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Is There an Edge to Evolution? Part 3

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October 23, 2010 Tags: Design
Is There an Edge to Evolution? Part 3

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 his previous post, Dr. Ussery showed that Behe’s analysis of the probability of getting beneficial mutations is flawed at fundamental levels. Beneficial mutations do occur, new genes do evolve and he cited some research articles that demonstrate this and then showed the interested reader how to gain access to the vast scientific literature that exists. He expresses concern that Michael Behe has not chosen to make the general public aware of what is being done in this arena.

In today’s post he goes on to examine what Behe states is the limit of what Darwinian evolution can and cannot do.

Chapter 4 - What Darwinism Can Do

The title for this chapter is a bit deceptive, in that most of this chapter is not really about what evolution CAN do, but rather what the limits to evolution are (the topic for the next chapter). There is a short description of genome sequence analysis and the types of mutations observed in the laboratory, but in my opinion this chapter is really missing a thorough discussion of the astounding variety and diversity we find when we examine genomes.

Again, Behe emphasizes that he has no problem with evolution by common descent:

Over the next few sections I'll show some of the newest evidence from studies of DNA that convinces most scientists, including myself, that one leg of Darwin's theory - common descent - is correct. (page 65).

Once again, the problem is random mutations:

The bottom line is this. Common descent is true; yet the explanation of common descent – even the common descent of humans and chimps – although fascinating, is in a profound sense trivial. It says merely that commonalities were there from the start, present in a common ancestor. It does not even begin to explain where those commonalities come from, or how humans subsequently acquired remarkable differences. Something nonrandom must account for the common descent of life. (page 65, emphasis in the original).

I absolutely agree with Behe – there must be a ‘non-random’ account. But I’m a bit confused here, because natural selection is, by definition, definitely non-random. That’s the whole point! There is (random) variation, and then those variants that are better are selected. It is not at all random. But Behe’s claim here is that there are not enough random variants produced for evolution to occur. 150 years ago, at the time of Darwin’s writing, it was not known whether the variation was random or produced in some other manner – and in a sense this did not matter.

What was important for Darwin was that the variation was there, and that the method for non-random selection – also known as “natural selection” – could account for the non-random common descent of life. One of the analogies Darwin used was “artificial selection”, where, for example, dog breeders would breed certain traits, giving rise to a large variety of dogs within a short amount of time – merely by [non-randomly] selecting for desired traits. Darwin reasoned if this worked for breeders, why couldn’t it work in natural environments? And as far as “random variations” go, we have quite a bit of variance in dogs, from tiny toy poodles to St. Bernards.

More than half the chapter is devoted to species that have had duplications of their entire genome. Behe focuses especially on yeast, although he mentions in a footnote that other whole genome duplications have been documented. But again, the text written is more within the framework of the limits of evolution—what it can’t do, which should be the subject for the next chapter (I suspect a chapter strictly about what Behe thought evolution could do would be quite thin). The claim that “genome duplication…. has not given baker’s yeast any advantage it wouldn’t otherwise have had” (page 74) seems pretty harsh, especially now that more than two dozen different strains of yeast have been sequenced, and there are clear advantages in survival associated with duplication of many of these genes.

Perhaps, once again, Behe is not familiar with the literature and not willing to have a look at what has been published. I encourage the interested reader to go ahead and have a look at what is out there—go to PubMed, and type in the words “yeast genome duplication evolution” and have a look at the articles found. Today when I did this, I found 420 articles. The second one on the list has this statement in the concluding sentence of the abstract: “Our results provide a scenario for how evolution like a tinker exploits pre-existing materials of a conserved post-transcriptional regulon to regulate gene expression for novel functional roles.” Behe concludes the chapter by saying that “although Darwin hoped otherwise, random variation doesn't explain the most basic features of biology” (page 83).

