David Burges critiques evolutionary creationism in The Testimony - 3

The frequency with which I emphasise both the difference between evolution as fact (common descent) and evolution as theory (the modern evolutionary synthesis) and the fact that problems real or imagined with the modern evolutionary synthesis do not mean that common descent is false or that special creationism magically becomes real reflects the amount of times these elementary mistakes are made by special creationists. Burges alas is no different, failing both to grasp the difference between evolution as fact and evolution as theory, as well as peddling demonstrably false claims that it is 'mathematically impossible' for evolution to occur. 

Given that an evolutionary natural history has not been in doubt for well over a century, the burden of proof lies solely on Burges and other science denialists to show that the evidence for common descent is better explained by special creation, and given that the evidence for common descent is spread across multiple scientific disciplines ranging from biogeography to comparative genomics to palaeontology, that demands more than a few lines from secondary sources. Burges needs to demonstrate both familiarity with the primary literature, as well as evidence that he has discussed his antievolution arguments with a considerable number of eminent professionals.

This he has not done. Unsurprisingly, Burges does not make his claim exclusively from the primary literature, but credits an obscure special creationist technician with a background in molecular biology for advice [1], citing an extremist YEC website TrueOrigins (about as credible a source on evolution as Jack Chick's tracts are on soteriology) as well as leaning uncritically on arguments from ID apologist Michael Behe and the philosopher/mathematician John Lennox.

Burges appears to recognises that one of the difficulties plaguing discussion on evolution and creation is a failure to define terms properly, Unfortunately, he contributes to the problem by failing to grasp the essential difference between evolution as fact and evolution as theory, and peddling instead the tiresome special creationist  microevolution / macroevolution dichotomy. Inevitably, his argument degenerates into the usual special creationist errors:

• Microevolutionary change over time cannot effect large-scale evolutionary change
• The fossil record does not show a 'slow accumulation of many small changes'
• Evolution is mathematically impossible

All of these assertions are flat out wrong, and once again demonstrate Burges' lack of experience in the relevant fields.

Evolution as Fact and Theory

There is no excuse for special creationists failing to differentiate between evolution as fact and theory as this distinction was made by Darwin at least twice. Four years after the first edition of the Origin of Species was published, Darwin went out of his way to make this point clear:

Whether the naturalist believes in the views given by Lamarck, or Geoffroy St.-Hilaire, by the author of the ‘Vestiges,’ by Mr. Wallace and myself, or in any other such view, signifies extremely little in comparison with the admission that species have descended from other species and have not been created immutable; for he who admits this as a great truth has a wide field opened to him for further inquiry. [3]

This distinction was readily grasped by 19th century scientists, who as Darwin notes en passant, accepted the fact of evolution, but rejected natural selection, Darwin's proposed mechanism to explain how evolution occurred:

Some of those who admit the principle of evolution, but reject natural selection, seem to forget, when criticising my book, that I had the above two objects in view; hence if I have erred in giving to natural selection great power, which I am very far from admitting, or in having exaggerated its power, which is in itself probable, I have at least, as I hope, done good service in aiding to overthrow the dogma of separate creations. [3]

Since then, the evidence for common descent, which was compelling during Darwin's day has become overwhelming to the point that as Douglas Futuyma says:

Darwin provided abundant evidence for the historical reality of evolution—for descent, with modification, from common ancestors. Even in 1859, this idea had considerable support. Within about 15 years, all biological scientists except for a few diehards had accepted this hypothesis. Since then, hundreds of thousands of observations, from paleontology, biogeography, comparative anatomy, embryology, genetics, biochemistry, and molecular biology, have confirmed it. Like the heliocentric hypothesis of Copernicus, the hypothesis of descent with modification from common ancestors has long held the status of a scientific fact. No biologist today would think of publishing a paper on "new evidence for evolution," any more than a chemist would try to publish a demonstration that water is composed of hydrogen and oxygen. It simply hasn't been an issue in scientific circles for more than a century/ [4]

Burges' unawareness of this evidence does not make it go away.

Mathematical claims of Darwin's death are greatly exaggerated - Why Behe is wrong (again)

Burges relies heavily - and uncritically - on special creationist secondary sources in order to make his claim, rather than going to the trouble of actually going through the primary literature to make his case. One of his favourite sources is the ID biochemist Michael Behe, to whose obscure 2007 book The Edge of Evolution he appeals:

…the malaria parasite, with its enormous population size and rate of reproduction, together with a high level of genetic mutation, offers a clear test case of the possibilities of Darwinian evolution. Its acquiring of resistance to the drug chloroquine was possible because the huge numbers of generations eventually produced the required genetic mutations, which then spread by natural selection through the population; yet just one significant comparable change in the much smaller human population would require a period many times longer than the purported age of the universe. [5]

Anyone who reads The Edge of Evolution however will find out that Behe  accepts common descent, and makes his reasons for accepting it perfectly clear:

When two lineages share what appears to be an arbitrary genetic accident, the case for common descent becomes compelling, just as the case for plagiarism becomes overpowering when one writer makes the same unusual misspellings of another, within a copy of the same words. That sort of evidence is seen in the genomes of humans and chimpanzees. For examples, both humans and chimps have a broken copy of a gene that in other mammals helps make vitamin C As a result, neither humans nor chimps can make their own vitamin C. Of an ancestor of the two species originally sustained the mutation and then passed to both descendant species, that would neatly explain the situation. 

