Behe, Lenski and the “Edge” of Evolution, Part 1: Just the FCTs, Please

| By on Letters to the Duchess

In this series, we reexamine the claim made by Intelligent Design proponent Michael Behe to have found a limit to “Darwinian” evolution in light of recent results from the laboratory of Richard Lenski.

Revisiting the Long Term Evolution Experiment (LTEE)

Readers may recall that in a previous series on how new biological information arises during evolution we discussed an ongoing experiment on the bacterium E. coli taking place in the laboratory of Richard Lenski. Named the Long Term Evolution Experiment, or LTEE, this research is very simple in its approach. As we described previously, the experiment merely allows twelve separate populations of E.coli to replicate in a controlled environment, and notes what changes appear over time:

The LTEE started in 1988 with twelve populations of the bacterium E. Coli all derived from one ancestral cell. The design of the experiment is straightforward: each day, each of the twelve cultures grow in 10ml of liquid medium with glucose as the limiting resource. In this medium, the bacteria compete to replicate for about seven generations and then stop dividing once the food runs out. After 24 hours, 1/10th of a ml of each culture is transferred to 9.9 ml of fresh food, and the cycle repeats itself. Every so often, the remaining 9.9 ml of leftover bacterial culture is frozen down to preserve a sample of the population at that point in time – with the proper treatment, bacteria can survive for decades in suspended animation. Early in the experiment this was done every 100 generations, and later this was shifted to every 500 generations. A significant feature of the LTEE is that these frozen ancestors can be brought to life again for comparison with their evolved descendants: in essence, the freezers in the Lenski lab are a nearly perfect “living fossil record” of the experiment.

To date, the most dramatic change that has been noted is that some bacteria in one of the twelve cultures have acquired the ability to use citrate under aerobic conditions (i.e. when oxygen is present). While E. coli have the ability to import citrate and use it as a carbon source when oxygen is absent, they cannot do so when it is present. Since the LTEE takes place under aerobic conditions, this new ability, labeled “Cit+”, was very advantageous, since it allowed Cit+ bacteria to use a new food source in the culture medium that the rest of the culture could not. In very short order, the Cit+ bacteria nearly took over one of the twelve cultures. We have discussed this result as an evolutionary gain of information before, though the precise nature of the mutations that led to the Cit+ phenotype was not known at that time.

Behe and the LTEE

Lenski’s work on the LTEE has also been of significant interest to promoters of Intelligent Design, such as biochemist Michael Behe. Behe discusses the Lenski LTEE in his 2007 book, The Edge of Evolution at some length, and uses it as an example of, in his view, “what Darwinism can do” – i.e. slightly modify or destroy existing biological systems: 

Even in a controlled lab culture where bacteria are warm and well fed, the bug that reproduces fastest or outcompetes the others will dominate the population. Like gravity, Darwinian evolution never stops.

But what does it yield? … By now over thirty thousand generations of E. coli, roughly the equivalent of a million years in the history of humans, have been born and died in Lenski’s lab. Over the whole course of the experiment, perhaps ten trillion, 1013, E coli have been produced. Although ten trillion seems like a lot (it’s probably more than the number of primates on the line from chimp to human), it’s virtually nothing compared to the number of malarial cells that have infested the earth. In the past fifty years there have been about a billion times as many of those as E. coli in the Michigan lab, which makes the study less valuable than our data on malaria.

Nonetheless, the data has pointed in the same general direction. The lab bacteria performed much like the wild pathogens: A (sic) host of incoherent changes have slightly altered pre-existing systems. Nothing fundamentally new has been produced. No new protein-protein interactions, no new molecular machines. As with thalassemia in humans, some large evolutionary advantages have been conferred by breaking things… The fact that malaria, with a billion fold more chances, gave a pattern very similar to the more modest studies on E. coli strongly suggests that that’s all Darwinism can do. (pp 141-142)

Behe, then, appears to see “Darwinism” as capable of “breaking things” to gain an evolutionary advantage, but unable to produce “fundamentally new” things. While The Edge of Evolution predates the report from the Lenski group (in 2008) describing the evolution of Cit+ E. coli in the LTEE, a paper published by Behe in 2010 does address this new development. However, as we have noted above, the precise nature of the mutations leading to Cit+ remained a mystery at the time.

In his 2010 paper, Behe reviews a large swath of experimental evolution studies, including the LTEE, with a view to placing the observed changes into one of three categories. These categories center around what Behe defines as a Functional Coded elemenT, or “FCT”:

An FCT is a discrete but not necessarily contiguous region of a gene that, by means of its nucleotide sequence, influences the production, processing, or biological activity of a particular nucleic acid or protein, or its specific binding to another molecule. Examples of FCTs are: promoters; enhancers; insulators; Shine-Dalgarno sequences; tRNA genes; miRNA genes; protein coding sequences; organellar targeting- or localization- signals; intron/exon splice sites; codons specifying the binding site of a protein for another molecule (such as its substrate, another protein, or a small allosteric regulator); codons specifying a processing site of a protein (such as a cleavage, myristoylation, or phosphorylation site); polyadenylation signals; and transcription and translation termination signals.

With this definition in hand, Behe then undertakes a large review of work in experimental evolution with bacteria and viruses. Understandably, loss-of-FCT mutations predominate, since mutations can easily break genes, and gene losses in some environments can be an advantage for the organism. Similarly, adaptive modification-of-FCT mutations are relatively common. Gain-of-FCT mutations, however, are rare. Once again Behe returns to the LTEE experiment as a prime example to consider:

With a cumulative population size of about 1014 cells, Lenski’s investigation is large enough and long enough to give solid, reliable answers to many questions about evolution.

After a thorough review of the results of the LTEE, however, it becomes clear that one of the “solid, reliable answers” that Behe has in mind is that Lenski’s work demonstrates the paucity of gain-of-FCT mutations, much like his critique of the LTEE in Edge of Evolution. Since the nature of the mutation that led to the ability to use citrate under aerobic conditions (Cit+) was at that time unknown, Behe speculates as to which category it will fall into, and discusses some possible underlying molecular mechanisms for the Cit+ mutation:

If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.

The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.

This point is a major one in Behe’s paper: the LTEE is the best experiment of its kind to date, and all there is to show for it are loss-of-FCT and modification-of-FCT mutations. Though Behe is blunt in The Edge of Evolution, and more subtle in the review, the same point is clear in both sources. According to Behe, we’ve been watching what evolution can do for quite a while, and what it can do amounts to “not much.”

Fortunately for us, the Lenski lab kept watching, and working diligently to understand the changes that led to the Cit+ development. As we will examine tomorrow in Part 2 of this series, what they have discovered does not square easily with Behe’s ideas. Indeed, a careful analysis of their findings and Behe’s key arguments in The Edge of Evolution is in order, and that’s what we’ll do in tomorrow’s post.




Venema, Dennis. "Behe, Lenski and the “Edge” of Evolution, Part 1: Just the FCTs, Please" N.p., 22 Oct. 2012. Web. 23 February 2018.


Venema, D. (2012, October 22). Behe, Lenski and the “Edge” of Evolution, Part 1: Just the FCTs, Please
Retrieved February 23, 2018, from /blogs/dennis-venema-letters-to-the-duchess/behe-lenski-and-the-edge-of-evolution-part-1-just-the-fcts-please

References & Credits

Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York: Free Press, 2007).

Michael J. Behe (2010). Experimental evolution, loss-of-function mutations, and “The first rule of adaptive evolution”. The Quarterly Review of Biology 85(4); 419-445.

About the Author

Dennis Venema

Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia and Fellow of Biology for BioLogos. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. 

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