For more on what evolution CAN do, I mention “The Edge of Evolution” in a footnote in the last chapter (Evolution of Microbial Communities) of my textbook on Comparative Genomics. It is in a section on “Where Does Diversity Come From?”, and I make the statement that some anti-evolutionists “claim that there is not enough diversity in bacterial populations for evolution to occur.” I encourage the interested reader to have a look at this section, as I think it is a nice culmination of a story I’ve slowly built up through the previous chapters on bacterial genomics.

I readily admit that this is something that takes time to understand and cannot easily be explained in a 10-second sound bite – this textbook came from a course I’ve taught at the Technical University of Denmark since 2000. Currently the course meets in the autumn semester, for 8 hours a week, for 13 weeks; this year I have 54 students. So this takes time to explain, but my point here is that the claim that nothing has changed over the past 10 years, in terms of evidence for evolution and documented diversity, is simply wrong.

Chapter 5 - What Darwinism Can't Do

The title of this chapter reminds me of a book by Lenny Moss, called What Gene’s Can’t Do. I think this is a wonderful book, kind of countering the “gene-centric” popular culture. It’s a well-written book, and in my opinion he makes some valid scientific points. Unfortunately, although Behe could have had a similar good discussion here, instead we are treated to poor quality left-overs. This chapter is kind of an update on “irreducible complexity” as outlined in Behe's previous book, Darwin's Black Box. In spite of strong protestations from many (including myself) in their reviews of that work, Behe still clings to the idea that no one has ever published anything about the evolution of these complex molecular machines. “Despite the amazing advance of molecular biology as a whole, despite the sequencing of hundreds of entire genomes and other leaps in knowledge, despite the provocation of Darwin's Black Box itself, in the more than ten years since I pointed out that a situation concerning missing Darwinian explanations for the evolution of the cilium is utterly unchanged” (page 95).

Again, the interested reader is invited to visit PubMed, type in “cilium evolution” and see for oneself: are we to believe that articles with titles like “The evolution of the cilium and the eukaryotic cell” and 'Origin of the cilium: novel approaches to examine a centriolar evolution hypothesis” simply don't exist? Perhaps if one closes their eyes, and clicks their heels three times, thinking, “They don't exist, they don't exist”, maybe these articles can simply vanish!

Last week I gave a lecture in my course about the 10th anniversary of sequencing the human genome. In the field of genomics, much has happened in the past 10 years. There has been an explosion in the amount of genomic data available, and also in the strong, clear evidence for evolution in exactly the manner Behe claims is impossible and will never happen. To put this in perspective – when I first came to the Center for Biological Sequence Analysis in 1997, there were four bacterial genomes sequenced. Last week, in my course I showed an update of the currently sequenced genomes: there are now more than four thousand genomes sequenced, and the number is growing on a daily basis. And the more genomes we sequence, the more we learn about how evolution works. When I was growing up, the preacher in our church used to say, “Did you hear about the guy who said ‘It can’t be done?’ Well he got run over by the guy doing it!” I think there is some truth in this – Behe says it can’t be done, and a decade later, despite this vast amount of data, he claims things remain “utterly unchanged”.

In my next post, I will examine Behe’s discussion of whether random mutation hitched to natural selection is a biological explanation for various molecular phenomena.

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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sy - #37293

October 29th 2010


I am still confused. Perhaps its because I came in here in the middle, and I dont know what your original point was. I dont see what you mean about Meyer fudging and lying. Of course peptidyl transferase is an important function during translation, but it is the aaRS that activates the amino acids to allow the peptide synthetic reaction to occur, and that provides the crucial link between tRNA and the corect amino acid.

Perhaps you could fill me in a bit about the details of the argument or direct me to the appropriate thread. Thanks.

sy - #37294

October 29th 2010


I found your earlier comments about peptidly transferase, as well as Meyer’s discussion on the topic. I dont find anything in the latter to support your claim of fudging and lying. I am looking at pages 306-308 inlcuding note 24 to Chapter 14 in Signature In the Cell.  Could you be more specific?