More compelling evidence of the shared ancestry of humans and other primates comes from their hemoglobin - not just their working haemoglobin, but a broken haemoglobin gene, too. In one region of our genomes humans have five genes for proteins that act at various stages of development (from embryo through adults) as the second (betalike) chain of haemoglobin. This includes the gene for the beta chain itself, two almost identical copies of a gamma chain (which occurs in fetal haemoglobin), and several others. Chimpanzees have the very same genes in the very same order. In the region between the two gamma genes and a gene that works after birth, human DNA contains a broken gene (called a "pseudogene") that closely resembles a working genre for a beta chain, but has features in its sequence that preclude it from coding successfully for a protein.  

Chimp DNA has a very similar pseudogene at the same position. The beginning of the human pseudogene has two particular changes in two nucleotide letters that seem to deactivate the gene. The chimp pseudogene has the exact shame changes A bit further down in the human pseudogene is a deletion mutation, where one particular letter is missing. For technical reasons, the deletion irrevocably messes up the gene's coding. The very same letter is missing in the chump gene. Towards the end of the human pseudogene another letter is missing. The chimp pseudogene is missing it too.  

The same mistakes in the same gene in the same positions of both human and chimp DNA. If a common ancestor first sustained the mutational mistakes band subsequently gave rise to these two modern species, that would very readily account for both why both species have them how. It's hard to imagine how there could be stronger evidence for common ancestry of chimps and humans.  

That strong evidence from the pseudogene points well beyond the ancestry of humans. Despite some remaining puzzles, there's no reason to doubt that Darwin had this point right, that all creatures on earth are biological relatives.  (Emphasis mine) [6]

What Behe rejects is not evolution as fact, but the currently accepted theoretical explanation for how evolution occurred, a position that puts him very much in the scientific minority. By failing to point out that Behe not only accepts that the genomic evidence for human-ape common ancestry, but expresses his belief that it is "hard to imagine how their could be stronger evidence for common ancestry of chimps and human" in the same book to which he appeals in an effort to bolster his assertion that evolution is impossible, Burges is seriously misleading his readers.

Burges also fails to inform his readers that Behe's 2007 book - and his claim that it is mathematically impossible for Darwinian evolution to generate a genetic change in humans comparable to the evolution of chloroquine resistance in malaria - have been comprehensively debunked by the mainstream scientific community. [7] Molecular biologist David Levin [8] points out that:

Behe’s thesis of evolutionary limits hangs on the assumption that important evolutionary steps require multiple simultaneous mutations without the benefit of cumulative selection. However, there is no evidence to support this claim. His error is evident even in his example of chloroquine resistance, which, by his logic, should not have involved evolutionary intermediates. But the scientific data say otherwise. The existence of natural isolates of malarial strains that possess one or the other of the supposedly critical mutations suggests not only that evolution of chloroquine resistance is a stepwise process, as has been argued by others, but that there are multiple mutational paths to resistance.

Levin points out a significant omission in one of Behe's examples of what he believes Darwinian evolution can do:

Under the heading of "What Darwinism Can Do," he describes the stepwise evolution of an antifreeze protein from a digestive enzyme in Antarctic fish. This was an important evolutionary adaptation that allowed fish that possess this protein to survive in frigid Antarctic waters. However, he omits an interesting detail from his description - the antifreeze protein has sugars added to it (by an enzyme), whereas the protein from which it evolved does not. Therefore, a new protein-to-protein interaction must also have evolved to allow modification of the antifreeze protein. In fact, this beautiful example of evolution involves the construction of significant complexity. [9]

To say that this undercuts Behe's assertion is something of an understatement. Evolutionary biologist Nick Matzke takes apart Behe's reasoning that multiple protein-protein binding site evolution is less probable than the double mutation resulting in the evolution of chloroquine resistance:

Here is the flabbergasting line of argument. First, Behe admits that CQR evolves naturally, but contends that it requires a highly improbable simultaneous double mutation, occurring in only 1 in 10^20 parasites. Second, Behe asserts that protein-protein binding sites require several simultaneous point mutations and are therefore even less probable than the alleged double-mutant CQR. Behe’s last step is to square 10^20 to produce 10^40, the number of organisms required to evolve two binding sites linking three proteins. Since fewer organisms than this are available in Earth’s history, any complex of three or more proteins is beyond the reach of mutations not guided by ID. 

The argument collapses at every step. Behe obtains the crucial 10^20 number from an offhand estimate in the literature that considered only the few CQR alleles that have been detected because they have taken over regional populations. What is needed, however, is an estimate of how often any weak-but-selectable CQR originates. A study conducted where CQR is actively evolving shows that high-level CQR is actually more complex than two substitutions, but that it is preceded by CQR alleles having fewer substitutions, and Behe’s two mutations do not even always co-occur. As a result CQR is both more complex and vastly more probable than Behe thinks. This sinks Behe’s 1 in 10^20 estimate for CQR, as well as his notion that protein-protein binding sites are more complex and therefore less probable than CQR. Behe’s decision to square the probability for two binding sites depends on the assumption that two binding sites would have to evolve at once, but the assumption is false for the same reasons that Behe’s “irreducible complexity” argument failed in the first place. The squaring assumption is further contradicted by any experiment that accidentally evolves two proteins binding to different sites on a target protein instead of just one. [10]

Behe's argument that the evolution of chloroquine is the edge of Darwinian evolution as Matzke points ouit is blown apart by the fact that the evolution of chloroquine resistance is "both more complex and vastly more probable than Behe thinks." Any argument based on CQR being the edge of evolution falls apart.

