On the Evolution of Citrate Use

Those who follow the long-term evolution experiment (LTEE) with E. coli know that the most dramatic change we have observed to date is the origin of the new ability to grow on citrate. It’s dramatic for several reasons including the fact (external to the LTEE) that E. coli has been historically defined as a species based in part on its inability to grow on citrate in oxic environments and the fact (internal to the LTEE) that it was so difficult for the bacteria to evolve this ability that only one of the populations did so, and that it took over 30,000 generations even though an abundance of citrate has been present in the medium throughout the LTEE. Even after 64,000 generations, only the Ara–3 population has evolved that new ability.

Zachary Blount, formerly a graduate student and now a postdoc in my lab, has spent the last decade studying the evolution of this population and its new ability. His two first-authored papers in PNAS (2008) and Nature (2012) demonstrated, respectively, that (i) the origin of the ability to grow on citrate in the LTEE was contingent on one or more “potentiating” mutations that happened before the “actualizing” mutation that conferred the new function first appeared, and (ii) the actualizing mutation was a physical rearrangement of the DNA that brought together a structural gene, citT, that encodes a transporter and a previously unconnected regulatory region to generate a new module that caused the phenotypic transition to Cit⁺. These papers presented and discussed much more than these two points, of course, but they are the key findings. More recently, Zack was a coauthor on a paper in eLife (2015) by Erik Quandt, Jeff Barrick, and others that identified two mutations in the gene for citrate synthase—one that potentiated the evolution of citrate utilization, and another that subsequently refined that new function.

So we were keenly interested when we saw a new paper titled “Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA” by Dustin Van Hofwegen, Carolyn Hovde, and Scott Minnich. The paper is posted online as an accepted manuscript by the Journal of Bacteriology. What follows here are some overall impressions of their paper that Zack and I put together. We may follow these impressions later with some further analysis and comments.

* * * * *

Let’s begin by saying that it’s great to see other groups working on interesting systems and problems like the evolution of citrate utilization in E. coli.

Moreover, the actual science that was done and reported looks fine and interesting, though we have a few quibbles with some details that we will overlook for now. By and large, the work confirms many of the findings that were reported in our papers cited above:

(i) the ability to grow on citrate in the presence of oxygen can and does evolve in E. coli (Blount et al., 2008);

(ii) when aerobic growth on citrate evolves, it does not do so quickly and easily (Blount et al., 2008) but instead takes weeks or longer—more on that below;

(iii) all strains that have evolved this new ability have physical rearrangements that involve the citT gene and appear also to involve a so-called “promoter capture” whereby a copy of this transporter-encoding gene acquires a new upstream regulatory region (Blount et al., 2012); and

(iv) genetic context matters—the strain one uses affects the likelihood of evolving the Cit⁺ function (Blount et al., 2008) and the resulting ability to grow on citrate (Blount et al., 2012; Quandt et al., 2015).

The problem, then, is not with the experiments and data. Rather, the problem is that the results are wrapped in interpretations that are, in our view, flawed and fallacious.

“No new genetic information”

The authors assert repeatedly (last sentence of their Importance statement, and first and last paragraphs of their Discussion) that “no new genetic information evolved.” However, that statement flatly contradicts the fact that in their experiments, and ours, E. coli gained the new ability to grow on citrate in the presence of oxygen. We would further add (which we have not emphasized before) that these Cit⁺ strains can grow on citrate as a sole carbon source—when E. coli grows anaerobically on citrate, it requires a second substrate for growth in order to use the citrate (a phenomenon called “co-metabolism”).

The claim that “no new genetic information evolved” is based on the fact that the bacteria gained this new ability by rearranging existing structural and regulatory genetic elements. But that’s like saying a new book—say, Darwin’s Origin of Species when it first appeared in 1859—contains no new information, because the text has the same old letters and words that are found in other books.

In an evolutionary context, a genome encodes not just proteins and patterns of expression, but information about the environments where an organism’s ancestors have lived and how to survive and reproduce in those environments by having useful proteins, expressing them under appropriate conditions (but not others), and so on. So when natural selection—that is, differential survival and reproduction—favors bacteria whose genomes have mutations that enable them to grow on citrate, those mutations most certainly provide new and useful information to the bacteria.