John - #37356

October 29th 2010

Meyer, p.128:
“A protein within the ribosome known as a peptidyl transferase then catalyzes a polymerization (linking) reaction involving the two (tRNA-borne) amino acids.”

As for pp. 304-306, it complements the above falsehood in that there’s no indication to the naive reader that the peptidyl transferase in every one of their own ribosomes today is a ribozyme, not a protein. Meyer’s fudging consists of only grudging admissions about what ribozymes CAN do, when the most powerful evidence relates to what they actually DO, right now.

Why would an intelligent designer use RNA for this purpose? It’s clear why evolutionary mechanisms would have a hard time replacing it with protein.

Do you know of two other similar examples omitted by Meyer, sy?

John - #37358

October 29th 2010

sy wrote:
” but it is the aaRS that activates the amino acids to allow the peptide synthetic reaction to occur, and that provides the crucial link between tRNA and the corect amino acid.”

But there’s good evidence for direct associations of tRNAs with amino acids, and it clearly is much easier to substitute a protein for these less-specific direct associations.

In your mind, does homology between protein sequences represent common design?

Chip - #37383

October 29th 2010

What happened to the latest post from DU?  Since it seems to have been removed, I’ll reply here: 


While I agree that any conclusions that are drawn about your person are not valid, I do think those who claim that you misrepresented Behe are completely correct.  While others may have steps they need to take, perhaps if you would actually respond to the objections in this regard that have already been noted, we’d see more light and less heat. 

Since you didn’t respond before, I’ll restate the objection I raised earlier (Part II of your series).  Here’s what Behe actually says: 

there have been absolutely no studies that document that large animals change in the way that Dawkins supposes. (E of E, p42, w/my emphasis.  Readers are encouraged to read the entire context at google books)

Without any question, the dependent clause beginning with “that” puts strict limits on the “no studies” noun phrase that it modifies.

Chip - #37388

October 29th 2010

You, however, said: 

Behe goes on to claim that there are “absolutely no studies” to document a molecular basis for the “coherent development of a single trait in a Darwinian arms race.” But this is highly erroneous. True, the example he gives us is not a “good mutation” - but to just blatantly claim that nothing has been done is showing his ignorance of the literature.

This is completely false (with the “nothing has been done” comment graduating to beyond the pale) since in the very same paragraph, he says “although there have been some studies showing modest arms races with smaller animals…” (ibid p42, again with my emphasis)

The only thing “highly erroneous” here is your representation of Behe.  I’m not an expert in your field, but I am educated and I can read.  At best, the argument that you’ve presented here is careless and sloppy. 

And yes, it does raise significant questions in my mind:  if Behe is so wrong, why is it that so many of his orthodox critics can’t criticize him—and not a straw-man distortion of him?

I agree with the tone of what you said in the now-removed piece; while frank, I’ve been civil.  Care to respond?

John - #37421

October 29th 2010

Chip wrote:
“Here’s what Behe actually says:

there have been absolutely no studies that document that large animals change in the way that Dawkins supposes. (E of E, p42, w/my emphasis.  Readers are encouraged to read the entire context at google books)”

Is that statement true, Chip?

Nick Matzke - #37424

October 29th 2010

“We had a conversation about this at BioLogos a month or two back. If memory serves me correctly, I think the number was well under 10%, more like 2%. Paul Nelson is the only one that comes to my mind out of >36 Fellows.”

The ID leadership is not majority YEC, but there is more than one!  E.g., DI fellows who are YECs include Paul Nelson, John Mark Reynolds, Nancy Pearcey, and Dean Kenyon.  Others, like Forrest Mims, are apparently agnostic on the age of the Earth, which is probably an even more bankrupt position than YEC.

John - #37425

October 29th 2010

After all, Behe also wrote:
“We can look high or we can look low in books or in journals, but the result is the same. The scientific literature has no answers to the question of the origin of the immune system.”