Sean Carroll, professor of molecular biology at the University of Wisconsin-Madison, and vice president for science education at the Howard Hughes Medical Institute points out two fundamental errors Behe makes. The first is to minimimise "the power of natural selection to act cumulatively as traits or molecules evolve stepwise from one state to another via intermediates." This as Carroll points out betrays an astonishing ignorance of evolution:

Behe begrudgingly allows that only “rarely, several mutations can sequentially add to each other to improve an organism's chances of survival.” Rarely? This, of course, is the everyday stuff of evolution. Examples of cumulative selection changing multiple sites in evolving proteins include tetrodotoxin resistance in snakes (3, the tuning of color vision in animals (4), cefotaxime antibiotic resistance in bacteria (5), and pyrimethamine resistance in malarial parasites (6)—a notable omission given Behe's extensive discussion of malarial drug resistance. 

Behe seems to lack any appreciation of the quantitative dimensions of molecular and trait evolution. He appears to think of the functional features of proteins in qualitative terms, as if binding or catalysis were all or nothing rather than a broad spectrum of affinities or rates. Therefore, he does not grasp the fundamental reality of a mutational path that proteins follow in evolving new properties.

The second blunder Behe makes arises from a flawed understanding of what is needed for the evolution of protein site interactions:

This lack of quantitative thinking underlies a second, fatal blunder resulting from the mistaken assumptions Behe makes about protein interactions. The author has long been concerned about protein complexes and how they could or, rather, could not evolve. He argues that the generation of a single new protein-protein binding site is extremely improbable and that complexes of just three different proteins “are beyond the edge of evolution.” But Behe bases his arguments on unfounded requirements for protein interactions. He insists, based on consideration of just one type of protein structure (the combining sites of antibodies), that five or six positions must change at once in order to make a good fit between proteins—and, therefore, good fits are impossible to evolve. An immense body of experimental data directly refutes this claim. There are dozens of well-studied families of cellular proteins (kinases, phosphatases, proteases, adaptor proteins, sumoylation enzymes, etc.) that recognize short linear peptide motifs in which only two or three amino acid residues are critical for functional activity [reviewed in (7–9)]. Thousands of such reversible interactions establish the protein networks that govern cellular physiology. 

Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given two-amino acid motif is likely to occur at random in every protein in a cell. (There are 399 dipeptide motifs in a 400-amino acid protein and 20 × 20 = 400 possible dipeptide motifs.) Any specific three-amino acid motif will occur once at random in every 20 proteins and any four-amino acid motif will occur once in every 400 proteins. That means that, without any new mutations or natural selection, many sequences that are identical or close matches to many interaction motifs already exist. New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction (9). Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes. Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution. [11]

Ian Musgrave, molecular pharmacologist at the University of Adelaide takes aim at Behe's failure to recognise that complex protein-protein interactions can evolve, as well as his implicit assertion that these complex protein-protein interactions evolved at once:

Behe claims that for even a simple binding site composed of two amino acids in specific locations that you would need a population of around 10^20 organisms to evolve it. Since for large organisms, such as humans, whales, wildebeests and wolverines, this is many orders of magnitude larger than the total population of these organisms over their entire history on this planet, Behe claims we cannot have developed many protein-protein binding sites by natural means. Yet our cells have over 10,000 protein-protein binding sites! Thus, Behe says, multisubunit protein complexes must be the work of a (unknown) designer.

Let’s just stand back for a moment and quickly summarise Behe’s claims:

1) Protein-protein binding sites must be produced by multiple, simultaneous mutations in a specific sequence. 

2) There are lots and lots of protein-protein binding sites in modern organisms, far more than could be produced during the lifetime of any given species.

To take the second claim first, note the slight of hand involved. Humans do have lots of protein-protein binding sites, but we didn’t develop them de novo. The vast majority we inherited from our common ancestor with the chimpanzees. That hominid in turn inherited most of its protein binding sites from its ancestors, and so on. Indeed, the majority of the most impressive protein-protein complexes evolved in single celled organisms over hundreds of millions, if not billions, of years. The populations of these organisms far exceed the measly 10^20 that Behe invokes. But reading “EoE” Behe certainly gives the impression that all these protein-protein complexes must have evolved relatively recently, without a deep history. Take the proteasome, it didn’t evolve in some slow reproducing, lumbering multicellular organism, it evolved in bacteria back in the deep Precambrian. For someone who claims that he accepts evolution and natural selection, Behe certainly ignores it when considering protein-protein binding.

Behe's acceptance of common descent makes his blunder here even harder to fathom as he would realise that many of these protein-protein binding sites were inherited, rather than evolved de-novo. Furthermore, as Musgrave notes, we have evidence that important protein-protein interactions have evolved with only one mutation occurring:

This paper was looking at the basis of the binding of bovine seminal ribonuclease. Ribonuclease is an enzyme that, as its name suggests, breaks down ribonucleaic acid. These enzymes are typically monomers, but bovine seminal ribonculease is a modified duplicate of standard ribonuclease which is a dimer. The question that researchers were interested in was which mutations were responsible for binding. At stake was a particular model of how proteins bind to each other. To explain this, I have to briefly diverge into a discussion of protein folding. 

