Join us April 17-19 for the BioLogos national conference, Faith & Science 2024, as we explore God’s Word and God’s World together!

Forums
By 
David Ussery
 on December 04, 2010

Is There an Edge to Evolution?

After sharing his own philosophical and personal perspective, David Ussery carefully critiques the arguments made by Michael Behe in The Edge of Evolution.

Share  
Twitter
Facebook
LinkedIn
Print

After sharing his own philosophical and personal perspective, David Ussery carefully critiques the arguments made by Michael Behe in The Edge of Evolution.

In this article, David Ussery carefully critiques the arguments made by Michael Behe in The Edge of Evolution. Ussery begins with the statement that this series is for those who have read or who are going to read Behe’s book, and that it is detailed in nature. Then, he gives a short synopsis of his background, both personal and philosophical. He proceeds to comb through all nine chapters of the book, pointing out the strengths and weaknesses of various arguments made in each.

An Analysis of Michael Behe’s book, The Edge of Evolution

In the 12th century, the Danish king set aside a large area of forest along the eastern coast of the island of Zealand, as a Royal Hunting grounds. The area was fenced-off a few hundred years later, and is now open to the public. Fortunately for me, I live close to the “Deer Park,” and early in the morning, before many people get out of bed, I go for a run there. I am often truly impressed by what I see in nature, such as the majestic stare of a stag looking at me, as I go by, or the noise and sight of a flock of geese flying overhead. As an individual, I have no problem saying that what we see around us can point towards transcendence – there is grandeur and beauty. When discussing the Intelligent Design movement with my oldest brother, Steve, he asked me what was wrong with the idea that we can see God in nature—that is, that the goodness and design we see around us is surely an argument pointing towards God. I told him I don’t have problems with this line of thinking. Having thought about this some, I realized that this idea is very common in the Bible, and for example Jesus often seemed to point to this in parables. However, as a scientist, I am deeply skeptical of claims that one can use science to somehow ‘prove’ God exists (or to ‘prove’ there is no God, for that matter). In 1661, around the same time the Danish king fenced-off the area around the “Deer Park,” one of the first chemists, Robert Boyle, wrote a book called The Sceptical Chemist. (Hence the title of this review.) Boyle was a devout Christian as well as a very good scientist; I will come back to Boyle later.

This brings me to mention the target audience of this review. Of course anyone can read this, but it is intended mainly for educated readers who are interested in the science/religion dialogue, and in particular are interested in Intelligent Design, and either have read or want to read The Edge of Evolution: The Search for the Limits of Darwinism, by Michael Behe (Free Press, New York, 2007). I have heard from some of my friends and family that they find this book “convincing” from a scientific point of view. Before I go into a discussion of the book, I want to give the reader a bit more perspective about myself. I grew up in Springdale, Arkansas, and am the youngest of five children. Some (not all) of the members of my family are “young earth creationists,” that is, they think that the world is less than 10,000 years old. I first heard of Mike Behe about 25 years ago, when I was a Ph.D. student, working on showing that alternative DNA helical structures could exist inside of living cells. Behe had published a paper with Gary Felsenfeld, showing that methylation of certain DNA sequences could greatly facilitate the formation of left-handed Z-DNA, and that Z-DNA did not like to be wrapped around the nucleosome. Probably for most people, that last sentence doesn’t make much sense, but for me, this was a paper that I was very fond of, as these results pointed in the direction of perhaps some sort of biological meaning. I eventually got my Ph.D. (in biochemistry/molecular biology from the University of Cincinnati College of Medicine), did a post-doc at the Institute of Molecular Medicine, Oxford University, and about 12 years ago moved to Denmark, where I have been the leader of the comparative microbial genomics group at CBS (the Center for Biological Sequence analysis, a bioinformatics center in the Department of Systems Biology, at the Technical University of Denmark).

Now that I’ve laid down my philosophical and personal perspective I can get on with the review. I feel that this is a necessary background as, after I reviewed Darwin’s Black Box more than 10 years ago, I was accused by several readers of being critical of Behe not based on the science, but because I “wanted to promote atheism,” which is certainly not the case. I will struggle to give what is written in Edge of Evolution a fair hearing – let’s see how well the scientific evidence supports what is written in the book.

