Richard Lenski’s "Unicorns"


 by Sean Pitman

Originally Posted: December 7, 2013

Updated: November 2016


Richard E. Lenski is an American evolutionary biologist, best known for his 25-year long-term E. coli evolution experiment and his work with digital organisms using Avida.  What is especially impressive about Dr. Lenski's efforts is that he is trying to show how random mutations and natural selection (the Darwinian mechanism for evolution) can create functionally complex systems within living things.  He argues that very small gradual changes can add up over time to produce very dramatic functional changes, exactly as Darwin predicted.
Of course, those who favor the concept of intelligent design or the Biblical concept of Creation have long argued that "micro-evolution" is possible, but "macro-evolution" is not.  In other words, small changes cannot add up over time to produce highly complex biological systems.  In fact, the demonstration of macro-evolution is claimed to be equivalent to finding the mythical unicorn. 

So, who is right?  Has Dr. Lenski really found the elusive "unicorn"?  Has he actually shown how macro-evolution via the Darwinian mechanism is really a plausible theory?

Well, in 2012 Dr. Lenski and a few others published a very interesting paper claiming to have demonstrated this very thing (
Link, Link).  He produced E. coli bacteria that, after ~31,000 generations, evolved the ability to use citrate for energy under oxygenated conditions - something they weren't able to do before.  And, they achieved this novel function via random mutations and natural selection - right in line with predictions for the Darwinian mechanism. Of course, many people got very excited over the implications of this experiment.  In September of 2012 the well-known science journal Nature published an article about Lenski's experiment entitled, "Evolution: How the unicorn got its horn", by Hendrickson and Rainey.  Here's part of what they wrote about the implications of this experiment:
The discovery of the Cit + mutants in Lenski’s experiment has been a mote in the eye for those suggesting that major phenotypic innovations cannot be explained by micro-evolutionary (gradual) processes. Indeed, for anti-evolutionists, lack of mechanistic detail has even allowed room for divine intervention. After several attempts to politely address the concerns of one critic, Lenski responded publicly in what has proven to be one of the most competent and direct defenses of science versus dogma for some time. It includes the memorable phrase, “In other words, it’s not that we claim to have glimpsed ‘a unicorn in the garden’ — we have a whole population of them living in my lab!”. (Link)
Game over!

Finally, those pesky creationists and IDist have been put in their place once and for all!

Not so fast . . .

As is generally the case, especially for claims regarding the creative abilities of the Darwinian mechanism, the devil is in the details.  And, when one looks a bit more closely at the details of the Lenski experiment, it loses quite a bit of its luster.
What Dr. Lenski did was to grow E. coli under oxic (oxygenated) conditions in citrate-rich media. E. coli bacteria are generally unable to use citrate under oxic conditions as a source of energy. However, they can use it under anoxic conditions. In other words, they already have the gene for citrase in their genome. It is just that it is normally turned off under oxic conditions. How is it turned off? Well, the promoter for the gene that transports citrate into the bacterium (citT) is not active under oxic conditions. So, all that needs to happen is to move the citrate transport gene close to a promoter that is actually active under oxic conditions. Once this is done, citrate will enter the bacterium and be used for energy. And, this is exactly what happened. Nothing structurally new needed to be evolved. After about 31,000 generations, in a large population of bacteria, there was a single genetic mutation in a bacterium that ended up moving the citT gene and placing it under the control of a promoter (rnk) that is active under oxic conditions. The fact that just this single translocation mutation took so long to achieve should clue everyone in to how difficult it is to achieve even such low-level changes in function via random mutations. The protein product, however, remained the same – i.e., <500aa with no required amino acid changes to achieve a selectable effect. All that was required was to move a pre-existing gene close to a promoter to turn it on during oxic conditions. That's it. The protein itself didn't need to be changed for a useful advantage.

Now, at this point, multiple copies of the gene were rapidly produced in some colonies. However, having just one copy was enough to produce a selectable growth/survival advantage in the citrate-rich environment. It doesn't matter if there are 1 – 9 copies of the gene – the same function is realized to different levels – i.e., the cit+ function can exist, to a selectable degree, with just one copy of the gene producing the the very same protein. Additional "refinements" are easy once at least a minimum useful level of a particular type of function is realized – not a problem at all.