When proteins are synthesized in a cell, they have to fold up into their final, three dimensional shapes. In this process, loops on the protein chain fit into pockets in the protein chain. Sound familiar? It’s the same process the produces protein-protein binding. One of the simplest ways for two proteins to bind to each other is if the loop of one binds into the pocket of the other (see the diagram). You can see that it would be very simple to set this up. In the end the researchers found there were multiple ways to get ribonulcease to dimerise. One mutation was all it took. So we have evidence that in nature, single mutations are all it takes to produce important protein-protein complexes. And we have had this evidence for sometime. Why didn’t Behe address this?

Exactly. Behe forgets that many of these protein-protein sits not only would have been inherited from ancestors (a fact he implicitly acknowledges given his acceptance of common descent), and ignores that complex interactions can evolved from only single binding suite mutation. Musgrave concludes:

Behe claims that there are a huge number of protein-protein binding sites, and that even one protein-protein binding site is extraordinarily difficult to evolve. However Behe greatly overestimates the difficulty of developing a binding site, ignores the fact that the majority of 10,000 binding sites in modern vertebrates are duplicate copies of each other, with there being only a much smaller number of basic binding motifs and ignores the fact that most of these basic binding motifs were developed in rapidly dividing single celled organisms with very large populations. 

Far from protein-protein binding pointing to an unknown designer, protein binding sites point directly to descent with modification and the “tinkering” of natural selection. [12]

One of Behe's assertions in Edge of Evolution - the impossibility of the evolution of carbapenem resistance was already two years out of date when the book was published. Behe asserted:

Recently, former University of Rochester microbiologist Barry Hall examined various antibiotics in a class called "carbapenems" which are chemically similar to penicillin. With unusual clarity of thought on the topic of evolution, Hall wrote, "Instead of assuming that [the chief kind of enzyme that might destroy these antibiotics] will evolve rapidly, it would be highly desirable to accurately predict their evolution in response to carbapenem selection" (emphasis added). Using clear lab techniques he invented, he showed that, although most of the antibiotics quickly failed, one didn't. The reason is that neither single nor double point mutations to the enzyme allowed it to destroy the certain antibiotic (called "imipenem"). Wrote Hall, "The results predict, with > 99.9% confidence, that even under intense selection the [enzyme] will not evolve to confer increased resistance to imipenem." In other words, more than two evolutionary steps would have to be skipped to achieve resistance, effectively ruling out Darwinian evolution." [13]

What Behe forgot to tell his readers is that moderate to high level carbapebem resistance was first detected in 2001, six years before his book was published. [14] Carbapenem-resistance Enterobacteriaceae are now a major clinical problem with one report showing they can contribute to mortality in  up to 50% in those those infected.  Behe it seems was flat-out wrong, and had been so well before his book was published.

Finally, it is worth noting that Edge of Evolution was instrumental in deconverting geneticist and Evangelical Christian Dennis Venema (of BioLogos fame) from intelligent design during his graduate student days:

As I had decided, I intended to start my research by reading Behe’s then-new book Edge of Evolution (EoE). I wanted to give the ID movement a fair chance to make its best case before I looked into the evidence for evolution. I checked with my pro-ID colleague down the hall, and sure enough he had a copy I could borrow. I poured myself a cup of coffee, closed my office door, readied note pad and paper, and settled in. 

To this day I wish I could have recorded myself reading those opening chapters of EoE. It was not long before the first suggestion of a frown would appear. Not many pages hence the frown would deepen into a furrow. I could hardly believe what I was reading: where was the Behe of Darwin’s Black Box that had so captivated me years ago? Though it is not polite to recount it (and I want to be clear that I hold no animosity towards Dr. Behe, but merely want to share my initial reaction) I clearly recall putting EoE down on my desk thinking, “What is this?” I was shocked: I had fully expected to once again be amazed and amused watching Behe take evolution down a peg or two. Yet here I was, knowing virtually nothing of evolution, and already I was seeing nothing but holes in Behe’s argument. Later on, when Behe began to discuss a topic I was familiar with (population genetics) I confirmed what I suspected: Behe was out of his area of specialty and out of his depth. Later work would convince me that this pattern applied to the whole of the book and the core of Behe’s arguments. My note pad was filling up, but not with what I had expected. 

Before I had finished Edge of Evolution, I was done with ID. I would lose my faith in ID not by comparing it to the science of evolution, but by reading one of its leading proponents and evaluating his work on its own merits. ID, I decided, was an argument from analogy, ignorance and incredulity. I was looking for an argument from evidence. Due to an interesting set of circumstances, I was able to read Behe both as a credulous lay reader and as a skeptical trained scientist. Behe, I realized, hadn’t changed: I had changed, and what a difference it had made. (Emphasis mine) [15]

That professional, well-regarded biologists at the peak of their careers have faulted Behe's book is hardly surprising, but arguably the most devastating blow is that a young graduate student who entered graduate school as an anti-evolutionist with strong ID leanings found Behe's book to be the work of a man completely out of his depth, and ended up accepting evolution in no small part because of it. It speaks volumes of Burges' utter ignorance of biology and blinkered approach to the subject that he would even consider advancing a discredited book as evidence against evolution.

