Analysis of the Lenski Paper

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The population designated Ara-3 (center) has evolved to use the citrate present in the growth medium.

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Zachary D. Blount, Christina Z. Borland, and Richard E. Lenski’s paper "Historical contingency and the evolution of a key innovation in an experimental population of Eschericha coli"[1] has received a lot of attention on the net. This is, in part, due to the apparent support for evolution given by the paper but, mostly, due to Andrew Schlafly’s remarkable correspondence with Professor Lenski.

The paper in question looks at a particular event in an experiment tracking the nature of bacteria over many generations that, so far, has lasted twenty years. One change observed was that a strain arose that was able to metabolise citrate (“eat it”), something this particular bacteria is normally unable to do in the presence of air. Whilst the paper is admirably clear, it is a technical paper requiring good knowledge of biology for a thorough understanding. We present here a layman's interpretation of the study.

The study is often hailed as demonstrating a beneficial mutation arising in the laboratory, and therefore it is considered to be waving the flag for evolution and challenging creationism on many levels. The paper itself, however, does not enter into this debate. Instead, the question reviewed is how the mutation arose and the implications of this for two conflicting views on how mutations come to be. The “Cumulative” view is that mutations appear largely at random, with the result that for any broadly enough defined trait, there is a high likelihood that this trait will be presented for natural selection to operate on. The “Contingent” view is that mutations are restricted not just in terms of chance and whether or not they survive to be passed on, but in the possibility of them arising in the first place.

## Contents

* 1 The team’s results
* 2 Wild conclusions (ours, not the team's!) and further questions
* 3 See also
* 4 External links
* 5 References

## The team’s results[edit]

The team found two things that would suggest that, at least in this case, the “Contingent” position is correct.

Firstly, the mutation in question arose after very many generations and quite enormous numbers of bacteria. In our poker analogy, our player had been playing from Monday to Sunday and first saw a pair of Aces on Sunday.

The chances of receiving a high pair are 119:2. We should not necessarily expect to receive two high pairs in the first 119 deals, but the more deals sat through without any high pairs, the more we can be confident that "something is going on". “Something”, thought the research team, “is going on”.

Finding what was going on depended on new research. The team repeated the experiment with different generations of the bacteria (they had preserved a sample of every 500th generation). They took bacteria from generation 20,000 and cultured them, from generation 10,000 and cultured them, etc. etc. In other words, they got the pack in use on Monday, the pack in use on Tuesday, etc. and started dealing. They found that the mutation re-occurred, but only from bacteria cultured from generation 20,000 and up. Re-culturing the strains from earlier generations simply didn’t reproduce the mutation.

This is what we would expect to see given the “Contingent” position and what we would expect not to see given the "Cumulative" position. If we pick up a deck of cards used on Monday and deal away, we get different results from a deck of cards used on Saturday. They are different decks; the results we see are not just chance variations in outcomes, but different ranges of outcomes determined by the history of that deck. The early generation decks have Baces and Dings. Aces and Kings entered the decks of cards in use from Saturday morning on. If we pick up one of the later decks and start to deal, and only if we pick up one of the later decks, we find our player receiving high pairs.

## Wild conclusions (ours, not the team's!) and further questions[edit]

The team’s next aim is to find out exactly how the genes of the mutant E. coli “code” for eating citrate. This is likely to involve firstly mapping all the mutations that have taken place and then trying to find which of the dozens that are expected results in citrate-eating.

Fortunately for us, we don’t actually have to do all this hard work and can run off into wild speculation.

1. A common criticism of evolutionary theories is the assertion that “no new information” arises as a result of mutations. This assertion is reconciled with the commonplace observation of apparently “new” features by reasoning that the feature was already there: the adaptations we see reveal potential, they do not create it. In the paper, we are presented with a description of something that is new: the potential to develop citrate-eating. It would appear that this, at least, is not “already present”; we can try and try to “reveal” it in early generations, but we will fail. You can shuffle a Monday deck all you like, but you won’t get any Aces. Of course, this is just one mutation (although others have been described).[2] The team has shown that new information can arise: it leaves open the question of whether enough arises.

2. Bio-diversity. As if we didn’t need telling, the team’s results add to the idea that once something is lost in nature, then it’s lost. A mutation arising depends on history as much as chance and we are unable to re-wind the clock.

3. “Punctuated Equilibrium”. There is quite a debate between those who think that evolution happens gradually by small, incremental steps, and those who think that evolution happens in “bursts”. Has a “burst” now been seen in the lab? The team has seen 30,000 generations of non-citrate-eating stability, a nice steady equilibrium, followed by a “massive population expansion” (p7904) of citrate-eating bacteria.

4. Who’s going to win? The team point out that citrate-eating and non-citrate eating E. coli co-exist quite happily. The citrate-eating bacteria are not as good as the non-citrate eating bacteria at munching glucose. The team wonders whether it is better to specialise in eating citrate and leave the glucose-eaters alone, or will the citrate eaters adapt to eat glucose as well and march on to lab domination?

5. Will the bacteria become new species? Lenski himself speculates on this in the paper: "Will the Cit+ and Cit- lineages eventually become distinct species?", and he concludes that more time is necessary to tell.

## See also[edit]

* Potentiating mutation
* Historical contingency
* Conservapedia:Schlafly's alleged Flaws in Lenski's Study

## External links[edit]

* See the Wikipedia article on nylon-eating bacteria.
* The Loom - one of the best descriptions of the experiment
* The Loom - follow-up questions
* PET Plastic Eating Bacteria

## References[edit]

1. ↑ Blount, Zachary D.; Borland, Christina Z.; Lenski, Richard E. (2008). "Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli". Proceedings of the National Academy of Sciences. 105 (23): 7899–906\. Bibcode:2008PNAS..105.7899B. doi:10.1073/pnas.0803151105. JSTOR 25462703. PMC 2430337. PMID 18524956.7899-906&rft.date=2008&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430337#id-name=PMC&rft_id=https://www.jstor.org/stable/25462703#id-name=JSTOR&rft_id=info:bibcode/2008PNAS..105.7899B&rft_id=info:pmid/18524956&rft_id=info:doi/10.1073/pnas.0803151105&rft.aulast=Blount&rft.aufirst=Zachary+D.&rft.au=Borland,+Christina+Z.&rft.au=Lenski,+Richard+E.&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430337&rfr_id=info:sid/rationalwiki.org:Analysis+of+the+Lenski+Paper" class="Z3988">
2. ↑ See the Wikipedia article on nylon-eating bacteria.