One 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.
Medicine & Health
Life Science
Comments
Got to love a longitudinal study. This was a very interesting article.
BTW, I've got a request out for the Smithsonian Guide to Human Origins in my library queue. Should have it in a day or two. Got to love the inter-library loan system in this state.
Posted by: Tony P | June 3, 2008 12:32 AM
Pure awesome.
Posted by: Hugo | June 3, 2008 12:57 AM
It's a fascinating discovery and thank you for providing an excellent summary.
I'm now really looking forward to seeing them isolate the protein(s) involved in this novel trait, and the genetic mechanisms that led to its evolution. It's great that they've been able to document the history of each line, and can just thaw out the ancestral bacteria to do any molecular experiments to answer some of the interesting questions that their discovery raises.
Posted by: NP | June 3, 2008 3:03 AM
This is fascinating stuff! I work in a lab undertaking some of the questions that underlie the results obtained. We study the marine bacteria SAR11 and some of the experiments we are in the process of conducting may shed a lot of light on the question of how this one-in-a-trillion chance actually maps out nucleotide by nucleotide. Perhaps natural selection is orders of magnitude more efficient then we ever thought...just think: If this is a one-in-a-trillion chance for one lineage in one lab, and there are an almost unimaginable number of lineages in nature...you do the math. Can't wait to read the paper...and see the genomes (if it's in the works).
Posted by: Paul C | June 3, 2008 3:06 AM
Link to the paper is broken. (At least for me. PNAS is notorious for having press releases on papers you can't find for a number of days).
Just finished Microcosm. Excellent book. Off to the book club to see if there's anything new over there about it.
Posted by: Ron | June 3, 2008 6:06 AM
Waaaaa! Link doesn't work. (If it's in press, will it appear in the "Early Edition" section soon?)
See, it's stuff like this that's totally re-igniting my interest in the sciences. Not that I'd lost interest, really - I just tucked it away as if it was a former life. Not so, anymore. This is, in part, due to intriguing writing like yours and partly because I forgot how much unexpected fun like this work can come from coli.
Re: species... Species distinctions have always seemed a bit fuzzy to me, anyways. When it gets down to precise divisions between species, it sort of feels like a semantic argument with different opinions arising due to what particular aspect of an organism an individual thinks in important.
I wonder if it's going to come down to whole genome comparisons as the only way to be definitive. But even then...
Posted by: clear as mud | June 3, 2008 8:23 AM
Clear as mud:
This excites me as much as it does you, and for the same reasons.
One of the things that has struck me in the writings on the species concept is that it is difficult because in defining species we are trying to create a discrete threshhold where none exists in nature. In trying to impose our own limits of imagination on nature, we are never going to be able to come up with "One size fits all" definition. The definition we learned in high school regarding viable, interbreeding offspring only ever applied to sexual reproduction.
Carl - thanks for this post. It has made my day, believe it or not.
Posted by: Mike Haubrich, FCD | June 3, 2008 8:50 AM
Wow, what a fantastic study and lucid summary. Thanks Carl, this is the most excited I've been about biology in a while.
A question: 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?
Posted by: Matt | June 3, 2008 11:16 AM
Matt,
It sounds to me like that's precisely what Lenski and his colleagues are planning on doing next. It could be any number of things, or any combination of them, that has resulted in the acquired functionality. It would not surprise me if, in the experiment described where they looked for lines that re-evolved the same citrate-eating functionality, there were different (though perhaps similar) mutations leading to the same result.
I'm sure that what's going on currently is an analysis of the sequences of the various lines over the generations that saw the rise of this new function to show exactly what happened when. After that's done, the protein work will need to be done to show how what happened at the sequence level altered the proteins involved.
This is really cool stuff!
Posted by: Baka | June 3, 2008 1:27 PM
In a way some of these results were prefigured in the Avida work (PDF) published by Lenski and colleagues in 2003. For example, there's this finding:
In the 2003 work they found that multiple lineages of digital critters evolved to perform the same logic function, but did so by different evolutionary trajectories through gene space.Then there's this:
One sees the same pattern in the evolutionary histories of the Avida runs.Further, my own analysis of the mutation by mutation trajectory of one of those Avida evolutionary histories shows that a fair number of mutations (25% or more) in the Avida runs are selectively neutral when they first occur, and only generations later are incorporated (after more mutations in other parts of the digital critters' code) into instruction strings that perform selectively advantageous functions. Teasing out those variables in E. coli is going to be a task!
Posted by: RBH | June 3, 2008 3:48 PM
Thanks, Baka. Very exciting stuff.
Posted by: Matt | June 3, 2008 3:51 PM
creationist "yeah, but it's still just a bacteria. Let me know when a bacteria evolves into a dog or a cat." /creationist
Posted by: Siamang | June 3, 2008 3:52 PM
@Matt: Hmmm, my memory is E. coli doesn't really do introns, though I've been out of the loop for a few years, so my mind has atrophied.
I'm gonna take a stab at a bad guess. Start with the DNA coding for a component of a nutrient uptake system that coli *does* have.
