A common challenge to Darwinism is whether anyone has actually seen Evolution in action. If you do a Google search on this question, you get the Physics Forum (link here) as the number one result. And a person asked a pretty basic question in the forum:
I know that it (Evolution) has been 'proven', but my question is, has it actually been observed by somebody? Yes, we can see the similarities between different subspecies and species but that alone is not proof that they evolved from each other. Has anyone actually seen it happen?
Has anyone seen Evolution actually happen? The responses are revealing as to why this is a problem for Darwinists. They suggested that getting a flu shot, seeing fruit flies, and the Peppered Moth are all claimed examples of Evolution in action. The flu shot is a good response, because that shows what Evolution can really do – it does a single or even a double point mutation in the gene which is a very small change, and that provides resistance to a drug or vaccination. And so, the flu shot changes every year. Great example, but it is very limited.
But the other responses (fruit flies and the Peppered Moth) are flat out wrong. So what is the best example of Evolution that is actually observed? My friend Ed rose to the challenge, and suggested E coli and the famous Lenski experiments provides a great example. Ed writes, "Creationists often make snide remarks about not seeing it happening, but now we have... Seen from the outside, this is like you having a baby that could suddenly eat wood chips... Seen from the inside, it's what we've been saying all along should happen... (link here). I thought it especially remarkable since Tom has used E. coli before in his poorly-understood attempts to falsify evolution..."
Wow! Ed, attacks me viciously (Ed is sweet, he only writes viciously), and comes up with a slam dunk example of Evolution that is actually observed from the Lenski E coli experiments – before they did not eat wood chips, but now they can. It sounds like this is a true beneficial mutation that helps E coli survive in different environments.
But alas, Ed is wrong. It turns out that the E-coli bacteria being able to eat wood chips / citrate, when before it did not, is not actually an evolutionary addition. But instead it turns out that this beneficial mutation in E-coli resulting from a break or deletion in a pre-existing gene. So if breaking what is already there is the best example of Darwinism in action, aren't Darwinists acknowledging that Evolution cannot actually create anything new?
Anyway, Lenski's E-coli experiments are fascinating. He is now up to over 50,000 generations (equal to 1 million animal years), and its results show that minor changes do happen (evolution works), and it benefits the whole community. But it doesn't do much more than that, in other words it is similar to what takes place in vaccination resistance. To explain it with a little more oomph, here is a recent (Nov. 13, 2012) letter from Professor Behe on this topic:
BEHE: Readers of my posts know that I'm a big fan of Professor Richard Lenski, a microbiologist at Michigan State University and member of the National Academy of Sciences. For the past few decades he has been conducting the largest laboratory evolution experiment ever attempted. Growing E. coli in flasks continuously, he has been following evolutionary changes in the bacterium for over 50,000 generations (which is equivalent to roughly a million years for large animals). Although Lenski is decidedly not an intelligent design proponent, his work enables us to see what evolution actually does when it has the resources of a large number of organisms over a substantial number of generations. Rather than speculate, Lenski and his coworkers have observed the workings of mutation and selection. For this, we ID proponents should be very grateful.
In a manuscript published a few years ago in the Quarterly Review of Biology (Behe 2010), I discussed laboratory evolution results from the past four decades up to that point, including Lenski's. His laboratory had shown clearly that random mutation and selection improved the bacterium with time, as measured by the number of progeny it could produce in a given time. He demonstrated without doubt that beneficial mutations exist and can spread quickly in a population of organisms. However, once Lenski's lab eventually identified the mutations at the DNA level (a difficult task), many of the beneficial mutations turned out to be, surprisingly, degradative ones. In other words, breaking or deleting some pre-existing genes or genetic regulatory elements so that they no longer worked actually helped the organism under the conditions in which it was grown. Other beneficial mutations altered pre-existing genes or regulatory elements somewhat.