First, I want to start on a positive note – there are (at least) two things that I liked about the book:

  1. Behe does a good job of describing the logical outcome of thinking in contemporary molecular biology. For example, IF in fact DNA is really some sort of computer code, where did this information come from, how is it maintained, and Who wrote it? IF in fact the mutational frequency of DNA is in the range of 1 change per hundred million base-pairs (that is, the DNA polymerase incorporates the “wrong” base about once ever hundred million times), then how can we explain the incredible diversity we see around us?
  2. Behe is writing from the point of view of a non-materialist. Thus, he seems to think that there is more to the world than what we see around us, and this is in contrast to many other vocal atheistic scientists

I will now make my way through the text, in order of the chapters. In my opinion, the book starts well, and then begins to veer off in strange directions – but I’m getting ahead of myself.

Chapter 1 – The Elements of Darwinism

I agree with Behe when he says that “Darwin’s theory has to be sifted carefully, because it’s actually a mixture of several, unrelated, entirely separate ideas”: random mutation, natural selection, and common descent. He then goes on to say that of the latter, “in brief, the evidence for common descent seems compelling,” but that he feels “random mutation is extremely limited.” Later in this chapter, he states “Evolution from a common ancestor, via changes in DNA, is VERY well supported. It may or may not be random.” [page 12, emphasis in the original] This will in fact be the main focus of the rest of the book – whether “random mutation” alone can generate enough diversity on which natural selection can work , in order for evolution to occur. So just to flesh this out a bit—in Behe’s defense, clearly he is not a “young earth” creationist, who thinks that the world is less than 10,000 years old. He has no problem with the world being about 4.5 billion years old, and life slowly evolving from the first single-cell bacteria appearing almost as soon as fossils could form, through another 4 billion years as mostly single-celled or tiny microscopic organisms, and the very recent appearance of larger plants and animals a bit less than a half-billion years ago. This is all fine and accepted to be true—it is just the MECHANISM for how this might have happened that is being considered. Just as a minor point, one thing in this chapter that is stated as fact, isn’t quite right in my opinion—“By far the most critical aspect of Darwin’s multifaceted theory is the role of random mutation. Almost all of what is novel and important in Darwinian thought is concentrated in this third concept.” Perhaps this is true today, but certainly when Darwin published his Origin of Species, the critical novel, important and new idea, in contrast to the current thought, was that of common descent—in fact Darwin hadn’t a clue about HOW diversity was generated, but the whole point of his book was to demonstrate the evidence for natural selection and change of species (common descent) over time, in contrast to the idea that each individual species had been recently created by God, a few thousand years ago. And common descent, Behe admits, is supported by “compelling evidence”—so we are in agreement here. Evolution has happened over billions of years, and there is “compelling evidence” for evolution by common descent.

Chapter 2 – Arms Race or Trench Warfare?

This chapter is about one of the classic examples of evolution: malaria and sickle cell anemia in humans. Behe observes (correctly, in my opinion) that the mutations that are responsible for helping some humans fight malaria are bad mutations. ‘The first point is that the two examples he cites, sickle and Hemoglobin C (HbC), (two mutations that help the body resist malaria), are quintessentially hurtful mutations because they diminish the functioning of the human body. A second point is that “the mutations are not in the process of joining to build a more complex, interactive biochemical system.” (page 34).

Fair enough—and it is well known that harmful mutations, in the sense of wrecking something or making a pathway not work, occur much more frequently than beneficial mutations. However, 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.

For example, consider this from the abstract of a recent review article, with the title “Origins, evolution, and phenotypic impact of new genes,” published in Genome Research. “The array of mechanisms underlying the origin of new genes is compelling, extending way beyond the traditionally well-studied source of gene duplication. Thus, it was shown that novel genes also regularly arose from messenger RNAs of ancestral genes, protein-coding genes metamorphosed into new RNA genes, genomic parasites were co-opted as new genes, and that both protein and RNA genes were composed from scratch (i.e., from previously non-functional sequences).” This is a new article, but many of the references in this article date to long before The Edge of Evolution was written, and some even date to before Darwin’s Black Box was published, more than a decade ago.

