier.”

So why doesn’t the DI provide them?


Dave Ussery - #38863

November 7th 2010

Hi Mike,

Concerning Simon Conway Morris, I do mention him in later in this review (I think it’s the last section, which will be part VI).  I would assume (but don’t know) that Morris is the type of person BioLogos would want to include - he gave one of the Boyle lectures recently (which is a series of lectures, still going on, in the UK - started in 1692, dedicated to showing positive feedback between Science and Christianity.

Mike, I’m curious about your prediction that aerobic respiration was ‘front loaded’ - I had a look at the link (thanks for providing it!), and see that it is to an article where this is based on looking at gene conservation in ‘673 complete genomes’ - but my point is, when I now look at MORE genomes [currently there are more than 1300 genomes available)], fincluding much more diverse types of bacteria (e.g., the GEBA project) I don’t find these cytochromes conserved. 

Further, YES, it could well be true that modern day anaerobes have these, but this is not the same as saying that they had them 2 billion years ago - or even perhaps 4.5 billion years ago.  So I’m curious - is there any evidence, OTHER THAN sequence-based alignments of modern genomes, to support you case here?


Dave Ussery - #38864

November 7th 2010

More on whether aerobic respiration was ‘front loaded’ as Mike has suggested….

There was an article in Science magazine a week or two ago, about this - kind of interesting.  I remember this because it was on the same day I was giving a talk at a meeting on synthetic biology.  The tittle of my talk was ‘using real biology [evoution] to design minimal genomes for synthetic life’.  I was thinking about this, with respect to the discussion forum here.  It would have been great if someone from the ID community could actually contribute something here - sounds like a lot of people interested in design / engineering.  Why not enter the modern era, and actually use these design principles to design new life?  I’m not trying to be mean or make fun of the ID community - this is a serious question here…


Dave Ussery - #38865

November 7th 2010

Here’s the article (not enough space in the previous comment)


http://www.nature.com/nature/journal/v467/n7318/edsumm/e101021-01.html

Editor’s Summary
21 October 2010

The bioenergetics of complexity

Since the first eukaryotic cell arose from prokaryotes about four billion years ago, prokaryotes have shown little tendency to evolve greater complexity. By contrast, eukaryotic (nucleated) cells form the basis of all complex multicellular life. All eukaryotes either have mitochondria, or once had them and later lost them, placing the origin of the mitochondrion and the eukaryotic cell as perhaps the same event. Why was it so advantageous? Nick Lane and William Martin suggest that, by enabling oxidative phosphorylation across a wide area of internal membranes, mitochondrial genes facilitated a 200,000-fold expansion in the number of genes that can be expressed, vastly increasing the repertoire of novel protein folds, protein interactions and regulatory cascades.


hmm - #38873

November 7th 2010

John:

“hmm:
“As far as I know, Yes.”

Meaning you don’t know. You never looked, right?”

Meaning that there are many kind of peer review practices and journals. For example Annals of the New York Academy of Sciences publishes invited papers based on conferences. Papers are reviewed before acceptance, but not by so many than in some other journals. For example Acta Biotheorica has a bit different peer review practices etc.:

http://www.springer.com/philosophy/epistemology+and+philosophy+of+science/journal/10441
http://www.editorialmanager.com/acbi/

But I’m wasting my time now. You have asked many questions. I’ve replied many times. I’ve asked only few questions. Instead of answering to me, you have just asked more questions.


Alan Fox - #38877

November 7th 2010

Dr Ussery remarks:

It would have been great if someone from the ID community could actually contribute something here…

It seems in the nature of discussions involving ID proponents that the focus is on the incompleteness of scientific theories and there inability to explain all aspects of the observed diversity of life. Paul Nelson observed in 2004:

“Easily the biggest challenge facing the ID community is to develop a full-fledged theory of biological design. We don’t have such a theory right now, and that’s a real problem.”

There are still no alternative theories to mainstream evolution that have any utility or explanatory power.


Alan Fox - #38878

November 7th 2010

Oops!