That’s how evolution works—it’s not as though new genes and functions somehow appear out of thin air. As the bacterial geneticist and Nobel laureate François Jacob wrote (Science, 1977): “[N]atural selection does not work as an engineer works. It works like a tinkerer—a tinkerer who does not know exactly what he is going to produce but uses whatever he finds around him, whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a tinkerer who uses everything at his disposal to produce some kind of workable object.”

To say there’s no new genetic information when a new function has evolved (or even when an existing function has improved) is a red herring that is promulgated by the opponents of evolutionary science. In this regard, it seems relevant to point out that the corresponding author, Scott Minnich, is a fellow of the Discovery Institute and was an expert witness for the losing side that wanted to allow the teaching of “intelligent design” as an alternative to evolution in public schools in the landmark Kitzmiller v. Dover case.

“Rapid evolution of citrate utilization”

In the title of their paper and throughout, Van Hofwegen et al. emphasize that, in their experiments, E. coli evolved the ability to grow aerobically on citrate much faster than the 30,000 generations and ~15 years that it took in the LTEE. That’s true, but it also obscures three points. First, we already demonstrated in replay experiments that, in the right genetic background and by plating on minimal-citrate agar, Cit⁺ mutants sometimes arose in a matter of weeks (Blount et al. 2008). Second, rapid evolution of citrate utilization—or any evolution of that function—was not a goal of the LTEE. So while it is interesting that Van Hofwegen et al. have identified genetic contexts and ecological conditions that accelerate the emergence of citrate utilization (as did Blount et al., 2008), that in no way undermines the slowness and rarity of the evolution of this function in the context of the LTEE (or, for that matter, the rarity of Cit⁺ E. coli in nature and in the lab prior to our work). Third, the fastest time that Van Hofwegen et al. saw for the Cit⁺ function to emerge was 19 days (from their Table 1), and in most cases it took a month or two. While that’s a lot faster than 15 years, it’s still much longer than typical “direct selections” used by microbiologists where a readily accessible mutation might confer, for example, resistance to an antibiotic after a day or two.

So while we commend the authors’ patience, we do not think the fact that their experiments produced Cit⁺ bacteria faster than did the LTEE is particularly important, especially since that was not a goal of the LTEE (and since we also produced them much faster in replay experiments). However, in a manner that again suggests an ulterior nonscientific motive, they try to undermine the LTEE as an exemplar of evolution. The final sentence of their paper reads: “A more accurate, albeit controversial, interpretation of the LTEE is that E. coli’s capacity to evolve is more limited than currently assumed.” Alas, their conclusion makes no logical sense. If under the right circumstances the evolution of citrate utilization is more rapid than it is in the LTEE, then that means that E. coli’s capacity to evolve is more powerful—not more limited—than assumed.

“Speciation Event”

To us, one of the most interesting facets of the evolution of the citrate-using E. coli in the LTEE is its implications for our understanding of the evolutionary processes by which new species arise. Part of the reason for this interest—and the one that’s most easily stated in a popular context—is that the inability to grow on citrate is part of the historical definition for E. coli as a species, going back almost a century. But the deeper interest to us lies not in labeling a new species or debating where to draw the line between species—various criteria are used by different scientists, and inevitably there are many cases that lie in grey areas. Rather, as evolutionary biologists, we are most interested in the process of speciation—the ecological and genetic dynamics that lead to changing biological forms that, over time, are more and more like a new species until, eventually, perhaps far in the future, there is no doubt that a new species has evolved.

In short, speciation is not an event. As Ptacek and Hankison (2009, in Evolution: The First Four Billion Years) put it, “[S]peciation is a series of processes, with a beginning stage of initial divergence, a middle stage wherein species-specific characteristics are refined by various forces of evolution, and an end point at which a new species becomes a completely separate evolutionary lineage on its own trajectory of evolutionary change with the potential for extinction or further diversification into new lineages.” We realize that scientists (ourselves included) often use shorthand and jargon instead of writing more carefully and precisely. We have no doubt that one can find solid scientific papers that talk about speciation events; but except for cases that involve hybridization leading to polyploids that are reproductively isolated in a single generation (as sometimes occurs in plants), this is simply an imprecise shorthand.