Did Behe stand by that claim under oath, or did he change it?

What about when Behe wrote:
“There have been no reports of new viral protein-protein interactions in HIV proteins.”

sy - #37442

October 29th 2010


When you speak of interactions between amino acids and tRNA, do you mean between specific amino acids and their cognate tRNAs? I would love to see a reference to that, since it is news to me.

I don’t agree that Behe is distorting the power of ribozymes. In fact I think he got it pretty right on. Yes, he made a mistake in stating peptidyl transferase as a protein, but he corrected it later, so that was bad editing rather than deception. And the fact is that ribozymes are really poor catalysts compared to proteins. His main point, which is valid, is the lack of coding ability of the ribozyme world, which simply doesn’t allow for the modern life system of finely tuned proteins coded for in a genetic code.

I cant answer your question about a designer, because I don’t understand it.

sy - #37449

October 29th 2010

To clarify, it was the first question you asked me about why a designer would use RNA that I didnt understand. In answer to your second question about protein homologies, no I dont believe that protein homologies are evidence of design, they are evidence of common descent.

John - #37467

October 30th 2010

sy wrote:
“When you speak of interactions between amino acids and tRNA, do you mean between specific amino acids and their cognate tRNAs?”

They wouldn’t need to be specific at first, just selective. Let’s iron out the more important point first.

“I don’t agree that Behe is distorting the power of ribozymes.”

We’re discussing Meyer, not Behe.

“In fact I think he got it pretty right on.”

How can you say that when you can’t name the other two cases he strategically omitted? One of them was the subject of yet another Nobel Prize!

“Yes, he made a mistake in stating peptidyl transferase as a protein,…”

If he made a mistake, he would be eager to correct it if one contacted him, correct?

“... but he corrected it later,…”

No, he did not. At no point did he ever let his audience know that the MODERN peptidyl transferase is RNA, not protein.

Your assertion from wishful thinking is empirically testable, sy. Can you think of a way to test whether his readers know that peptidyl transferase is not a protein? I can and have, and you’re wrong.

“... so that was bad editing rather than deception.”

Then he’s incompetent when it comes to OOL stuff, as are all of his friends who reviewed the book.

John - #37468

October 30th 2010

“And the fact is that ribozymes are really poor catalysts compared to proteins.”

Then an intelligent designer would never put a ribozyme in such an important position! Only a stupid designer would. How does Meyer explain the Designer’s choice of material?

“His main point, which is valid, is the lack of coding ability of the ribozyme world,…”

But he’s fudging all the critical evidence that he isn’t strategically omitting. He misrepresents the RNA World hypothesis itself, and he quote-mines Wally Gilbert.

“... which simply doesn’t allow for the modern life system of finely tuned proteins…”

Yet the modern system uses a ribozyme to form all peptide bonds. The point Meyer’s eliding is that your “modern life system” has ribozymes performing essential functions. No reader of his book would ever learn that fact.

So what are the two ribozymes that Meyer doesn’t even mention?

“... coded for in a genetic code.”

Sorry, sy, but that phrase makes no sense at all. The “genetic code” is a metaphorical term that working biologists (Meyer never was one and Behe quit being one) use to refer to the mapping of codons to amino acids and nothing else.

Lurker - #37476

October 30th 2010

Sy and John-
Forgive me for butting in, but I’d like to add to this exchange. I’m not particularly interested in proving Meyer is generally despicable, but I’m surprised, Sy, that you find his arguments convincing, insofar as you seem to be otherwise well-informed about biology.

As John points out, he never indicates that he understands that rRNA is the sole catalytic element in the ribosome. Moreover, he never explains that the ribosome is an RNA machine in which proteins play fundamentally ancillary roles and that this makes most sense if it first evolved when proteins weren’t around.