Then there’s another article about recent evolution of beneficial mutations in humans. There are many, many articles published on this sort of idea, and to claim that not a single study has been done is essentially a play on the ignorance of the readers! It is as if the hope is that the readers are ignorant of the scientific literature, and either too lazy or not competent to have a look through PubMed and see what is really out there.

Chapter 3 – The Mathematical Limits of Darwinism

One of my Ph.D. students was a mathematician, and I can still remember trying to read through his paper—lots of formulas—and sometimes they were difficult for me to understand. I have since learned that many people in math departments have a strong disliking for statisticians—I used to naively think that the two are the same. In this chapter, it looks as though Behe has confused mathematics (in the title) with statistics (what is actually discussed in the chapter). What’s worse, the numbers he uses are based on bad assumptions, and are way off from what is known in the field by experimentalists doing current research in this area. Thus, unfortunately, his conclusions are not as strong as they might seem at first glance.

First, in calculating the odds of a single mutation in a protein, one has to take into account the chances of a mutation in the DNA sequence, because this is where mutations happen in biology—this is part of the ‘central dogma’ of molecular biology—that the information flows from DNA to RNA to protein, but not from proteins back to DNA. Thus, if a protein has a particular amino acid changed, this can be traced back to a change in the DNA sequence. Behe says ”resistance to chloroquine has appeared fewer than ten times in the whole world in the past century”—but what is meant by this shorthand is that we have documented evidence of this happening only a few times – that’s not the same as knowing definitively that this HAS happened only those few times. Lots of things [like mutations leading to drug resistance] happen all the time that don’t get seen and documented.

Then, based on this vastly over-simplified estimate, he suggests that the odds of a parasite developing resistance to chloroquine is one in 1020, whilst the odds of developing resistance to another drug (atovaquone) is one in 1012. Since the former, he says, involves two amino acid changes, while the latter involves on one, from these two numbers, it is concluded that the chance of having mutations which change two amino acids in a protein is a hundred million times lower (10-20 vs 10-12) than that for just getting one.

But this just simply does not make sense. Even within E. coli, the well known work-horse of molecular biology, take the order of amino acids in any one of its 5000 or so proteins, and compare that arrangement to that in otherE. coli strains and you will find LOTS of differences. For many proteins in E. coli, the level of identity between strains is around 80%—that is, about twenty out of every hundred amino acids are different—so to say that the odds for a double mutation (2 amino acid changes out of 100), is essentially impossible, when we observe 10 times that amount of diversity (20 differences for every 100 amino acids) in natural populations is speaking from ignorance. We see ten times the number of changes which Behe says is almost impossible all around us within a single species without even the need to generate new mutations.

I’ll discuss the vast differences found with various sequenced E. coli genomes later, but getting back to this chapter and the mutations in the two different spots within a single gene, Behe concludes:

On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since this is many times the age of the universe, it’s reasonable to conclude the following: No mutation that is the same complexity of chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years. (page 61, emphasis in the original).

But again, if one takes a deep breath, and looks at what is known, the mutational frequency that we can actually measure in humans is many times greater than that upon which Behe’s assumptions are based. His argument is that the chances of getting useful mutations at two sites in the same gene are highly unlikely. But can we assess how likely mutations, which are likely to change the function of a gene, occur? One of the underlying assumptions of molecular biology is that sequence determines structure, and that this structure determines function. Hence, a major structural change is likely to have a different function. So how common are mutations that result in structural changes in proteins?

Surprisingly Common! One out of every 21 births in humans have some sort of STRUCTURAL change (and hence likely a functional change) in a protein, just from insertions from a single transposable element (alu), common in humans. It is already evident that Behe has a real problem with “random” mutations—but I think perhaps he is confusing ‘randomness’ with ‘purposelessness’.

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!

Recently 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.”

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.

Figure 1

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.