Evolutionary Innovation in E coli

Burges, like many special creationists fails to appreciate the impact that Richard Lenski's long-term evolutionary experiment has had on evolutionary biology, resulting in him pinning uninformed vacuous nonsense such as:

The ability of bacteria to acquire resistance to antibiotics is frequently cited as clear evidence of evolution. Yet the E. coli bacterium has been studied through more than 25,000 generations, equivalent to about one million years of human development, with no real innovative changes. [16]

Burges' source for this is mathematician (not biologist) John Lennox, who asserts:

More recent work on the E. coli bacterium backs this up. In this research no real innovative changes were observed through 25,000 generations of E. coli bacteria. Biochemist Michael Behe points out that now more than 30,000 generations of E. coli have been studied, equivalent to about a million human years, and the net result is that evolution has produced: ‘Mostly devolution. Although some marginal details of some systems have changed during that thirty thousand generations, the bacterium has repeatedly thrown away chunks of its genetic patrimony, including the ability to make some of the building blocks of RNA. Apparently throwing away sophisticated but costly molecular machinery saves the bacterium energy. Nothing of remotely similar elegance has been built. The lesson of E. coli is that it’s easier for evolution to break things than to make things.’ [17]

What Burges neglects to inform his readers (there is a pattern here, alas) is that Lennox is merely parroting what Behe says in Edge of Evolution. That Lennox relies on a book which has been comprehensively trashed by mainstream scientists hardly bodes well for Lennox's competence as an informed, credible commenter on evolutionary biology. [18]

The other reference to which Lennox appeals is a 1999 PNAS paper by Dimitri Papadopoulos et al that examined genomic evolution in a 10,000 generation E.coli experiment (not a 25,000 generation experiment as Lennox asserts.) Far from being a failure, as Papadopoulos et al note:

Our results demonstrate that these experimental populations of E. coli underwent rapid molecular evolution, leading to extensive changes in their genome structure, during ~4 years of adaptation to an environment in which they received nutrients every day. Divergence from the ancestor increased over time, as did genetic diversity within each population. The amounts of evolutionary divergence and genetic diversity were roughly similar to those seen after ~30 years of storage without any nutrient inputs. Therefore, we conclude that constant, long-term starvation was not necessary to either substantially restructure the genome or to maintain a high level of genetic diversity, contrary to previous suggestions. [19]

One of the co-authors of the Papadopoulos was Richard Lenski who has achieved considerable fame with his Long Term Evolutionary Experiment showed even more evolutionary innovation. As both Richard Lenski and the LTEE are hardly household names, some elaboration is needed.

Richard Lenski is an evolutionary biologist and professor of microbial ecology at Michigan State University. In 2006, Lenski was elected to the National Academy of Sciences, one of the highest honours bestowed on American scientists. Apart from his work in microbial evolution, he is also well-regarded in the field of digital evolution, in which evolution is simulated in a computer environment.

Lenski's purpose was not to 'evolve a new species of bacterium', though the experiment did result in the creation of two distinct populations of bacteria which differed from each other enough for the question of speciation to be raised. As respected science writer Carl Zimmer puts it:

If E. coli is defined as a species that can't eat citrate, does that mean that Lenski's team has witnessed the origin of a new species? The question is actually murkier than it seems, because the traditional concept of species doesn't fit bacteria very comfortably…In nature, E. coli swaps lots of genes with other species. In just the past 15 years or so, for example, one disease-causing strain of E. coli acquired hundreds of genes not found in closely related E. coli strains…Another hallmark of  E. coli is its ability to break down lactose, the sugar in milk. But several strains have lost the ability to break it down. (In fact, these strains were originally given a different name--Shigella--until scientists realized that they were just weird strains of E. coli.) 

Nevertheless, Lenski and his colleagues have witnessed a significant change. And their new paper makes clear that just because the odds of such a significant change are incredibly rare doesn't mean that it can't happen. Natural selection, in fact, ensures that sometimes it does. And, finally, it demonstrates that after twenty years, Lenski's invisible dynasty still has some surprises in store. [20]

Lenski's purpose [21] in creating the LTEE was to:

1. Examine the dynamics of evolutionary change to see whether it is exclusively gradual, or shows bursts of rapid change even if the environment remains unchanged.
2. See whether evolutionary outcomes are contingent on previous events, or whether evolutionary outcomes are repeatable if one could rewind time and start again.
3. Out together the results on genetic and phenotypic changes to see if patterns of change in the genetic data are concordant with phenotypic change.

The short generation time of bacteria allowed Lenski and his team to examine evolutionary change over tens of thousands of generations - something simply not possible in animal or plant species within the professional life of a single researcher. Finally, as Lenski says, bacteria had been largely ignored by evolutionary biologists:

"Yet, until recently bacteria have been largely ignored by evolutionary biologists, who perhaps regarded them as tools of molecular biology and lacking in the obviously colourful phenotypes of many plants and animals. The importance of bacteria in nature, along with their very different genetic systems, combine to make them an interesting area for evolutionary research. [22]

Lenski's set up his experiment in 1988 by creating 12 identical lines of E. coli, and placing each in a solution containing glucose, which the bacteria would use as food. Each day, 1% of each population was transferred to a new container, with the remaining population discarded. Every 500 generations, samples of each population were frozen to act as a 'fossil record', allowing Lenski to effectively go back in time and compare ancient and modern bacterial lines. In addition, the bacterial lines were regularly examined to determine their genetic fitness among other tests.