In our first paper on the citrate-using E. coli that arose in the LTEE, we clearly emphasized that becoming Cit⁺ was only a first step on the road to possible speciation (Blount et al., 2008). One criterion that many biologists would apply to investigate speciation is whether a later form merely replaced an earlier form (evolution without speciation) or, alternatively, one lineage split into two lineages that then coexisted (incipient speciation). In fact, we showed that, after the new function evolved, the Cit⁺ and Cit^– lineages coexisted (and their coexistence was confirmed using genomic data in Blount et al., 2012). We concluded the 2008 paper by asking explicitly: “Will the Cit+ and Cit– lineages eventually become distinct species?” (emphasis added) and discussing how we might assess their ongoing divergence.

By contrast, Van Hofwegen et al. dismiss the idea of speciation out of hand, not only by calling it an event but by treating the issue as though it hinges, literally, on the individual mutations that produced a Cit⁺ cell. For example, they write: “[B]ecause this adaptation did not generate any new genetic information … generation of E. coli Cit⁺ phenotypes in our estimation do not warrant consideration as a speciation event.” And in the penultimate sentence of their paper, they say: “[W]e argue that this is not speciation any more than any other regulatory mutant of E. coli.” (We also note that this is a rather bizarre generalization, as though the gain of function that gave access to a new resource is equal in regards to its speciation potential to, say, the loss of regulation of a function that is no longer used by a lineage in its current environment. Both might well be adaptations, but one seems much more likely to begin the process of speciation.)

In conclusion, Van Hofwegen, Hovde, and Minnich have done some interesting experiments that shed further light on the nature of the mutations and ecological conditions that allow E. coli cells to evolve the ability to grow aerobically on citrate, a function that this species cannot ordinarily perform. However, they misunderstand and/or misrepresent the relevance of this system for evolutionary biology in several important respects. 

And the meaning of historical contingency

The paper by Hofwegen et al. is accompanied by a commentary by John Roth and Sophie Maisnier-Patin. Their abstract begins: “Van Hofwegen et al. demonstrate that E. coli rapidly evolves ability to use citrate when long selective periods are provided. This contrasts with the extreme delay (15 years of daily transfers) seen in the long-term evolution experiments of Lenski and coworkers. Their idea of ‘historical contingency’ may require reinterpretation.”

Historical contingency is a complicated notion, but it essentially means that history matters. In Blount et al. (2008), we made it clear what we mean by historical contingency in the context of the evolution of the Cit⁺ lineage in one of the LTEE populations. Was this an extremely rare event that could have happened at any time? Or did it instead depend on the occurrence of a sequence of events, a particular history, whereby an altered genetic context evolved—a potentiated background—in which this new function could now evolve?

Roth and Maisnier-Patin’s suggestion that our idea of “historical contingency” may require reinterpretation reflects a false dichotomy between historical contingency, on the one hand, and the effects of different selection schemes, on the other. The fact that evolution might be fast and not contingent on genetic background (though the evidence of Van Hofwegen et al. is, at best, ambiguous in this regard) in one set of circumstances has no bearing on whether it is contingent in another set of circumstances. The historical contingency of Cit⁺ evolution is not mere conjecture. We showed that the evolution of this new function in the LTEE was contingent. In replay experiments, Blount et al. (2008) showed that that the Cit⁺ trait arises more often in later-generation genetic backgrounds than in the ancestor or early-generation backgrounds. Moreover, Blount et al. (2012) performed genetic manipulations and showed that a high-copy-number plasmid carrying the evolved module that confers the Cit⁺ function had very different phenotypic effects when put in a Cit^– clone from the lineage within which Cit⁺ evolved than when placed in the ancestor or even other late-generation lineages not on the line of descent leading to the emergence of the Cit⁺ bacteria. In the clone on the line of descent, this module conferred strong, immediate, and consistent growth on citrate. In the other genetic backgrounds, growth on citrate was weak, delayed, and/or inconsistent.

The hypothesis of historical contingency is not mutually exclusive with respect to causal factors of an ecological or genetic nature—it simply says that factors that changed over time were important for the eventual emergence of Cit⁺. Moreover, historical contingency was invoked and demonstrated in a specific context, namely that of the emergence of Cit⁺ in the LTEE—it does not mean that the emergence of Cit⁺ is historically contingent in other experimental contexts, nor for that matter that other changes in the LTEE are historically contingent—in fact, some other evolved changes in the LTEE have been highly predictable and not (or at least not obviously) contingent on prior mutations in the populations (e.g., Woods et al., PNAS, 2006). [For more on historical contingency and the LTEE, you can download a preprint of Zack’s latest paper from his website: Blount, Z. D. A Case Study in Evolutionary Contingency. Studies in the History and Philosophy of Biology and Biomedical Sciences.]

