They're Still Just Bacteria, Mr. Zimmer!
In his August 15th column Matter in the New York Times, popular science writer Carl Zimmer discussed a recent research study of the Pseudomonas aeruginosa bacteria (P-a) published by a team from Sloan-Kettering in New York City. At the end of his article, readers were able to leave comments, and it was the comments from some of the readers that prompted Zimmer to write a second article appearing on the website The Loom in order to criticize some of the comments made to the New York Times column. The offending remarks were some version of "but they were still bacteria", which a couple of the responders suggested. Zimmer takes offense at this as demonstrating ignorance of evolution on the part of the critics, which I'll get to in a moment.
The study itself, led by Joao Xavier of Memorial Sloan-Kettering Cancer Center, took a look at how the P-a bacteria, a rather insidious bacterium that appears just about everywhere and often invades humans with dangerous infections, searches for food. Essentially, the study found, the P-a bacteria emit a molecule that forms a slick road for them to travel across, in a process called swarming. The P-a will use their flagella, a whip-like tail, to propel themselves down the slick roadway and devour whatever sustenance comes their way.
This study was the first time the process had ever actually been filmed and it is quite interesting to see this process in action. Helpfully, Zimmer includes a couple of the videos in his column. What Xavier and his team wanted to figure out was exactly how the P-a swarms. In the experiment, they set up a petri dish and deposited a few hundred or so of the P-a into it and then just let them do their thing. They hypothesized that if allowed to reproduce, the P-a would generate mutations from time to time and that some of those would be beneficial to helping the P-a survive and thrive in the new environment. Which is exactly what did happen. Each day, the researchers extracted a small sample from the petri dish and re-deposited them in a new one. Within a few days, the P-a had developed a mutation of multiple flagella that enabled those with it to swarm better and devour more food than their fellows stuck with just one tail. Essentially, it was survival of the fittest in action. Xavier and his team called the new phenomenon "hyperswarmers."
However, there was a cost to the P-a bacteria in evolving this new trait: a diminished capacity to make biofilm. That was important, because it is the ability to create the biofilm that helps make the P-a more resistant to anti-biotic treatments. As an advance in being able to combat a rather pesky bacteria, this was surely something gained. If the P-a could be induced through treatment to become hyperswarmers, and thus have a decrease in the biofilm, then antibiotics might be more successful in killing them.
What is interesting here, though, is that rather than focusing on the obvious medical benefit of this experiment, they instead chose to frame it as an advance in understanding evolution. In their summary of the study Xavier and his team write:
Most bacteria in nature live in surface-associated communities rather than planktonic populations. Nonetheless, how surface-associated environments shape bacterial evolutionary adaptation remains poorly understood. Here, we show that subjecting Pseudomonas aeruginosa to repeated rounds of swarming, a collective form of surface migration, drives remarkable parallel evolution toward a hyper-swarmer phenotype. In all independently evolved hyperswarmers, the reproducible hyperswarming phenotype is caused by parallel point mutations in a flagellar synthesis regulator, FleN, which locks the naturally monoflagellated bacteria in a multiflagellated state and confers a growth rate-independent advantage in swarming. Although hyperswarmers outcompete the ancestral strain in swarming competitions, they are strongly outcompeted in biofilm formation, which is an essential trait for P. aeruginosa in environmental and clinical settings. The finding that evolution in swarming colonies reliably produces evolution of poor biofilm formers supports the existence of an evolutionary trade-off between motility and biofilm formation.In other words, what intrigues the researchers about this study isn't so much that they might have hit on a way to eradicate a harmful bacteria with antiobiotic treaments, but that their study shows convergent evolution in action. Consider what they wrote in their conclusion of the research report:
Here, we show that evolution in surface-associated swarming colonies produces parallel molecular evolution of multiflagellated hyperswarmers. Swarming motility in P. aeruginosa is a social trait involving many molecular ... and a priori prediction of evolutionary trajectories is complicated due to its multifactorial nature. So, the consistent emergence of hyperswarmers in independent lineages is surprising all the more because all hyperswarmers have single-point mutations in the same region of the flagellar synthesis regulator FleN. This is a striking example of parallel molecular evolution. In addition, the emergence of the most predominant mutation--FleN(V178G)--in experimental evolution started from a clinical isolate shows the convergent molecular evolution in strains other than PA14.These results raise an intriguing question: if P. aeruginosa can be transformed from a monoflagellated (monotrichous) into a polar multiflagellated (lophotrichous) bacterium by single-point mutations, why is P. aeruginosa monoflagellated in nature? The answer to this question may lie in the fact that hyperswarmers are poor biofilm formers that lose against wild-type in biofilm competitions. Because biofilms are an essential part of the P. aeruginosa lifestyle, hyperswarmers likely face a strong counterselection in the wild, preventing their fixation there. Interestingly, nonflagellated mutants are also poor biofilm formers...suggesting that fine-tuning of flagellar motility is essential for biofilm formation.So, the reason we only see the P-a bacteria in the wild with just one tail is because those that mutate the FleN and gain additional tails don't survive as well because of the reduction in biofilm formation...an evolutionary tradeoff. Or, as they put it, an example of "fine-tuning". One has to wonder exactly how this fine-tuning takes place.