What conspicuously was not seen in his work were beneficial mutations that resulted from building what I dubbed new Functional Coded elemenTs, or "FCTs." Roughly, a FCT is a sequence of DNA that affects the production or processing of a gene or gene product (see my review for a more rigorous definition). In short, improvements had been made by breaking existing genes, or fiddling with them in minor ways, but not by making new genes or regulatory elements. From this information I formulated "The First Rule of Adaptive Evolution": Break or blunt any functional coded element whose loss would yield a net fitness gain. To say the least, the First Rule is not what you would expect from a process, such as Darwinian evolution, which is touted as being able to build amazingly sophisticated molecular machinery.
Before my review was published, the Lenski lab observed a mutant strain in their experiments that could metabolize citrate in the presence of oxygen, which unmutated E. coli cannot do. (Blount et al. 2008) (Importantly, however, the bacterium can metabolize citrate in the absence of oxygen.) This allowed the mutated bacterium to outcompete its relatives, because the growth medium contained a lot of citrate, as well as oxygen. It was an intriguing result, and was touted as a major innovation, but at the time Lenski's lab was unable to track down at the DNA level the exact mutations that caused the change.
Now they have. In a recent publication in Nature (Blount et al. 2012) they report the multiple mutations that confer and increase the ability to transport citrate in an atmosphere containing oxygen. They divide the mutations conceptually into three categories: 1) potentiation; 2) actualization; and 3) refinement. "Actualization" is the name they give to the mutation that first confers a weak ability to transport citrate into the laboratory E. coli. (It turns out that the bacterium is lacking only a protein to transport citrate into the cell in the presence of oxygen; all other enzymes needed to further metabolize citrate are already present.) The gene for the citrate transporter, citT, that works in the absence of oxygen is directly upstream from the genes for two other proteins that have promoters that are active in the presence of oxygen. A duplication of a segment of this region serendipitously placed the citT gene next to one of these promoters, so the citT gene could then be expressed in the presence of oxygen. Gene duplication is a type of mutation that is known to be fairly common, so this result, although requiring a great deal of careful research to pin down, is unsurprising.
Over time the mutant got better at utilizing citrate, which the authors called "refinement." Further work showed this was due to multiple duplications of the mutant gene region, up to 3-9 copies. Again, gene duplication is a fairly common process, so again it is unsurprising. In another experiment Lenski and co-workers showed that increasing the concentration of the citrate transporter gene was sufficient in itself to account for the greater ability of E. coli to grow on citrate. No other mutations were needed.
A more mysterious part of the whole process is what the group called "potentiation." It turns out that the original E. coli they began with decades ago could not benefit from the gene duplication that brought together a citT gene with an oxygen-tolerant promoter. Before it could benefit, a preliminary mutation had to occur in the bacterium somewhere other than the region containing the citrate-metabolism genes. Exactly what that mutation was, Lenski and coworkers were not able to determine. However, they examined the bacterium for mutations that may contribute to potentiation, and speculated that "A mutation in arcB, which encodes a histidine kinase, is noteworthy because disabling that gene upregulates the tricarboxylic acid cycle." (They tried, but were unable to test this hypothesis.) In other words, the "potentiation" may involve degradation of an unrelated gene.
Lenski's lab did an immense amount of careful work and deserves much praise. Yet the entirely separate, $64,000 question is, what do the results show about the power of the Darwinian mechanism? The answer is, they do not show it to be capable of anything more than what was already known. For example, in my review of lab evolution experiments I discussed the work of Zinser et al. (2003) where a sequence rearrangement brought a promoter close to a gene that had lacked one. I also discussed experiments such as Licis and van Duin (2006) where multiple sequential mutations increased the ability of a FCT. Despite Lenski's visually startling result -- where a usually clear flask became cloudy with the overgrowth of bacteria on citrate -- at the molecular level nothing novel occurred.
So the Question of whether anyone has actually seen Evolution in action, actually is another arrow in the quiver of Intelligent Design. Evolution does little changes in the battle against malaria like malaria's ability to develop resistance to chloriquine. It doesn't do the heavy lifting of what we see in our world. Evolution doesn't create and doesn't develop anything new. So, I hope that you see from this post that something else (or more precisely SomeOne else) is going on here. Investigate the examples of Evolution, and don't be afraid. Evolution's Iron Gates are paper mache thin.
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