Chapter 8 – Objections to the Edge

I agree with Behe when he says “Time is actually not the chief factor in evolution—population numbers are.” (page 153). Perhaps an analogy can help explain this. In my line of work, we rely heavily on computers. For example, I want to do a comparison of a thousand bacterial genome sequences—if it takes a few days to do a calculation on one genome, then it would take literally YEARS to do the calculations for a thousand genomes. How do we get around this? By using lots of processors in parallel. If we have 1000 CPUs, then in principle, assuming the computers are free and all goes well, we can do the calculation in a few days. Thus, by using parallel processing, one can speed things up tremendously. The argument goes for evolution as well. Although the mutational frequency might be small, if you have enough genomes, the chances of getting the ‘right combination’ is much greater, especially if it happens in parallel along with the occasional recombination of genomes.

Behe’s argument in this chapter is essentially that even with more than several hundred million years of evolution, this is simply not enough time for the ‘right mutations’ to occur in order for the complexity we see around us, in terms of plants and animals, to have evolved via ‘random processes’. On page 163, Behe poses the question: “Yet if it can do so little, why is random mutation/natural selection so highly regarded by biologists?” He then goes on to compare the idea of random mutations with that of “ether”, that mysterious substance hypothesized to exist more than a hundred years ago, but thoroughly discredited by Einstein. It is quite clear from this comparison that Behe thinks “random mutation” is a myth believed by most biologists on faith, with little evidence to back it up.

I disagree. I do believe that life’s history is infused with purpose and that this process is God’s process. The question here, from my perspective, is not whether there is purpose or not, but whether the scientific arguments presented in Behe’s book make sense and are valid, based on what is currently known in biochemistry and molecular biology. It is those arguments that I address here. To really understand the potential of mutations to build new protein interactions you need to see a much bigger picture than Behe paints. Bacteria have been around since the first ecosystems, more than 4 billion years ago, and are still the most predominant life form on the planet today. I have a table I love to show my students when I’m teaching. It comes from a review article published about a year ago. There are 1031 bacteriophages (viruses that attack bacteria) on the earth, and if one were to stretch out their genomes, end-to-end, they would be about a thousand times the length of the Milky Way galaxy! If one were to stretch out all of the bacterial DNA from the planet, it would be close to a MILLION times the length of the Milky Way! So this is an enormous amount of DNA. Since bacteria have very short lifetimes (less than a day) that means that more than that amount of DNA is being replicated every day. With each replication there is an opportunity for genetic change in parallel lines which have the opportunity to mix and match every so often in the history of life. In examining a tiny, tiny fraction of that, a ‘mere’ thousand bacterial genomes, I am absolutely astounded at the amazing diversity. As I’ve said before, not a single protein is conserved amongst just this tiny sampling of bacteria we’ve looked at so far, and many bacterial ‘species’ have less than half the proteins of one genome found in another genome—of the same species! To what extent does Behe appreciate this vast opportunity to build new combinations of proteins?

Behe makes an astonishing conclusion. He states “the formation of even one helpful intracellular protein-protein binding site may be unattainable by random mutation.” (page 157). Let’s start off by examining what has been published. Go to PubMed, search their more the 20,000,000 articles online. If you type in “evolution, protein binding sites” you will see the article, “Structural features and evolution of protein-protein interactions” along with 5400 other articles on the topic. The abstract for this article includes the sentence:

Here, the interfaces of 750 transient protein-protein interactions as well as 2,000 interactions between domains of the same protein chain (obligate interactions) were analyzed to obtain a better understanding of molecular recognition and to identify features applicable for protein binding site prediction.

This is just one article. Would you agree that perhaps Behe’s statement “the formation of even one helpful intracellular protein-protein binding site may be unattainable by random mutation” is likely not to be too meaningful? It seems that it might be a little premature to bring his summary of the state of biological research to a public audience as he did in this book. There is no question that Behe’s story is very incomplete. You are especially urged to read Kelsey Luoma’s excellent article on this. She is an undergraduate student who did what all good science students do—she went back to check the literature. The literature clearly demonstrates the evolution of new protein interactions.

Relative amount of genetic material assayed in Malaria experiments, compared to the amount that has existed in all cells which have existed in the history of life.