Again, Dr. Lenski's pet "unicorn" is a very low-level example of evolution in action where nothing structurally new was produced to achieve the function in question. The only thing that happened was a mutational move of a pre-existing gene from one location to another within the genome so that it could be turned on in a particular environment. That's not a problem at all for the Darwinian mechanism.  Statistically, such a mutation is very likely to happen, within a few tens of thousands of generations, or even sooner, given a fairly large colony of bacteria.
In fact, other researchers, have experimented on evolving aerobic citrate-utilizing E. coli. In 2016 Dustin Van Hofwegen et al., working in the lab of Scott Minnich, were able to isolate 46 independent citrate-utilizing mutants of E. coli in just 12 to 100 generations using highly prolonged selection under starvation, during which the bacteria would sample more mutations more rapidly (Link). In their research, the genomic DNA sequencing revealed an amplification of the citT and dctA loci and rearrangement of DNA were the same class of mutations identified in the experiment by Richard Lenski and his team (Link). Hofwegen et al., concluded that, "We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved" (Link). 
Of course, Blount and Lenski responded by arguing:
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. (Link)
Of course functionally "new" information was evolved in these citrate utilization experiments. It just was just very very low-level functional information that didn't require the evolution of anything structurally new.  If all that has to happen in the transfer of one particular "word" or "phrase" in a book to another particular spot in the book for some new functionality to be realized, well, the odds of success are very high indeed. Again, all that happened here is that a pre-formed gene was transferred from one place to another fairly specified place within the genome. That's it. Clearly, that's statistically likely in relatively short order.

But, that's not the real problem for the Darwinian mechanism or for the Theory of Evolution in general.  The real challenge is in explaining how random mutations can search through the vastness of protein sequence space (a space comprised of all possible sequences of a particular length) to find the extremely rare islands of novel beneficial sequences that could produce something qualitatively new - an entirely new type of function that requires an new protein-based system - a new physical structure.  Such unicorns are much harder to find because random mutations have to search through vast oceans of non-beneficial sequences before they can find the very rare isolated islands of beneficial sequences.  The question is, are there any examples of this sort of evolution actually happening?

Well, yes, there are many examples were truly novel protein sequences with selectably beneficial functionality are discovered by random mutations.  Most of these examples are single-protein enzymes and the like that require a minimum of no more than a few hundred specifically arranged amino acid residues (amino acids are the building blocks of proteins, with a total of 20 different amino acid "characters" within the "alphabet" of proteins).  However, there are no examples of evolution in action producing any protein-based system that requires a minimum of more than 1000 specifically arranged amino acid residues - not even close. The reason for this is because sequence space at this level is unimaginably enormous (i.e., 201000 = 1e1301 sequences).  To get an idea as to how large this number is, consider that the total number of atoms in the visible universe is about 1e80 atoms.  What is more important, however, is that the ratio of potentially beneficial vs. non-beneficial sequences in the 1e1301 sequence space is incredibly tiny - so minuscule that any cluster of beneficial sequences in the enormity of sequence space is surrounded, on all sides, by an enormous ocean of non-beneficial sequences that is so vast that, if the beneficial islands of sequences were like stars in the sky, no other stars would be visible in the universe from the perspective of one of these islands.  That means that getting from one of these islands to the next closest beneficial island, by random mutations, would take trillions upon trillions of years of time.

As a real life example, consider that the famous rotary flagellar motility system that exists within various types of bacteria requires a minimum of over 5000 specifically arranged amino acid residues.  No such system has ever been shown to evolve nor has anyone presented any statistically tenable argument for how random mutations and natural selection could gradually build such a system. The problem is that the proposed beneficial steppingstones in a pathway of a complex multi-protein system, like a flagellar motility system, are themselves far far too widely separated in protein sequence space, by distances that would cover many universes, for random mutations to get across any of the non-beneficial gaps this side of trillions of years of time.  That is why evolutionary progress stalls out, in an exponential manner, with each step up the ladder of functional complexity (i.e., minimum size and/or specificity requirements for a system to work to a selectable level of usefulness).

For further information on the statistical limits to the Darwinian mechanism see the "Steppingstone Problem".