Tag: Microcosm: The Book

Microcosm on MSNBC, Podcasts

By Carl Zimmer | June 5, 2008 8:21 pm

I spoke Tuesday on Seattle, and there’s proof now! Alan Boyle, MSNBC’s science guru, wrote a great piece on both the talk and the subject, my book Microcosm. Meanwhile, folks from Real Science were taping, and now you can listen to the talk at their web site. If I had lots of free time, I’d combine the audio with my slides and post them, but I’m swamped for now.

I also completely spaced out last week and forgot to mention that I was interviewed on the Skeptic’s Guide to the Universe. You can listen here.


More Goings-on at the Scienceblog Book Club

By Carl Zimmer | June 5, 2008 1:09 pm

Don’t forget to check in for the latest posts going up over at the Scienceblog Book Club. My book Microcosm has gotten us into a debate about the nature of life.


E. coli Evolution Follow-up

By Carl Zimmer | June 5, 2008 11:06 am

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 supressed 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 bateria 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 a 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.


Reminder: A Double-Header in Seattle Today

By Carl Zimmer | June 3, 2008 8:34 am

The microbial march continues! I’ll be in Seattle today, giving two talks on Microcosm: E. coli and the New Science of Life. The first is a 1:30 talk at Microsoft Research. Then I’ll be giving a public talk at Town Hall at 7:30 as part of their science series.


A New Step In Evolution

By Carl Zimmer | June 2, 2008 9:41 pm

Lenski.jpgOne of the most important experiments in evolution is going on right now in a laboratory in Michigan State University. A dozen flasks full of E. coli are sloshing around on a gently rocking table. The bacteria in those flasks has been evolving since 1988–for over 44,000 generations. And because they’ve been so carefully observed all that time, they’ve revealed some important lessons about how evolution works.

The experiment was launched by MSU biologist Richard Lenski. I wrote about Lenski’s work last year in the New York Times, and in more detail my new book Microcosm. Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.

Based on what scientists already knew about evolution, Lenski expected that the bacteria would experience natural selection in their new environment. In each generation, some of the microbes would mutate. Most of the mutations would be harmful, killing the bacteria or making them grow more slowly. Others would be beneficial allowing them to breed faster in their new environment. They would gradually dominate the population, only to be replaced when a new mutation arose to produce an even fitter sort of microbe.

Lenski used a simple but elegant method to find out if this would happen. He froze some of the original bacteria in each line, and then froze bacteria every 500 generations. Whenever he was so inclined, he could go back into this fossil record and thaw out some bacteria, bringing them back to life. By putting the newest bacteria in his lines in a flask along with their ancestors, for example, he could compare how well the bacteria had adapted to the environment he had created.

Over the generations, in fits and starts, the bacteria did indeed evolve into faster breeders. The bacteria in the flasks today breed 75% faster on average than their original ancestor. Lenski and his colleagues have pinpointed some of the genes that have evolved along the way; in some cases, for example, the same gene has changed in almost every line, but it has mutated in a different spot in each case. Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.

Last year Lenski was elected to the National Academy of Sciences. This week he is publishing an inaugural paper in the Proceedings of the National Academy of Sciences with his student Zachary Blount and postdoc Christina Borland. Lenski told me about the discovery behind the paper when I first met him a few years ago. He was clearly excited, but he wasn’t ready to go public. There were still a lot of tests to run to understand exactly what had happened to the bacteria.

Now they’re sure. Out of the blue, their bacteria had abandoned Lenski’s their glucose-only diet and had evolved a new way to eat.

After 33,127 generations Lenski and his students noticed something strange in one of the colonies. The flask started to turn cloudy. This happens sometimes when contaminating bacteria slip into a flask and start feeding on a compound in the broth known as citrate. Citrate is made up of carbon, hydrogen, and oxygen; it’s essentially the same as the citric acid that makes lemons tart. Our own cells produce citrate in the long chain of chemical reactions that lets us draw energy from food. Many species of bacteria can eat citrate, but in an oxygen-rich environment like Lenski’s lab, E. coli can’t. The problem is that the bacteria can’t pull the molecule in through their membranes. In fact, their failure has long been one of the defining hallmarks of E. coli as a species.