So Behe is clearly wrong when, on page 154, he says that since “we see no new protein-protein interactions developing in 1020 cells, we can be reasonably confident that, at least, no new cellular systems needing two new protein-protein interactions would develop in 1040 cells—in the entire history of life…” Depending upon your math background you might be tempted to think that the difference between 1020 and 1040 is not that great. Just in case that is the case, let’s examine how different those numbers are with a little illustration. The DNA from 1020 cells of bacteria would be about 18 light years long—that’s a lot of DNA! However, the length of the DNA from all bacteria, on the face of the planet, living right now (roughly 1031 cells), is about 100,000,000,000 LIGHT YEARS long. However, that is just is just the amount of bacterial DNA present right now. Bacteria duplicate as often as once every five minutes. So compared to the DNA in 1020 cells (18 light years) the amount of DNA in 1040 cells is 1,800,000,000,000,000,000,000 light years. That’s a lot of DNA. (Remember there are 180,000 miles in one second of a light year. That’s a lot of DNA.) Let’s be careful about telling the public “we can be reasonably confident that, at least, no new cellular systems needing two new protein-protein interactions would develop in 1040 cells—in the entire history of life…” The generation of this amount of DNA provides for a lot of opportunity for mutations that would generate new protein interactions.

“We see no new protein-protein interactions developing in 1020 cells, [therefore] we can be reasonably confident that, at least, no new cellular systems needing two new protein-protein interactions would develop in 1040 cells – in the entire history of life…” – Michael Behe, Edge of Evolution, page 154

Let’s look further at what really was done in the experiment with 1020 cells he discusses in the quote from page 154 where he clearly states that no new protein-protein interactions were seen. The fact is that in this experiment they didn’t search the proteome for new protein-protein interactions—they were only looking for one particular type of mutation. So not only did Behe’s extrapolate from a “pin-prick” sample size (1020 cells) to a larger than universe-sized sample size (by comparison), the authors of this study didn’t even begin exhaustively comb the “pin-prick” sample for new protein-protein interactions. It is dangerous to extrapolate over “zillions” of orders of magnitude (from 1020 to 1040) even at the best of times. However, Dr. Behe did it for a parameter that had not even been carefully searched to begin with. The investigators did not design the experiment to search for any new protein-protein interactions in the entire protein repertoire of cells—they were just probing for one particular phenotype. Behe is correct that they didn’t see them, but to conclude that they didn’t find ANY new protein-protein interactions is a bit far-fetched, since they weren’t looking for them. They were only looking for a small number of highly specific changes, not the proteome as a whole. True, no one reported finding beneficial mutations in the samples studied, for this particular case, but to conclude that they can in general never or only rarely happen is just a hopeful extrapolation.

Total Amount of DNA in Bacterial Cells

An Evaluation of Behe’s Edge of Evolution, Chapter 9—The Cathedral and The Spandrels

This series of posts has been going through Michael Behe’s book, The Edge of Evolution, chapter by chapter. This penultimate chapter focuses on the findings of one of the most fascinating new topics in biology today, evolutionary developmental biology (evo-devo). In essence this is a field that couples two sub-disciplines, evolutionary biology and developmental biology using the tools of molecular biology. Chapter 9 is moving on to “higher levels of biological organization,” and Behe readily admits that things are now a bit less well-defined, and “the arguments in this chapter will necessarily be more tentative and speculative than for previous chapters” because now the subject will be dealing with more complicated things—plants and animals, and “much less is known about what it takes to build an animal than to build a protein machine” (pages 172-173).

As often happens in science when one examines a phenomenon through a different window, many new and often surprising insights come into view. In 1940, for example, few people studying genetics imagined that DNA would be the genetic material; most everyone thought it would be proteins. However, soon afterwards the tools of microbiology began to reshape how biologists viewed the genetic material, and that in turn opened the window for Watson and Crick to see the gene’s true molecular nature. With that, the now-famous double helix came into view for the first time.