With that background of the study in hand, let's return to Carl Zimmer and his second article from The Loom, which he entitled "Experimental Evolution and the False Solace of "They're Still Bacteria". In this article Zimmer laments "While the response to my column has been generally enthusiastic (thanks), I have gotten some negative comments that echo an old refrain I often hear when I write about experimental evolution. Basically: they're still bacteria." He then cites some tweets, especially from one V. Hugo who had the audacity to tweet that "So the bacteria......remained a bacteria." Another tweeter named Navathir wrote "That's not biological evolution, but rather pattern formation: Dogs' offsprings' color change, right?" Zimmer finds all this just plain ignorant and responds with:
"Opponents of evolution often like to decree what evolution really is. That way, when scientists study evolution, they can declare, "That's not evolution."In other words, adaptation! A point mutation created a trait, additional tails improving motility in this case, that gave the hyperswarmers a selective advantage over their fellows in a controlled environment (recall why hyperswarmers don't appear in the wild - the loss of biofilm - that "fine-tuning" thing to which Xavier and his team allude.) This is a good example of a mutation giving you more of something you already have, not something new. Zimmer, of course, doesn't refer back to any of that. Instead he continues his sneer at the critics: "It's very hard for me to see how evolving from a single tail to up to half a dozen tails-all of which work together rather than getting tangled up with each other-is not a new trait. But even if we go along with V. Hugo this far, his sort of argument still fails, because it's not an argument at all. He's just creating a personal definition of evolution in order to scoff at scientific research. The origin of new traits is part of evolution, but so is the spread of beneficial mutations due to natural selection."
Nevathir, for example, claims that that what happened in this experiment is just "pattern formation," which apparently refers to how dogs give birth to puppies that have different color patterns. (That's not actually called pattern formation, but I have to guess here.)
Puppies get different color patterns because (among other reasons) they inherit different combinations of genes from their parents. The experiments I wrote about this week are not "pattern formation" in this sense of the phrase. They started with genetically identical bacteria, which divided, producing identical clones except when new mutations arose. Those mutations were then passed down to their descendants. Mutations to one gene in particular led to the emergence of "hyperswarmers." Hyperswarmers were genetically programmed to make more tails, which allowed them to swim faster than their ancestors. And they quickly drove slower bacteria extinct as they came to dominate the population.
That is evolution-evolution in under a week, in fact.
A "personal definition of evolution"? It is difficult to see how the results of this experiment are really much different than, say, the variation in finch beak sizes on the Galapagos Islands or the coloration of the Peppered Moth on the trees in England. So what does Zimmer even mean by "a personal definition"? The finch beak and coloration adaptations have long been used as examples of "evolution in action" by Darwinists, even though they were still "just finches" or "just moths" in spite of the changes. Zimmer clearly just assumes what this study does not demonstrate: that the ability to mutate these multiple flagella translates to explaining how we get from bacteria to man, even though the study in reference didn't get quite that far. Well, it's the time involved, as Zimmer explains:
[Critics]...aren't satisfied with this experiment because it isn't a large-scale episodes of evolution-the split between species, for example, or the origin of an eye or a hand. (I'm guessing here, but it's a guess educated on many previous such comments.) Large-scale episodes take time, typically stretching across thousands or millions of years. The scientists who study bacteria over the course of a few weeks don't expect to witness such transformations. Instead, they are finding that they can dissect the mechanisms of evolution. They can even document the emergence of new genes, as mutations accidentally duplicate stretches of DNA, which can then begin to take on new functions.Again, Zimmer is implying the very thing not present in the study: that this observation of "evolution in action" can explain bacteria to man. He finds the "but its still bacteria" complaint to be just "wrong-headed" and concludes with: "Such a remark isn't just wrong-headed about evolution, though. It reveals a misunderstanding of bacteria. Bacteria originated about 3.5 billion years ago and have been diversifying into many different forms ever since. Some bacteria float in the ocean, turning sunlight into carbon. Others breathe iron. Others make squid glow. Watching bacteria evolve in a Petri dish helps us to understand not just evolution in general, but bacteria in all their particulars."
In other words, 3.5 billion years later, we have many divergent types of bacteria, but they are all "still just bacteria". What's the problem?