In 2009, Richard Lenski produced some of the most detailed documented evidence of the production of new novel traits through natural selection. In this case, E. coli bacteria developed the ability to transport citrate through their cell wall in oxygenated conditions before metabolizing it. The mutation chain that occurred was documented in detail and the experiment is notable in giving biologists a much better understanding of the role of potentiating mutations.
These mutations don't produce benefit alone, but are necessary intermediates in the production of new traits. It is of importance to note that when bacteria containing the potentiating mutation that led to the citrate transport trait were frozen, they retained the ability to re-evolve it. That demonstrated that the potentiating mutation is a necessary intermediate, providing further verification for the causal chain of mutations.
In addition to the potentiating mutation, subsequent mutations occurred that provided increasing benefit. The initial ones allowed the bacteria to metabolize a small amount of citrate. Eventually though, the mutations greatly improved the function, allowing those bacteria to consume the food source, outcompeting their neighbors.
This experiment isn't about a single chance mutation leading to some benefit. It is the complete evolution of a new trait through a series subsequent mutations. The addition of a new feature. Again the premise of evolution is very simple. Given a set of organisms, and a set of environmental conditions and states, a certain number of organisms will survive. The ones that survive will continue to produce offspring and pass on their genes, the others perish and do not. Random mutation provides some variety to the mix. Change over time driven by the selection of a given set of organisms over another set that are better able to survive in an environment.
In the following I present Answer's In Genesis's (AIG) response to the results of the experiment, and my rebuttal to their response.
Many evolutionists state that the bacteria are experiencing “adaptive evolution.” However, this is not evolution but rather adaptation. Molecules-to-man evolution requires an increase in information and functional systems. Instead, these bacteria are likely experiencing a loss of information and functional systems as has been observed in other mutant bacteria in Lenski’s lab. While these changes are beneficial in the lab environment, they do not lead to a net gain that moves bacteria in an upward evolutionary direction.The bacteria in question didn't lose anything. The E. coli actually gained the ability to transport citrate through its cell wall. That is not a loss of any kind. They go on to quote a study on how E. coli can transport and metabolize citrate in low oxygen conditions
Previous research has shown that wild-type E. coli can utilize citrate when oxygen levels are low.6 Under these conditions, citrate is taken into the cell and used in a fermentation pathway. The gene (citT) in E. coli is believed to encode a citrate transporter (a protein which transports citrate into the cell).6 When oxygen levels are high, it is thought that the citrate transporter does not function or is not produced (even though they still possess the enzymes necessary to utilize citrate).Lenski's paper itself, also points this out.
The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions.The evolved trait is not the ability to utilize citrate, but to transport it through its cell wall. This involves several mutations, and each of them in the chain was documented by Lenski's experiment. In fact, by freezing different strains at various points in the evolutionary chain, Lenski was able to restart the process at different points repeatedly, and demonstrate the causal chain conclusively. He reconfirmed the link between the mutation and trait. The AIG response is simply speculating about what might have happened, which they need not do since reading Lenski's paper, the precise mutation chain is laid out.
Lenski’s lab has not yet identified the genetic alterations of the Cit+ E. coli line, but he believes that there are multiple mutations involved. Studies of the “fossil record” of this line indicate that one or more mutations occurred around generation 20,000 which he terms “potentiating” mutations that were necessary before additional mutations around generation 31,500 led to Cit+ cells. Lenski thinks that the mutations may have activated a “cryptic” transporterLenski's lab has found the genetic alterations. AIG's response is old, so I grant them the benefit of the doubt here. There have been further publications from Lenski on the subject further confirming the results.
While the fitness of the bacteria has increased (as compared to the starting bacteria), it has come at a cost. For example, all the lines have lost the ability to catabolize ribose (a sugar).3 Some lines have lost the ability to repair DNA.4 These bacteria may indeed be more fit in a lab setting, but if put in competition with their wild-type (normal) counterparts in a natural setting, they would not stand a chance.Let's quote Lenski's paper for context.
Previous analyses of this experiment have shown numerous examples of parallel phenotypic and genetic evolution.All twelve populations underwent rapid improvement in fitness that decelerated over time (2, 3, 22, 23). All evolved higher maximum growth rates on glucose, shorter lag phases upon transfer into fresh medium, reduced peak population densities, and larger average cell sizes relative to their ancestor (22–26). Ten populations evolved increased DNA supercoiling (27), and those populations examined to date show parallel changes in global gene-expression profiles (4, 28, 29). At least three genes have substitutions in all 12 populations (30, 31), and several others have substitutions in many populations (27–30), even though most loci harbor no substitutions in any of them (32). At the same time, there has also been some divergence between populations. Four have evolved defects in DNA repair, causing mutator phenotypes (3, 33). There is subtle, but significant, between population variation in mean fitness in the glucose-limited medium in which they evolved (2, 23). In media containing other carbon sources, such as maltose or lactose, the variation in performance is much greater (34). And while the same genes often harbor substitutions, the precise location and details of the mutations almost always differ between the populations (27–31).I don't see where Lenski states they lost the ability to catabolize ribose, but citation 31 is a reference to documented instances where the ability was lost in E. coli. (Cooper VS, Schneider S, Blot M, Lenski RE (2001) Mechanisms causing rapid and parallel losses of ribose catabolism in evolving populations of E. coli B. J Bacteriol 183:2834–2841.) I have bold-faced the part where he documents defects in DNA in four of the populations. Not all the resulting Lenski populations had DNA defects. More from AIG
Lenski states (based on calculated mutation rates in E. coli), “It is clearly very difficult for E. coli to evolve this function. In fact, the mutation rate of the ancestral strain from Cit- to Cit+ is immeasurably low . . . .”1 If developing the ability to utilize citrate under certain conditions using random mutations of a pre-existing citrate utilization system is so rare, then how even more improbable is it to believe that these same random mutations can lead to completely new information and functional systemsYes, but as Lenski points out in an exasperated response to Andrew Layton Schlafly
Did you know that your own bowels harbor something like a billion (1,000,000,000) E. coli at this very moment? So remember to wash your hands after going to the toilet, as I hope your mother taught you. Simple calculations imply that there are something like 1020 = 100,000,000,000,000,000,000 E. coli alive on our planet at any moment. Even if they divide just once per day, and given a typical mutation rate of 10-9 or 10-10 per base-pair per generation, then pretty much every possible double mutation would occur every day or so. That’s a lot of opportunity for evolution.Indeed there continue to be publications and journal articles written that continue to confirm and reconfirm the results of Lenski's work. Along with providing specific genomic evidences for the mutations involved the results demonstrate the specific chain of mutations. Studies of Lenski's E. coli strains continue to provide insight into evolution of new traits.