Examining the surprises that appear when one looks at a phenomenon from a new vantage point is what makes science so engaging. Scientists love surprises. In this chapter, Behe focuses on one of the most exciting scientific discoveries of the past thirty years, and implies that because evolutionary biologists were surprised, that evolutionary theory had reached the edge of its scientific limits. Let’s examine the basis of the surprise and then explore whether Behe is justified in concluding that the scientific surprises discussed in Chapter Nine correspond to a cliff-edge. Is Behe correct in concluding that going beyond that edge, one enters into territory that can only be explored by inserting a [supernatural] Intelligent Designer into the scientific “equations?” Is Behe’s edge simply a window of opportunity to see where mainstream biological tools will take us, or is it a blank wall? Behe believes it is a blank wall. Why?

In an earlier post our colleague, David Kerk, described the tinman gene, the gene required for making a heart. It is one of the many conserved “master” genes whose functions are now understood, through the new perspectives afforded by evo-devo. These genes serve as genetic switches that have the capability of activating particular developmental programs. A given switch (i.e. a master gene) is often structured quite similarly throughout the animal world even when comparing widely disparate species like flies and frogs. This high degree of conservation shocked evolutionary biologists. It was startling, for example, to realize that the same gene that served as a switch to turn on eye development in flies was found in humans, because if you think about it, the eyes of flies are a lot different than human eyes! Indeed, the mouse master gene for making eyes has been transplanted into fruit flies where it still works. Fly cells respond to the mouse switch by making eyes—fly eyes, not mouse-like eyes—but eye tissue nonetheless. Biologists didn’t expect genes to be conserved through the greater than 550 million years since mice and flies had a common ancestor. However, even though it was a surprise, it is extremely consistent with evolutionary theory. Despite the surprise, the finding is completely consistent with natural selection and common descent. Master genes are conserved through the parade of life. Like the hour hand on a ticking clock, they change, but only at a crawl.Actually, the surprise comes from just how beautifully consistent the view is from this vantage point. Scientists were expecting consistency, but certainly not in such an eye-popping, mind-boggling manner.Behe chooses to view things differently. This is evidence, he says on page 190, that:… the best minds in science have been misled. They justifiably expected randomness and simplicity…

These scientists were NOT expecting randomness and they were most certainly NOT expecting simplicity. What they were expecting was greater complexity—not the degree of simplicity they found. The same genes are being used to build insects as what are used to build mammals. What could be simpler than that? So from this perspective, it is difficult to even begin to grasp Behe’s point about expected simplicity.

Let’s go back though to his statement regarding the notion that the scientists’ “expected randomness.” Why would he tell a general audience that? Natural selection is the very converse of a random process with an unanticipated outcome. They knew it would be non-random—natural selection is by definition non-random. What surprised them—what shocked them actually—was just how foundationally simple and non-random evolutionary mechanisms turn out to be. Evo-devo is not inconsistent with the core of evolutionary theory. Quite the opposite actually—natural selection is by definition a non-random process.

It is important to be fair to Behe here. He has stated clearly that the data as a whole are consistent with common descent. This is not in question for him. Indeed, it would probably have been good for him to emphasize in this chapter that these data are beautifully consistent with his own premise—common descent. One can track the lineage of the “genetic toolkits.” The toolkits get modified slightly and one can trace their modifications as one examines the tree of life. But there is a tree—one tree—Mike agrees with this! Indeed his entire approach to intelligent design is grounded in common descent. So in that regard Behe is in total alignment with mainstream biology. In that regard BioLogos and Behe are truly at one. We wish he would say that more often. There is a sense in which Mike Behe is more closely aligned with BioLogos than with many of his colleagues at the Discovery Institute including Bill Dembski and Stephen Meyer, who, although they waffle on occasion, have come out against common descent. Neither Bill nor Steve are biologists. It would be great if they would listen to their own biochemist. If they would, then perhaps Mike Behe’s statement on page 191 would take us to a whole new day:

Let’s acknowledge that genetics has yielded yet more terrific (and totally unanticipated) evidence for common descent.

Do you hear that, members of the ID Movement? Perhaps the single most important figure in the ID movement over the past fifteen years has called for an acknowledgement that common descent has occurred. Implied in this statement is evidence for common descent all the way from single cells to human beings. If the leaders and followers who do not have credentials in biology and biochemistry would get on board with their expert who does, then half of the concerns with the ID movement would be over.