Initially, each line increased its mean fitness with respect to the ancestral strain; these gains eventually levelled off at around the 20,000 generation mark. At approximately the 33,000th generation, one of the strains evolved the ability to use citrate (a chemical substance also included in the growth medium) as a source of energy, and increased in size considerably.

Population expansion during evolution of the Cit+ phenotype. Samples frozen at various times in the history of population Ara-3 were revived, and three DM25 cultures were established for each generation. Optical density (OD) at 420 nm was measured for each culture at 24 h. Error bars show the range of three values measured for each generation.(Blount et al. PNAS 2008)

This was significant for two reasons. The first is its inability to utilise citrate as a source of energy under oxic conditions:

Throughout the duration of the LTEE, there has existed an ecological opportunity in the form of an abundant, but unused, resource. DM25 medium contains not only glucose, but also citrate at a high concentration. The inability to use citrate as an energy source under oxic conditions has long been a defining characteristic of E. coli as a species. [23]

This of course raises the question of whether the strain of E coli that evolved the ability to metabolise citrate under oxic conditions is a new species, and as Carl Zimmer noted earlier, this is not a clear-cut question to answer. Lenski et al however point out that two distinct bacterial populations emerged after the evolutionary vent; one that could now metabolise citrate under oxic conditions, and the other which continued as an exclusive glucose metaboliser:

The origin of the Cit+ function also had profound consequences for the ecology and subsequent evolution of that population. This new capacity was refined over the next 2,000 generations, leading to a massive population expansion as the Cit+ cells evolved to exploit more efficiently the abundant citrate in their environment. Although the Cit+ cells continued to use glucose, they did not drive the Cit- subpopulation extinct because the Cit- cells were superior competitors for glucose. Thus, the overall diversity increased as one population gave rise evolutionarily to an ecological community with two members, one a resource specialist and the other a generalist. [24]

Lenski and his colleagues explicitly address the question of speciation towards the end of their paper:

Will the Cit+ and Cit- lineages eventually become distinct species? According to the biological species concept widely used for animals and plants, species are recognized by reproductive continuity within species and reproductive barriers leading to genetic isolation between species. Although the bacteria in the LTEE are strictly asexual, we can nonetheless imagine testing this criterion by producing recombinant genotypes. In particular, we could move mutations that are substituted in the evolving Cit+ lineage into a Cit- background to test whether they reduce fitness in their ancestral context. One could also perform the reciprocal experiment, although we anticipate more rapid evolution in the Cit+ lineage because it has acquired a key innovation that substantially changed its ecological niche. Such experiments would require, of course, controls to examine the fitness effects of the same mutations in the lineage where they arose. If the Cit+ lineage is indeed evolving into a new species, then we expect, with time, that more and more of the beneficial mutations substituted in that lineage would be detrimental in the ecological and genetic context of its Cit- progenitor. [25]

By far the more significant aspect of the LTEE is the way in which E. coli evolved the ability to metabolise citrate under oxic conditions. Did it evolve through an unusually rare mutation, or did it require an initial mutation which 'primed' that line for another mutation which permitted the evolution of citrate metabolism under oxic conditions? This is where the frozen samples were invaluable in that one could effectively go back in time, and regrow samples of bacteria from previous generations, and see whether only those after a certain generation would evolve the ability to metabolise citrate under oxic conditions, as one would expect if a potentiating mutation was needed.

Alternative hypotheses for the origin of the Cit+ function. According to the rare-mutation hypothesis, the probability of mutation from Cit− to Cit+ was low but constant over time. Under the historical-contingency hypothesis, the probability of this transition increased when a mutation arose that produced a genetic background with a higher mutation rate to Cit+. (Blount et al. PNAS 2008)

Lenski performed three replay experiments to test the hypotheses, and the results showed that Cit+ mutants evolved more often from later generations (around the 20,000 generation mark):

These analyses compel us to reject the hypothesis that a rare mutation could have produced a Cit+ variant with equal probability at any point in the LTEE. Some unusually rare mutation might be involved, but its rarity does not provide a sufficient explanation for the unique and exceptionally slow evolution of this new function during the LTEE. Our results instead support the hypothesis of historical contingency, in which a genetic background arose that had an increased potential to evolve the Cit+ phenotype. [26]

It is the way in which this new function evolved in E. coli which has produced no little excitement in the evolutionary biology community. In pragmatic terms, what we have seen is not inconsistent with incipient speciation. Lenski notes:

The citrate-eaters still eat glucose, but they aren’t quite as successful at competing for that sugar as they were before. As a consequence of that tradeoff, their cousins persist as glucose specialists. So the bacteria in this simple flask- world have split into two lineages that coexist by exploiting their common environment in different ways. And one of the lineages makes its living by doing something brand-new, something that its ancestor could not do. 