Erik Quandt offers this analogy to illustrate our point that contingency depends on context: “It’s kind of like the difference between being an average person attempting to dunk a basketball when all by yourself, with unlimited time, and maybe even with a trampoline versus having to get to the rim in a game with LeBron James and the Cavs playing defense. Just because you can do it by yourself under optimal conditions, does this negate the difficulty of doing it in an NBA game or say anything about the kind of history (training and/or genetics) that you would need for that situation?”

* * * * *

Advertisement

Science Communication: Where Does the Problem Lie?

When concerns arise about the public’s understanding of science—say, on the efficacy of vaccines vs. their risks—I see many articles, tweets, etc., bemoaning poor scientific communication. Communication involves multiple parties and several steps. The science must be published, discussed widely, explained openly, and eventually stated in terms that non-specialists can understand. It also must be heard—and not merely heard, but fairly considered, carefully weighed, and then accepted, rejected, or put on hold by the intended receiver. That’s not all, of course. There are generally intermediaries—including teachers, reporters, doctors, business interests, politicians, religious leaders, and others—who must also convey the scientific information, but who may block, change, confuse, or distort the message either accidently or deliberately. And none of this is a one-way flow of information. There are multiple voices, and there are feedbacks as questions are asked, answered in new words or with new evidence, and so on. So it’s a complex problem, too complicated for a poll to shed much light. And of course, a poll here will get a highly non-random sample—mostly scientists, students, and others with an interest in science. But perhaps some professional pollster or organization interested in the communication of science can develop a proper poll along these lines (with information about a respondents’ professions, ages, affiliations, etc.), and with proposals about how to improve the situation at the various roadblocks. (Or maybe similar polls already exist. Please feel free to suggest useful references in the comments.) It might also be interesting to run the same poll except with prompts about different issues such as vaccinations, global change, and evolution. So here’s the poll: If you had to say, which one of the following groups shoulders the greatest blame, and thus has the greatest room for improvement, when it comes to the problems of communicating science?

• Scientists
• Professional intermediaries such as teachers, reporters, and doctors
• Other intermediaries such as businesses, politicians, and religious leaders
• The public

[The image below is from the British Council / BBC World Service site on teaching English. It is shown here under the doctrine of fair use.]

Zachary Blount on “Ham on Nye” Debate, Follow-up #3

I’m very pleased to present this guest post written by Dr. Zachary Blount, aka Dr. Citrate, as an in-depth follow-up to the “Ham on Nye” science versus creation debate.  Zack did his undergraduate studies at Georgia Tech, and then obtained a masters degree from the University of Cincinnati.  After that, he came to MSU, where he completed his Ph.D. in 2011.  With his doctoral work generating so many interesting results and new questions, Zack stayed on here as a postdoctoral researcher.  His current research is funded by a grant from the John Templeton Foundation Program on Foundational Questions in Evolutionary Biology.

Zack has devoted years to studying the evolution of the ability to grow on citrate that occurred in one of the 12 populations from the long-term evolution experiment (LTEE) with E. coli.  We still don’t fully understand all of the steps involved.  But a simple “on/off” switch it is not!

However, even if it had been a single, simple mutation that allowed the cells to grow on citrate, that still would have been evolution … it still would have been a beneficial mutation in the context of the experiment … and it would still have demonstrated the acquisition of new information encoded in the genomes of the bacteria that fits them to their environment.  Of course, if it were so easy as a single, simple mutation, then we would have seen that capability evolve in many or all of the populations. But after almost 60,000 generations to date, only one population has evolved that ability.

You can read about the technical details of our findings in two papers here and here, as well as in a recent paper from a team at the University of Texas, Austin.

In what follows, the nomenclature Cit⁺ refers to the bacteria that evolved the ability to grow on citrate in the presence of oxygen, while Cit^– refers to the bacteria – their ancestors and other E. coli – that lack that ability.