If citrate-eating bacteria invade the flasks, however, they can feast on the abundant citrate, and their exploding population turns the flask cloudy. This has only happened rarely in Lenski’s experiment, and when it does, he and his colleagues throw out the flask and start the line again from its most recently frozen ancestors.

But in one remarkable case, however, they discovered that a flask had turned cloudy without any contamination. It was E. coli chowing down on the citrate. The researchers found that when they put the bacteria in pure citrate, the microbes could thrive on it as their sole source of carbon.

In nature, there have been a few reports of E. coli that can feed on citrate. But these oddballs all acquired a ring of DNA called a plasmid from some other species of bacteria. Lenski selected a strain of E. coli for his experiments that doesn’t have any plasmids, there were no other bacteria in the experiment, and the evolved bacteria remain plasmid-free. So the only explanation was that this one line of E. coli had evolved the ability to eat citrate on its own.

Blount took on the job of figuring out what happened. He first tried to figure out when it happened. He went back through the ancestral stocks to see if they included any citrate-eaters. For the first 31,000 generations, he could find none. Then, in generation 31,500, they made up 0.5% of the population. Their population rose to 19% in the next 1000 generations, but then they nearly vanished at generation 33,000. But in the next 120 generations or so, the citrate-eaters went berserk, coming to dominate the population.

This rise and fall and rise suggests that the evolution of citrate-eating was not a one-mutation affair. The first mutation (or mutations) allowed the bacteria to eat citrate, but they were outcompeted by some glucose-eating mutants that still had the upper hand. Only after they mutated further did their citrate-eating become a recipe for success.

The scientists wondered if other lines of E. coli carried some of these invisible populations of weak citrate-eaters. They didn’t. This was quite remarkable. As I said earlier, Lenski’s research has shown that in many ways, evolution is repeatable. The 12 lines tend to evolve in the same direction. (They even tend to get plump, for reasons yet to be understood.) Often these parallel changes are the result of changes to the same genes. And yet when it comes to citrate-eating, evolution seems to have produced a fluke.

To gauge the flukiness of the citrate-eaters, Blount and Lenski replayed evolution. They grew new populations from 12 time points in the 33,000-generations of pre-citrate-eating bacteria. They let the bacteria evolve for thousands of generations, monitoring them for any signs of citrate-eating. They then transferred the bacteria to Petri dishes with nothing but citrate to eat. All told, they tested 40 trillion cells. Here’s a movie of what that looks like…

Out of that staggering hoard of bacteria, only a handful of citrate-eating mutants arose. None of the original ancestors or early predecessors gave rise to citrate-eaters; only later stages in the line could–mostly from 27,000 generations or beyond. Still, even among these later E. coli, the odds of evolving into a citrate-eater was staggeringly low, on the order of one-in-a-trillion.

Now the scientists must determine the precise genetic steps these bacteria took to evolve from glucose-eaters to citrate-eaters. In order to eat a particular molecule, E. coli needs a special channel in its membranes through which to draw it. It’s possible, for example, that a channel dedicated to some other molecule mutated into a form that could also take in citrate. Later mutations could have fine-tuned it so that it could suck in citrate quickly.

If E. coli is defined as a species that can’t eat citrate, does that mean that Lenski’s team has witnessed the origin of a new species? The question is actually murkier than it seems, because the traditional concept of species doesn’t fit bacteria very comfortably. (For the details, check out my new article on Scientific American, “What is a Species?”) In nature, E. coli swaps lots of genes with other species. In just the past 15 years or so, for example, one disease-causing strain of E. coli acquired hundreds of genes not found in closely related E. coli strains. (See my recent article in Slate.) Another hallmark of E. coli is its ability to break down lactose, the sugar in milk. But several strains have lost the ability to break it down. (In fact, these strains were originally given a different name–Shigella–until scientists realized that they were just weird strains of E. coli.)

Nevertheless, Lenski and his colleagues have witnessed a significant change. And their new paper makes clear that just because the odds of such a significant change are incredibly rare doesn’t mean that it can’t happen. Natural selection, in fact, ensures that sometimes it does. And, finally, it demonstrates that after twenty years, Lenski’s invisible dynasty still has some surprises in store.