That sounds a lot like the origin of species to me. [27]

Returning to the main subject - the role of contingency in evolution, another aspect of this experiment is that it has the potential to show why some animals change, whereas others have remained relatively stable over millions of years. This is a point that Massimo Pigliucci, an evolutionary biologist who specialises in evolvability makes:

Dr. Pigliucci said that evolvability could explain a number of important patterns in nature, like why some animals come in many different forms while their close relatives have not changed much in hundreds of millions of years. That would mean that evolvability would need to be present in the generation-by-generation struggle for survival. And Dr.Lenski’s experiment documents that it can indeed make a difference for real organisms. [28]

If we return to Lennox's assertion that "no real innovative changes were observed through 25,000 generations of E. coli bacteria" it becomes clear that after 33,000 generations, a major innovation, analogous to speciation occurred. One is left wondering why Burges never once referred to this.

As a coda to the LTEE, I'll mention a recent paper  by Justin Meyer, one of Lenski's doctoral students, who has shown how viruses can evolve completely novel ways to infect bacteria:

The standard way for lambda to get into a cell is to latch onto its outer membrane, attaching to a particular kind of molecule on the surface of E. coli. It can then inject its genes and proteins into the microbe. 

Mr. Meyer set up an experiment in which E. coli made almost none of the molecules that the virus grabs onto. Now few of the viruses could get into the bacteria. Any mutations that allowed a virus to use a different surface molecule to get in would make it much more successful than its fellow viruses. “It would have a feast of E. coli,” Dr. Lenski said. 

The scientists found that in just 15 days, there were viruses using a new molecule — a channel in E. coli known as OmpF. Lambda viruses had never been reported to use OmpF before.

Mr. Meyer was surprised not just by how fast the change happened, but that it happened at all. “I thought it would be a wild goose chase,” he said. 

To see if this result was just a fluke, Mr. Meyer ran his experiment again, this time with 96 separate lines. The viruses in 24 of the lines evolved to use OmpF.

The researchers sequenced the genomes of the evolved viruses and were surprised to find that this transformation always required four mutations. In all the lines that could grab OmpF, those four mutations were identical, or nearly so. No single mutation could allow the viruses to start latching onto OmpF. Even three out of four mutations brought no change. Only after they developed all four mutations could the viruses make the switch. 

The results suggest the mutations help the viruses do a better job of hooking onto the original molecules after they became scarce. “When you put all four together, you get this entirely new function,” Mr. Meyer said...

The chances that a single virus would acquire so many mutations at once are certainly small. In the case of lambda viruses, Mr. Meyer estimates the chance of all four mutations arising at once is roughly one in a thousand trillion trillion. 

Yet the lambda viruses repeatedly acquired all four mutations in a matter of weeks. “There’s this thinking that it all has to come together at once,” Dr. Lenski said. “But that’s just not how evolution works.” (Emphasis mine) [29]

The significance of Lenski's comments on the evolution of four mutations at once in a matter of weeks again shows that Behe's comments about the alleged 'edge of evolution' are pure nonsense. They also once again show that Burges is hopelessly out of his depth in this subject.

Conclusion

Burges like almost all special creationists has perpetuated the inaccurate division of evolution into 'microevolution' and 'macroevolution', and recited the long-rebutted assertion that it is 'mathematically impossible' for microevolution to produce macroevolutionary change. Burges' main problem of course is failing to differentiate evolution properly: evolution is both fact and theory. The evidence for common descent has been regarded as overwhelming for well over a century, with contemporary research looking at how evolution occurs, rather than if it has occurred. That is simply no longer an issue.

Burges leans uncritically on a discredited book by ID biochemist Michael Behe as well as a recent book by mathematician / philosopher John Lennox who also relies uncritically on the same work by Behe, meaning Burges' list of recognised authorities collapses back down to Behe, whose book as shown has been thoroughly rebutted by mainstream biologists.

Finally, Burges fails to inform his readers that Behe accepts common descent, and makes that point clear in the very book he cites as evidence against evolution.  Burges' failure to make any of this known to his readers indicates either a deliberate omission, or substandard research. Both options hardly reflect well on the credibility of his article.

References

1. Special creationists who claim that they are scientists forget that possession of an advanced degree alone does not make one a scientist. Outside of evolutionary biology, it is possible for a special creationist to contribute to scientific knowledge. However special creationists assume a priori that evolution is impossible based purely on a fundamentalist reading of the Bible which they privilege above all the evidence. When it comes to this subject, they have ceased behaving as scientists. Anyone who signs - or agrees with - the AiG statement of faith which specifically rejects all evidence that conflicts with their dogma has lost the right to call themselves a scientist.

2. Darwin CR. Letter: Origin of species. Athenaeum 9 May: 617; 1863.

3. Darwin C. The descent of man, and selection in relation to sex. (1871: London: John Murray)

4. Futuyma D Evolutionary Biology (1998: Sinauer) p 12

5. Burges D "Is Theistic Evolution Compatible With Faith in God's Word?" The Testimony (2014) 84:143-147

6. Behe M The Edge of Evolution: The Search for the Limits of Darwinism (2007: Free Press) p 71-72

7. This alas is similar to Burges' review of Behe's 1996 review of Darwin's Black Box which likewise was thoroughly trashed, a point about which Burges neglected to inform his readers. 