 — Richard Lenski

* * * * *

My work on the evolution of aerobic growth on citrate in one of the LTEE populations has received a fair amount of attention over the years.  (Sometimes there is a bit of a dream-like quality to it all.  I still have a hard time conceiving that people unknown to me know about what this here kid from north Georgia has done.)  The attention is rather gratifying because I’ve spent many years and a great deal of effort in school and in the lab to become an evolutionary biologist. But why did I do all that in the first place? Because I find evolution to be endlessly fascinating, beautiful, and even inspiring.

It means a lot to know that the work I spent several thousands of hours toiling away on has made a contribution to science.  Even more satisfying is that my work has come to be viewed as a go-to example of evolution in action that may, perhaps, inspire in others some of the same feelings that have motived me.

Of course, this attention has also been a bit troubling because it has led to repeated disparagement, dismissal, distortion, and misrepresentation of my work by both professional and amateur creationists.  These creationists often get entirely wrong the work my colleagues and I toiled long and hard to do, likely because they haven’t bothered to read our papers, learn the details and methods, or think much about the results.  (I suspect some duplicity is in there, too.)  Reflexive, unthinking dismissal bothers me – maybe because my parents and devoutly Southern Baptist Granny told me when I was a child that this is something that civilized folk simply should not do.

This brings me to the recent debate between the legendary science educator Bill Nye and the legendary obfuscator and anti-science showman Ken Ham.  It was the standard sort of set-up, with Nye defending evolution and science against creationism, and Ken Ham, well, doing what Ken Ham does.

Twice during the debate, Ham discussed my work with the LTEE population that evolved the capacity to grow aerobically on citrate.  The first time was at about 44 minutes, and included a video clip of Dr. Andrew Fabich, a “Biblical creationist” microbiologist at Liberty University.  [You can read the transcript here.]

The evolution of the new Cit⁺ function is, and has been discussed as, an instance of evolutionary innovation that arose in a controlled experiment in which we can drill down and figure out how it evolved. Ham and Fabich, however, dismissed Cit⁺ as an innovation or even an instance of evolution using two arguments suggesting that neither knows the work well at all and likely have not read our papers.  (In Ham’s case, this wouldn’t be surprising, as he has been called “willfully ignorant” even by other creationists, which is a bit like being called unkempt by Pig-Pen or in need of a haircut by Cousin Itt.  In Fabich’s case, however, it would betray a lack of professional courtesy, at best.)

First, Ham repeatedly said that some of the bacteria in the LTEE “seemed” to have developed the ability to grow on citrate.  This wording suggests either stupidity or duplicity on our part, as though we either didn’t check or just lied, but the fact of the matter is that there is no “seem” about it.  The Cit⁺ bacteria do grow on citrate, and they do so under conditions that E. coli normally does not.  This ability is something that is easy to demonstrate, and which I and my colleagues – not only in the Lenski lab but also other labs that are now working with these bacteria – have documented.  And it’s not as though we don’t have the evidence – as Rich has pointed out to another anti-evolution critic, we have many, many, many vials full of them in our freezers.

The second argument was more direct.  Both Ham and Fabich asserted that the Cit⁺ function did not evolve because using citrate did not involve “any kind of new information … it’s just a switch that gets turned on and off.”  (Fabich went on to state that this “switch” is what we reported.  That is emphatically not true.  It beggars belief that anyone, much less a trained microbiologist, could actually read our 2012 paper, where we reported the genetic basis of Cit⁺, and come away thinking this.) Variations on that wording are often used by creationists who discuss the citrate work because it implies that Cit⁺ arose because of a pre-existing regulatory switch and involved no evolution at all.  But that simply is not the case – that wording, dare I say it, is a lie.

If you take E. coli from a medium in which it is growing on glucose, and move it into a medium where the only thing to eat is something else, like lactose, it turns off the expression of some genes specific to growth on glucose, and it turns on other genes necessary to grow on lactose.  That is what is called gene regulation, and that is what biologists mean when they talk about switching functions on and off – existing genetic circuitry that allows an organism to respond to changes in the external and internal environment.  If you transfer normal, Cit^– E. coli from a glucose medium to a medium with only citrate to eat, they don’t grow.  They just sit there and starve.  Regular E. coli cells have no existing genetic regulatory circuitry that “flips a switch” to allow them to start growing on citrate in the presence of oxygen.  On the other hand, if you do the same thing with the Cit⁺ cells that evolved in the long-term experiment, the Cit⁺ cells will start growing happily on citrate.  This difference is not a matter of gene regulation, but an evolved difference between the ancestral strain and the Cit⁺ lineage that allows Cit⁺ cells to grow on citrate.