The entire chapter is plagued by inaccurate statements. You mentioned footnote 24, which has a good example. There he claims that while rRNA may catalyze peptide bonds, the ribosome as a whole, and by implication ribosomal proteins, provides ‘critical “substrate positioning”’. Review his citation (Rodina et al): it refers to the positioning of tRNA ends in the ribosomal active site, by rRNA, and in no way refutes the claim that protein synthesis is an RNA affair.

Tim - #37477

October 30th 2010


Are you still following this thread?  I finally have time now to begin responding to your previous questions and challenges, but want to make sure you’re still following this before I invest the time to respond.  Let me know.

Lurker - #37478

October 30th 2010

The point that RNA is a poor catalyst compared to proteins is not germane: RNA catalysts are still routinely capable of million-fold acceleration over uncatalyzed rates, and from its inception, the RNA World theory had proteins replacing ribozymes precisely because they were superior. I am unaware of any fundamental problem with RNA performing the enzymatic roles currently performed by proteins, I’m curious what causes you to disagree. Specifically, can you clarify what aspect of RNA makes it incapable of coded peptide synthesis? Are you primarily familiar with this field from Meyer’s book? As perhaps John is alluding to with his discussion of homology, Meyer doesn’t provide any of the phylogenetic and the biochemical evidence that indicate evolution of the translation apparatus, aaRS proteins included, from an RNA-based predecessor. Again, even if he finds reasons to discount this evidence, its absence is a pretty bad error.

Ok, this is too long as it is. I would be interested in your response.

John - #37479

October 30th 2010

Lurker wrote:
“The point that RNA is a poor catalyst compared to proteins is not germane:…”

It certainly is if we are to evaluate Meyer’s claims and conclusions for internal consistency.

Lurker - #37483

October 30th 2010

I’m not sure I understand your point, but my statement could be clarified. A protein enzyme can often accelerate its target reaction by billions to trillions of fold. Whether RNA can do this is still debated, as most ribozymes, natural or artificial, haven’t necessarily been evolved for high rates of activity. There are some reasonable structural and biochemical arguments that RNA wouldn’t be as good as proteins, but then again, in a few cases we have evidence that RNA is quite capable of extreme rate acceleration (the group I intron, I believe, can function at near optimal efficiency).

Regardless, we do know that ribozymes can at least routinely accelerate their reactions by millions of fold, and can do so for a broad variety of chemical transformations. There’s no ironclad law that life must operate with the rate constants we typically find now; in the absence of possibly superior proteins, ribozymes in the RNA world achieving million-fold rate enhancements would have been quite sufficient.

I doubt we disagree very much about the accuracy of Meyer’s claims, although I’m more willing than you to chalk up his errors to ignorance. But in what way has he been inconsistent about the rates of RNA catalysis?

John - #37488

October 30th 2010

“I doubt we disagree very much about the accuracy of Meyer’s claims, although I’m more willing than you to chalk up his errors to ignorance.”

I’d say given the way he touts himself on his very own site (gotta love the third person):
“Meyer’s research goes to the very source of the mystery of life: its origin, and more specifically the origin of biological information as represented in DNA,”

...when he’s never even done any research, being ignorant of these Nobel-winning findings (and strategically omitting others) means that he’s lying about his expertise. I think he’s smarter than that.

“But in what way has he been inconsistent about the rates of RNA catalysis?”

He hasn’t. His position is simply that RNA is an inferior catalyst, which then leads to the question of why an intelligent designer would use it instead of protein.

Meyer can’t answer this, so he resorts to blatant falsehood in one part of the book and careful fudging in another, so the reader lacks sufficient information (ribozymes play incredibly important roles in modern biology) to ask this obvious question.

Rich - #37499

October 30th 2010


Yes, I’m still following this thread, despite the fact that so much of it has been dominated since you left by one unpleasant individual whose posts are all heat and no light.  I’ve been awaiting your return so that we could again pick up the notion of irreducible complexity.  I’m hoping that you will have given the passages I cited from Behe and Dembski another look.

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