I’m back at last from the west coast leg of the Microcosm tour.
Portland had a cloudy, melancholy charm, and at Powell’s I gave a reading in front of a collection of hand-made black velvet paintings from the nearby Velveteria. When the audience’s eyes drifted off of me, I couldn’t tell if they were lost in thought or distracted by Jimi Hendrix or a smoking clown.
The next day I headed for San Francisco, where I talked to Moira Gunn for her show Tech Nation (link to come). Then I had lunch with Kirsten Sanford, who will be interviewing me on tomorrow’s edition of This Week In Science. Then off to Santa Cruz, to talk to Robert Pollie at KUSP for his show Talk of the Bay (link to come). Finally I made my way over to Kepler’s in Menlo Park. I spoke there a few years ago, and since then they closed and were saved by the community. I was glad to be able to come back.
In the morning I flew to Seattle. I headed for Microsoft Research to give a talk, which I’m told will be online before long. I was a little spooked by the experience, because, in addition to the lunchtime crowd in the room, there were lots of people watching online elsewhere–in some cases in other countries. I had to resist the instinct to talk very loudly so that people over in China could hear me.
Then I made a quick appearance on KOMO, the ABC affiliate in Seattle. The anchor started talking about E. coli in hamburger and spinach, and I responded by describing the billions of E. coli in her. I saw her eyes widen a little in what I’m guessing was suppressed horror, but she handled it like a pro.
Finally I went to Town Hall and waited for intrepid souls to wade through the downpours to hear me talk. It was great to see familiar faces (like this mug). I met blogger Geoff Arnold, who showed me Microcosm on Kindle, and since I couldn’t autograph his screen, he took a picture. (I think Town Hall will also be posting my talk–will update.)
Along the way, I wrote a blog post about some new advances in the research I describe in Microcosm. The response was terrific (thanks in part to a link from reddit), and the comments have been multiplying faster than E. coli on a warm day.
There were a few questions that came up that I thought I’d address in follow up.
–First off, the paper itself is finally online now.
—Matt asks
how are they sure this citrate eating adaptation was a result of mutations, and not, say, an existing sequence of dna that was just locked in an intron or something, and then eventually shuffled to a coding region of the genome? Could they follow the genetic changes point by point, or are they still trying to figure that out?
Introns are segments of protein-coding genes that get edited out as the DNA sequence is read by a cell. E. coli and other bacteria don’t have introns. But E. coli does sometimes shuffle segments of DNA around its genome. Whether the mutations involved were shuffles, or changes to single nucleotides of DNA, or accidental duplications of DNA, etc.–all that remains to be seen.
–Phishrow asks
how common are experiments of this scale and duration? You hear about 20 odd year studies on human populations from time to time; but how many situations like this one do we have bubbling away?
Good question. I’m having a hard time thinking of anything that’s run anywhere near as long as Lenski’s 20 yr experiment (I’m thinking specifically of evolutionary experiments). A lot of great work has been done on bacteria and viruses over the course of a few hundred or few thousand generations. It’s not easy to keep something running for decades, though–especially to find the funding for it.
Ian asks
Carl – Are you aware of any long-running experiments like this where the initial bacterium has accumulated sufficient mutations that in the end it would be classified as a different type (genus or something higher) of bacterium from what it started out? The “Shigella” comment in the article above comes close.
Actually, the Shigella case shows just how hard it is to use conventional taxonomy to understand the evolution of bacteria. Shigella seemed so different from E. coli when it was first discovered that it was put in a different genus. It seemed different because it makes us sick by invading cells, something harmless strains don’t do. There are also lots of other differences–Shigella lacks some key enzymes E. coli has. But studies on their DNA revealed that several strains of E. coli had independently evolved into “Shigella” strains. What is clear is that in this cluster of lineages, there has been some dramatic evolutionary change. And now Lenski has seen some dramatic evolutionary change over the course of a few thousand generations.