No, the ability to grow on citrate is not a matter of simply flipping a pre-existing regulatory switch.  Continuing the electrical metaphor, the evolved Cit⁺ function is instead about rewiring.  My dear little Cit⁺ cells gained their ability to partake of the previously forbidden citrate by a genetic duplication involving a gene, called citT, which encodes a transporter protein that is used during anaerobic growth on citrate.

This duplication did something very special.  You see, one of the major aspects of gene regulation is that genes have associated regulatory DNA sequences, including what are called promoters that control when genes are expressed.  The citT gene is normally controlled by a promoter that tells the cell to turn it on only when there is no oxygen present.  As shown in the Figure below, the gene duplication put one copy of citT next to, and under the control of, a promoter that normally controls another gene called rnk.  The rnk gene is normally turned on when oxygen is present.  The new association between citT and the rnk promoter – what we call the rnk-citT regulatory module – turns citT on when oxygen is present, and allows Cit⁺ cells to use citrate under the conditions of the LTEE.  (To really feast on the citrate involved additional evolutionary changes, both before and after this rewiring, but I’ll leave that point aside for this post.)

There is a very interesting consequence of how the rnk-citT module originated. While Ham did not make this argument, other creationists have asserted that Cit⁺ arose simply by a loss of gene regulation, because they have the notion that evolution can only break things.  However, the duplication that gave rise to the rnk-citT module caused no such thing.  There is still a copy of citT that is linked to the same adjacent DNA sequence as before, and there is still a copy of rnk that is under the control of its own promoter.  In other words, the cell got something new without losing anything old.

When they actually bother to explain all of that, creationists still dismiss Cit⁺ as being an instance of evolutionary innovation because it involved the rearrangement of existing components.  True, the duplication responsible for Cit⁺ did rearrange components that were already there, but that rearrangement generated a new association between components that did not previously exist, and it produced a new function that also did not previously exist.  To argue that rearrangements cannot produce innovation is akin to arguing that a novelist has done nothing creative in writing her novels because she only used words that already existed.

Ham also made a demand that is common among creationists that betrays a fundamental misunderstanding of evolutionary theory. In the later debate segment [starting at ~2:30], Ham says, “What Bill Nye needs to do for me is to show me example of something…uh, some new function that arose that was not previously possible from the genetic information that was there. And I would claim and challenge you that there is no such example that you can give… you’d have to show an example of brand new function that never previously was possible.  There is no such example, uh, that you can give anywhere in the world.”

According to Ham, evolution cannot be true if this burden can’t be met.  Consider that wording for a moment, though: “… show an example that never previously was possible.”  Not possible?  That’s kind of a high bar given that impossible things don’t happen by definition.  Moreover, it is clear from Ham’s words that he won’t regard any capacity that arises from modification of an existing genome to be an innovation, which means that he must think that evolutionary theory holds that new genes just pop into existence fully formed, without precursor states, like Athena from the head of Zeus.

This goes to the larger problem with how Ham, Ray Comfort, Michael Behe, Georgia Purdom, and others of their ilk approach evolution – they just don’t know much about it, and so what they end up arguing against isn’t the science, but a caricature of the science that exists only in their minds.  Evolutionary novelty does not arise from genes just popping into existence.  That is a silly idea, and one that no evolutionary biologist holds!

Instead, evolution innovates and creates through descent with modification of what already exists, a process that Nobel laureate François Jacob called “evolutionary tinkering”.  This modification arises by random mutations: base changes, deletions, duplications, insertions, and so on – and, depending on the organisms, horizontal genetic exchange and sexual recombination.  Natural selection then preserves and accumulates the useful changes – those that enhance survival and reproduction of the organism in its environment – across the generations.  Often, such innovations are based on just what we see with the Cit⁺ bacteria – novel rearrangements of old components.  Indeed, Jacob wrote that, “(Evolutionary) novelties come from previously unseen association of old material.  To create is to recombine.”

So Ham and other creationists dismiss how evolutionary theory says evolution works as not being evolution, and then they demand the impossible.  That strikes me as neither fair nor honest.  But in the end, their lies, distortions, misrepresentations, and ignorance don’t matter, just as debates, entertaining though they may be, don’t matter, because nature doesn’t care.  To paraphrase a bumper sticker I once saw, they may not believe in evolution, but nature does!