Behe goes on from there to demonstrate the complexity of the genetic circuitry needed to build various cell types. Vertebrates, for example have B lymphocytes to help fight off infections; invertebrates, he says, do not. The genetic circuitry to build any cell type is exceedingly complex. Organisms are placed into classification groupings, based on somewhat subjective human ideas. Vertebrates are member of the phylum, Chordata. Invertebrates are members of other phyla. Behe proposes that the differences between phyla are so large, that they require the invention of whole new cell types. Since new cell types require new protein interactions and since he believes he has already shown that new substantive protein interactions won’t occur without intervention, new phyla as he sees it cannot arise without intelligence.

Let’s be clear, there is an Intelligence behind all of life. So, even here we don’t disagree. The question is why Behe wants to draw a line (an edge) between presence of God and absence of God in life’s history—presence of intelligence and absence of intelligence. Perhaps it is because of the necessary “absence of intelligence” to serve as an experimental control for “presence of intelligence?” If so, this sounds as though his theology is flying free. It is not grounded in Scripture. The Bible asserts that “by him all things were created…He is before all things and in him all things hold together.” (Colossians 1:16, 17). It also says, “Through him all things were made, without him nothing has been made that has been made” (John 1:3).

Further, one could build a case that he has now floated free of his scientific roots as well. Based on the data available so far, Behe may be correct that we cannot successfully trace the step-by-step lineage of new particular cell types in certain phyla. Behe’s assertion that for scientific reasons, however, we must now insert an Outside Architect is deeply flawed. The only scientific evidence he lays out to support the scientific hypothesis of the need for this architect harbors back to the same sort of calculations on the probability of new protein/protein interactions. We have already demonstrated that those calculations are off by many orders of magnitude.

What are those calculations that show no new protein/protein interactions have occurred? What is the data he analyzes? On page 200 Behe suggests that out of a billion rats subjected to warfarin in the past 50 years, we might have expected “many new regulatory regions; none seemed to have helped against warfarin.” Did anyone check these billion rats to see if some had undergone changes in regulatory regions? It seems that this is really a premature conclusion to put forward to the public without vetting it before the scientific community first. From there he goes on to fruit flies that have been studied in the lab for 100 years. During this time “no new, helpful, developmental-control programs have appeared.” Is there some reason why we might have expected some new “helpful” program in flies? What sort of “new help” would Behe have envisaged for fruit fly development? How would it have been detected? Was anyone actually looking for such a thing?

In the chapter, Behe then goes on to report that the malaria parasite has evolved no new reported “cell forms or regulatory systems” in a hundred billion billion chances. How does he know this? It is true that no one reported new regulatory systems. But was anyone looking for them? For all we know the parasite might have been evolving and even changing elements of its regulatory system. A careful analysis might even have been able to show this.

Based on analyses like these, Behe ends his chapter by discussing spandrels, the space between the arches that hold up a great cathedral. The arches, he says are clearly designed by a great architect. The artwork that decorates the spandrels were added after the fact—after the architect had left the scene. Now moving towards a metaphor, he states that science, his science, has now shown that the major classification groups of animals are like the arches of a great cathedral—they have been designed by God, the Greatest Architect. Darwinian evolution comes in and decorates the spandrels with all sorts of species and maybe genera and families—but the existence of phyla requires an Architect. This is Professor Behe’s cathedral and although one has to give him credit for being creative, this is based on his claim that rats that don’t evolve new systems (for which no one was carefully looking, to be honest). It is based upon fruit flies that don’t seem to be developing new and better body plans than they already have, and it is based on billions of billions of malaria parasites that are not being analyzed for changes at the molecular level. Surely ID is now floating free of scientific data. A theology based on a God whose Presence in creation comes and goes is equally problematic. Is not ID also floating free of Scripture?

It doesn’t have to be this way. Professor Behe, since he accepts common descent, is already half way home towards accommodating the scientific community. As imperfect human beings, we are all wrong on occasion. As mentioned early on in the chapter, “the arguments are more tentative and speculative” here. But there’s also a danger that perhaps the arguments have strayed far from solid science as well as sound theology. It doesn’t have to be this way.


About the author