–Heather raises some concerns…
I’m not knowledgeable about bacteriology, nor am I opposed to evolution, but 2 facts in the article stand out: (1) contamination from foreign bacteria, including citrate-eaters, occurred often enough that the researchers had a procedure for it (toss the flask and start from the most recent frozen sample of the same line), and (2) the E Coli. can develop the ability to eat citrate by acquiring the plasmid DNA ring from a citrate-eater.
You can read the paper for the details, but the short response is that the researchers repeatedly checked for contamination and established that it was indeed E. coli that was eating citrate. Also, they set up the entire experiment to make it impossible for E. coli to pick up plasmids.
–Ken Finley writes
This is total horse crap. There’s nothing in the Bible to suggest that evolution exists. You’re just arbitrarily making up excuses.
If the bacteria changed, it was clearly because God willed it. He does that sometimes, you know.
Just because God helped the bacteria survived, you can’t just simply say it’s because we come from monkeys. That’s stupid and arrogant.
You’ll go to hell for your blasphemy
Sometimes I have a hard time figuring out when these sorts of posts are serious or jokes.
–Nate writes
This is a very interesting study, but I would like to point out to some people that seem to have misunderstood what happened. The bacteria did not develop a way to eat citrate, they mutated to a point where they were able to get it across their membranes. They already had the capability to digest it. Most likely a few bacteria had a few mutations which damaged their membranes and allowed citrate to get through. I would like to know what all the tradeoffs were in these bacteria as well. Losing several capabilities while gaining one doesn’t seem like a step forward to me, but in this situation it was advantageous to these bacteria because of the abundance of citrate.
He then follows up...
…it’s proof that an organism cannot gain a capability through mutations without losing several others. If, hypothetically, the same bacteria gained a dozen more capabilities, this research would tend to show that the bacteria would end up losing 3-4 times that many capabilities. If a bacteria did lose that many, it would most likely no longer be viable. It does prove microevolution occurs, which we already knew, but cannot be made to prove anything past that. That type or extrapolation is foolish and ignorant.
Nate, you may want to read the paper. You’re sounding a lot more certain about the nature of the mutations than the scientists themselves are. And you’re almost certainly wrong when you suggest that the citrate-eaters just have damaged membranes. You’d have to do some serious damage to its membranes to let citrate leak in–so much damage that lots of stuff would leak in and out. That’s clearly not the case here, because the bacteria are healthy. Bacteria use special channels to draw in these molecules.
As for tradeoffs, it’s true that these citrate-eaters may not do as well eating glucose as their ancestors. I have no idea where you get the “3-4 times that many capabilities” phrase. But so what? Evolution is not about “steps forward,” like some unhindered march of progress. It’s about change, and tradeoffs are an essential part of that change.
And if you’re going to call this “microevolution,” you’ll need to define your terms here for us. Here we have seen the evolution of a capability, the lack of which was significant enough that it marked E. coli as a species. What’s micro about that?
Andrew asks,
Forgive the question, as I’m not a scientist (just an interested dabbler), but I thought that evolution was, in general, a slow process that could not be observed so quickly? Is the situation different for bacteria? Is evolution something that can be observed in a matter of years for them?
Bacteria can divide several times a day, which makes them very fast breeders. And since they’re so small, hundreds of millions can fit in a small flask. Even though mutations are incredibly rare, these sorts of numbers make it inevitable that they will arise in bacterial colonies. And natural selection combined with these numbers means that over a few years you can see clear change occurring. There’s no compelling reason to think that these processes don’t happen in bigger, slower-breeding species (like us), but it’s harder to see the changes because they take decades, centuries, or millennia. It’s also worth bearing in mind that Lenski’s experiment is a tiny embodiment of evolution in bacteria. Just remember that bacteria pack the soils, the oceans, the sea floor, and our bodies. They’ve been evolving for billions of years. And they can pool their evolutionary potential by trading genes. That makes the evolution of a new trait in Lenski’s lab all the more important.
Originally published June 5, 2008. Copyright 2008 Carl Zimmer.