Source: Z.D. Blount, C.Z. Borland, and R.E. Lenski, “HI istorical Contigency and the Evolution of a Key Innovation in an Experimental Population of Escherichia coli.” PNAS in press (http://www.pnas.org/cgi/doi/10.1073/pnas.0803151105) [UPDATE: PDF AVAILABLE ON LENSKI’S SITE.]

Update: See my follow up here where I answer some questions from commenters.

CATEGORIZED UNDER: Microcosm: The Book

Microcosm in the Boston Globe: You Get Old, I Get Old…E. coli Gets Old

By Carl Zimmer | June 2, 2008 9:53 am

The French biologist Jacques Monod once famously said, “What is true for E. coli is true for the elephant.” At the time, he was referring to the universal rules of molecular biology–of DNA and proteins, for example, that are the same from one species to another. As scientists in the mid-1900s figured out the workings of E. coli, they were also figuring out the workings of life in general. In my new book Microcosm, I make the case that Monod’s words were more true than even he realized. In the Boston Globe today, I explain how scientists used to think that there was one big difference between E. coli and the elephant (and us)–we get old and E. coli doesn’t. But now it turns out that E. coli was not immortal after all. And that discovery means that E. coli may help reveal secrets about Alzheimer’s disease and other burdens of old age. Read it here.


Reminder: Talking Tonight at Kepler’s Bookstore in Menlo Park, CA

By Carl Zimmer | June 2, 2008 8:14 am

The E. coli epidemic spreads today to the Bay Area. Please come out to Kepler’s to hear me talk about Microcosm: E. coli and the New Science of Life.


Introducing the Scienceblog Book Club

By Carl Zimmer | June 1, 2008 8:00 pm

One of the best things to come out of blogging is the blog book club. (See, for example, the book club at Talking Points Memo.) In the bad old days, the only way writers could respond to books was with a one-shot book review. A blog book club, on the other hand, allows writers to have public conversations about books and the issues they raise. It also makes room for readers to get into the discussion as well.

Unfortunately, until now blog book clubs have mostly been dedicated to politics. Scienceblogs is now rectifying this imbalance with the launch of the Scienceblogs Book Club. And, oh frabjous day, the first title they’ve chosen to discuss is my new book, Microcosm.

A wonderful troika of writers have joined the club. P.Z. Myers, who blogs at Pharyngula, is on board, despite the fact that I am not writing about cephalopods at this moment. So is John Dennehy, a microbiologist at CUNY (a k a The Evilutionary Biologist). And rounding out the club is journalist Jessica Snyder Sachs, author most recently of the excellent Good Germs, Bad Germs, in which she tours the mysterious world of microbes in which we are immersed.

I’ve kicked things off with an introductory post. I hope you find the conversation that unfolds to be provocative (and perhaps intriguing enough to pick up a copy of the book).


Reminder: Talking Tonight at Powell’s Bookstore in Portland

By Carl Zimmer | June 1, 2008 8:03 am

I’m heading cross-country to talk about Microcosm. First stop–Powell’s bookstore in Portland tonight. Never been there before, so I’m looking forward to a bibliophile’s pilgrimage. Hope to see Portlanders there!


All Things E. coli

By Carl Zimmer | May 30, 2008 3:24 pm

ecolihub.jpgE. coli is, arguably, the one species that scientists know best. If you type the name “Escherichia coli” into PubMed, the database of the National Library of Medicine, you’ll get over a quarter of a million titles of scientific papers. Scientists have sequenced about 30 genomes of different strains of E. coli. It’s the microbe of choice for those who want to figure out how to tinker with life. There’s one problem with all this attention–how are scientists supposed to make sense of all this data? Scientists have created sites to aggregate E. coli data in one place. The newest and broadest site is now up: E. coli Hub. To put the site in historical context, the scientists who set it up asked me to write an essay. It’s now online here.


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The Loom

A blog about life, past and future. Written by DISCOVER contributing editor and columnist Carl Zimmer.

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