While they go on cycling through their old and ossified rhetoric according to their fixed and incorrect notions, evolution proceeds, MacGyvering the new from the old. Natural selection can’t do the impossible, but it is pretty darn spiffy at doing the improbable with the rare.

If you are interested in learning more, please visit my website, where you will find my papers available for download.  You can also watch my Ph.D. defense presentation, in which I go into much more detail about the evolution of the Cit⁺ E. coli.

— Zachary Blount

* * * * *

The figure below shows schematically the tandem duplication in the population that evolved the new ability to grow on citrate.  This duplication produced the new rnk-citT regulatory module by placing the second copy of the citT gene adjacent to the rnk promoter region.  The figure comes from Blount et al., 2012, Nature; it is shown here under the doctrine of fair use.

“Ham on Nye” Debate, Follow-up #2

Ken Ham spoke about the research in my lab at two points during the “Ham on Nye” science versus creation debate. The first segment also includes a video clip in which Dr. Andrew Fabich, a “biblical creationist” and microbiologist at Liberty University, talks about our work.

Dr. Zachary Blount is a postdoctoral researcher in my lab who performed most of the work that was discussed.  Zack produced these transcripts of Ham’s and Fabich’s presentations while preparing his response to their distortions and misrepresentations of our work.

First segment, beginning at ~44 minutes:

Ken Ham:

“Let me introduce you to another scientist, Richard Lenski of Michigan State University.  He’s a great scientist.  He’s known for culturing E. coli in the lab, and he found there were some E. coli that actually seemed to develop the ability to grow on substrate, um, on citrate substrate.  But, Richard Lenski is here mentioned in this book [Microbiology: An Evolving Science] and it’s called ‘Evolution in the Lab’.  So, the ability to grow on citrate is said to be evolution, and there are those who say, ‘Hey! This is, this is against the creationists.’  For instance, Jerry Coyne from the University of Chicago says, ‘Lenski’s experiment is also yet another poke in the eye for anti-evolutionists.’  He says, ‘The thing I like most is it says you can get these complex traits evolving by a combination of unlikely events.’  But is it a poke in the eye for anti-evolutionist?  Is it really seeing complex traits evolving?  What does it mean that some of these, uh, bacteria are able to grow on citrate?

Let me introduce you to another biblical creationist who is a scientist.”

[via video] Andrew Fabich:

“Hi, my name is Dr. Andrew Fabich.  I got my Ph.D. from the University of Oklahoma in Microbiology.  I teach at Liberty University, and I do research on E. coli in the intestine.  I’ve published in secular journals from the American Society for Microbiology, including Infection and Immunity, uh, and Applied and Environmental Microbiology, as well as several others.  My work has been cited even in the past year in the journals Nature, Science Translational Medicine, Public Library of Science, Public Library of Science Genetics.  I, um, it’s cited regularly in those journals, and while I was taught nothing but evolution, I don’t accept that position, and I do my research from a creation perspective.  When I look at the evidence people cite of the E. coli supposedly evolving over 30 years or over 30,000 generations in the lab, and people say that it is now able to grow on citrate.  I don’t deny that it grows on citrate, but it’s not any kind of new information. It’s …  The information’s already there, and it’s just a switch that gets turned on and off, and that’s what they reported in there.  There’s nothing new.”

Ken Ham: 

“See, students need to be told what’s really going on here.  Certainly there’s change, but it’s not change necessary for molecules to man.”

Second segment, beginning at ~2 hours, 30 minutes:

Ken Ham: 

“What Bill Nye needs to do for me is to show me example of something …uh, some new function that arose that was not previously possible from the genetic information that was there.  And I would claim and challenge you that there is no such example that you can give.  That’s why I brought up the example in, uh, my presentation of Lenski’s, uh, experiments in regard to E. coli.  And there were some that seemed to develop the ability to exist on citrate, but as Dr. Fabich said from looking at his research, he’s found that that information was already there.  It’s just a gene that’s switched on and off.  And so, uh, there is no example because, you know, information that’s there in, in the genetic information of different animals, plants, and so on.  There’s no new function that can be added.  Certainly great variation within a kind, and that’s what we look at, but you’d have to show an example of brand new function that never previously was possible.  There is no such example, uh, that you can give anywhere in the world.”