8.  Professor and Chair of the Department of Molecular and Cell Biology at Boston University's School of Dental Medicine

9. Levin DE "Review: The Edge of Evolution" Reports of the National Center for Science Education (2007) 27:38-40

10. Matzke NJ "The Edge of creationism" Trends in Ecology and Evolution (2007) 22:566-567

11. Carroll DB "God as Genetic Engineer" Science (2007) 316:1427-1428

12. Musgrave I "Behe versus ribonulease; the origin and evolution of protein-protein binding sites" Panda's Thumb April 13th 2008

13. Behe op cit p 236-237

14. Yigit H et al "Novel Carbapenem-Hydrolyzing β-Lactamase, KPC-1, from a Carbapenem-Resistant Strain of Klebsiella pneumoniae" Antimicrob Agents Chemother. 2001 45: 1151–1161

15. Venema D "From Intelligent Design to BioLogos, Part 4: Reading Behe" Science and the Sacred August 18th 2011

16. Burges op cit p 145

17. Lennox JC God's Undertaker: Has Science Buried God? (2009: Lion Hudson) p 110

18. Apart from uncritically leaning on Behe's discredited 2007 book Edge of Evolution, Lennox takes a leaf out of the YEC playbook by quote mining Gould and Eldredge on transitional fossils: "Stephen Jay Gould said, ‘The extreme rarity of transitional forms in the fossil record persists as the trade secret of palaeontology.’ His fellow palaeontologist, Niles Eldredge of the American Museum of Natural History, adds: ‘When we do see the introduction of evolutionary novelty, it usually shows up with a bang, and often with no firm evidence that the fossils did not evolve elsewhere. Evolution cannot forever be going on somewhere else. Yet that’s how the fossil record has struck many a forlorn palaeontologist looking to learn something about evolution.’" (p 114). 

The quote from Gould is a notorious quote mine, and its presence badly damages Lennox's credibility, as can be seen when the quote is taken in context: 

The extreme rarity of transitional forms in the fossil record persists as the trade secret of paleontology. The evolutionary trees that adorn our textbooks have data only at the tips and nodes of their branches; the rest is inference, however reasonable, not the evidence of fossils. Yet Darwin was so wedded to gradualism that he wagered his entire theory on a denial of this literal record:

The geological record is extremely imperfect and this fact will to a large extent explain why we do not find interminable varieties, connecting together all the extinct and existing forms of life by the finest graduated steps. He who rejects these views on the nature of the geological record, will rightly reject my whole theory.

Darwin's argument still persists as the favored escape of most paleontologists from the embarrassment of a record that seems to show so little of evolution [directly]. In exposing its cultural and methodological roots, I wish in no way to impugn the potential validity of gradualism (for all general views have similar roots). I only wish to point out that it is never "seen" in the rocks. 

Paleontologists have paid an exorbitant price for Darwin's argument. We fancy ourselves as the only true students of life's history, yet to preserve our favored account of evolution by natural selection we view our data as so bad that we never see the very process we profess to study. 

For several years, Niles Eldredge of the American Museum of Natural History and I have been advocating a resolution to this uncomfortable paradox. We believe that Huxley was right in his warning. The modern theory of evolution does not require gradual change. In fact, the operation of Darwinian processes should yield exactly what we see in the fossil record. It is gradualism we should reject, not Darwinism.

(Gould, S. J. 1980. "The Episodic Nature of Evolutionary Change" in The Panda's Thumb, pp. 179-185. New York: W. W. Norton & Company.)

In context, Gould clearly has no problems with the fossil record, and as he stated elsewhere, transitional fossils abound between larger groups:

Since we proposed punctuated equilibria to explain trends, it is infuriating to be quoted again and again by creationists -- whether through design or stupidity, I do not know -- as admitting that the fossil record includes no transitional forms. Transitional forms are generally lacking at the species level, but they are abundant between larger groups. 

Gould, SJ "Evolution as Fact and Theory" in Hens Teeth and Horse's Toes: Further Reflections in Natural History. (1983: New York: W. W. Norton & Co)  p. 258-260.

To say that such quote mining undermines Lennox's credibility is hardly an overstatement.

19. Papadopoulos D et al "Genomic evolution during a 10,000-generation experiment with bacteria" Proc. Natl. Acad. Sci. USA (1999) 96:3807-3812

20. Zimmer C "A New Step in Evolution" The Loom June 2nd 2008 

21. Lenski, Richard E. (2003). Janick, Jules. ed. "Phenotypic and Genomic Evolution during a 20,000-Generation Experiment with the Bacterium Escherichia coli" Plant Breeding Reviews (New York: Wiley) 24 (2): 225–65

22. ibid, p 229

23. Blount, Z.D, Borland C.Z., Lenski R.E. "Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli" Proc. Natl. Acad. Sci. USA (2008) 105:7899-7906

24. ibid, p 7904

25. ibid, p 7905

26. ibid, p 7902-3

27. Lenski R.E. "Evolution in Action: a 50,000-Geneation Salute to Charles Darwin" Microbe (2011) 6:30-33

28. Zimmer C "Tortoise and Hare, in a Laboratory Flask" The New York Times March 21 2011 

29. Zimmer C "Study Finds Virus to be Fast Learner on Infecting" The New York Times January 26 2012