Their inability to explain…


Alan Fox - #38879

November 7th 2010

Meaning that there are many kind of peer review practices and journals.

Indeed! The peer review process that took place with “Darwin’s Black Box” is a case in point.


pds - #38880

November 7th 2010

Dave,

Thanks for the apology and the explanation.

You said,

“Now, the question is what is it that you would like to discuss here on these BioLogos pages, about my review of Behe’s book.”

I have already said that several times.  I will repeat it:

“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?”

I get the impression that you are not interested in this for some reason.


hmm - #38883

November 7th 2010

Yes. Peer review is an amazing process…

http://iaria-highsci.blogspot.com/2008/12/we-have-letter-of-acceptance-fantastic.html
http://pdos.csail.mit.edu/scigen/

In fact, the author often cannot know, whether his/her paper is really read, understood and reviewed. Especially, if you (as an author) just get a message that your paper is accepted without any additional modification, you cannot usually know, how the publication decision was really done: was your paper so good, or referee so bad of hurry…


hmm - #38884

November 7th 2010

This is also funny page:
http://pdos.csail.mit.edu/scigen/blog/


Arthur Hunt - #38887

November 7th 2010

Dave @ #38865 quoted something from Nature:

Nick Lane and William Martin suggest that, by enabling oxidative phosphorylation across a wide area of internal membranes, mitochondrial genes facilitated a 200,000-fold expansion in the number of genes that can be expressed, vastly increasing the repertoire of novel protein folds, protein interactions and regulatory cascades.

200,000-fold expansion in gene number?  That’s just a silly number.


Dave Ussery - #38891

November 7th 2010

PDS wrote:

“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?”

I get the impression that you are not interested in this for some reason.

Nope, I am definitely interested in this….

PDS, I owe you yet another apology! - I did indeed answer this, several days ago, but if you remember it was just an abstract posted, and you missed it, when I asked you about it.  You said you would have a look at the article, and then get back to me.  So it looks like we were both waiting on each other….  again, we were not communicating clearly - I am sorry!

At any rate, I’ll put a link to the article here:
http://www.ncbi.nlm.nih.gov/pubmed/19253335

I will paste in the next comment,  the last paragraph from the article….


Dave Ussery - #38892

November 7th 2010

The evolution of the cilium, in part via 8 gene duplications

last paragraph from Hartman and Temple Smith’s article…
http://www.ncbi.nlm.nih.gov/pubmed/19253335

The evolution of the ciliary dyneins as discussed in this paper would have taken place in a simpler and much earlier form of the proto eukaryotic cell. The starting point would have been with the singlet microtubules of the cytoplasm along with the motor proteins of kinesin and a dynein providing transport of the various cargoes along these singlet microtubules. These motor proteins along with the singlet microtubules would have been involved in an early form of mitosis and an associated di- vision center without a complex centriole/basal body at its center. The evolution of the doublet microtubules of the cilium induced the ancestor of the Cyto 2 and IAD homodimers from the Cyto 1 homodimer. The ancestor of the IAD homodimer then underwent a series of gene duplications producing the ancestors of the axonemal HC-Dyneins.


Dave Ussery - #38893

November 7th 2010

actually, that was the last paragraph from the RESULTS section, before the discussion…  Pressed “submit” too soon again!


Mike Gene - #38894

November 7th 2010

Hi Dave,

but my point is, when I now look at MORE genomes [currently there are more than 1300 genomes available)], fincluding much more diverse types of bacteria (e.g., the GEBA project) I don’t find these cytochromes conserved.

I’m not sure I am following your point.  It sounds to me like you are saying that in order to conclude the cytochrome oxidases from various distantly related archaeal and eubacterial lineages are homologous, the oxidases would need to be universally present. Is that correct? I would also point out that according to the criteria you use - matches at least 50% of the length of the protein, and within that region have at least 50% identity –  ftsZ and tubulin would not be considered homologous.

So I’m curious - is there any evidence, OTHER THAN sequence-based alignments of modern genomes, to support you case here?

What other type of data would you count as evidence?  Are you saying you need fossil evidence of cytochrome oxidase?


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