It could either be:
(1) one that isn't required under the specific lab conditions, so it's ok to alter without affecting viability. or
(2) it could be a total gene duplication - which happens plenty enough, if I recall - allowing a copy to be maintained while the other becomes a target for tinkering.
What would be needed is an alteration possibly in the active site which normally binds to a different organic compound.
If there's enough of a tweak that, suddenly, the active site gains even a bit of new affinity for citrate, then - BINGO - that bug gets the upper hand - it has a new carbon source all to itself.
It can start as just a barely passable uptake system, but it could give the bug's descendants a toe-hold. From there, if the bug (and the gene) can endure over time, more tweaking would result in further overtaking of the population.
Or not.
I'm waiting to see the paper :D
Posted by: clear as mud | June 3, 2008 4:29 PM
Haven't seen the paper, but I'm willing to speculate a little....
I think we can rule out horizontal gene transfer, as these were supposedly "pure" E. coli lines. My semi-naive speculation is that it is a known transport system that mutated such that it can now move citrate across the membrane effectively plus some additional mutations (in other genes) to effectively metabolize citrate (my metabolic biochemistry is extremely rusty). So I'd agree with clear as mud to some extent. As to the exact nature of the events (mutation vs duplication and mutation), we'll have to wait for a comment from someone who knows or the paper. I think it is pretty clear that it is multiple events, though.
Posted by: Ron | June 3, 2008 5:29 PM
This is a really cool result(and a useful reminder that one-in-a-billion is only a synonym for "not happening" on a human scale). I'll be interested to see what they end up learning about the nature of the change that gave these guys citrate metabolism.
More broadly, 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?
Posted by: phisrow | June 3, 2008 7:08 PM
I am not sure this is the place to post this, but carlzimmer.com is blocked by Firefox 3 as a reported attack site.
To see the report, o to http://safebrowsing.clients.google.com/safebrowsing/diagnostic?client=Firefox&hl=en-GB&site=http://carlzimmer.com/articles/index.php?subaction=showfull&id=1212035493&archive=&start_from=&ucat=11&
Is this a new form of attack by one of scienceblog's many enemies?
Posted by: ramiro quai | June 3, 2008 9:10 PM
Thank you, thank you, thank you. This has made my evening, and reinvigorated my love for and interest in biology.
Brian
Posted by: Brian | June 3, 2008 10:22 PM
horde not hoard
Posted by: Josh | June 3, 2008 10:30 PM
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.
I'm tired of the creationists claiming this never happens. It would be nice if there were one of these marathon bacterial studies which had something like this as a result, whether intended or not.
Posted by: Ian | June 4, 2008 6:45 AM
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.
These facts cause several questions to arise that must be answered before we can start claiming to have "proven" evoloution:
*If contamination occurred from citrate-eaters was identified by the flasks becoming cloudy, how did the researchers ensure that there wasn't also contamination by other bacteria that don't conveniently provide visual presence?
*Could it be that there were citrate-eaters present, in a population too small for detection, in the flask, at the time it was frozen? In other words, is it possible that the last frozen sample was in some cases already itself contaminated?
*If the E coli can develop the ability to eat citrate by acquiring plasmids from citrate-eaters, is there perhaps another mechanism by which they could have acquired this ability? Since we know that contamination by foreign bacteria DID occur, I don't see how this can be ruled out.
I would greatly love to see this experiment repeated in such a way as to rule out contamination by other bacteria.
Posted by: Heather | June 4, 2008 9:20 AM
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.
Posted by: Ken Finley | June 4, 2008 9:21 AM
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.
Posted by: Nate | June 4, 2008 9:30 AM
Excellent proof of evolution...but all the bible bangers can't handle the truth...so they won't believe in scientific proof...but will instead believe in some imaginary god which is no different than childrens imaginary friends.
Posted by: Enlightenment | June 4, 2008 9:50 AM
Even though my education on biology pretty much stopped when I graduated from high school all those years back, I can still identify that this is a fantastically astounding result. A very good read.
Posted by: Lachlan | June 4, 2008 10:07 AM
Sorry, there is no substitution for the Holy Bible! Word!
JT
http://www.FireMe.To/Udi
Posted by: John Collins | June 4, 2008 10:20 AM
@Nate
In terms of fitness in their environment it is of course a step forward.
Posted by: Travis | June 4, 2008 11:03 AM
Enlightenment,
This is a very novel and significant finding. However, it is not a proof for anything, especially that God doesn't exist. If it is proof for anything is seems fairly obvious that 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.
Posted by: Nate | June 4, 2008 11:05 AM
My goodness, who knew E. coli could bring out the anti-science brigades.
"If it is proof for anything is seems fairly obvious that it's proof that an organism cannot gain a capability through mutations without losing several others."
Where on Earth did you get that from? Which abilities did they lose... or gain for that matter? Have you read the paper? I don't think most anyone else has since it hasn't been released yet.
Yes, making leaps in logic is a problem all people must combat. This result (whatever the specifics) is not a "disproof of God". Nor is it proof of what you suggested. "Disproves God!" and "Microevolution!" are keywords of people on different sides using their pre-conceived ideas to jump over the logic presented by the facts before them.
Posted by: clear as mud | June 4, 2008 11:59 AM
Heather, I'm not a bacteriologist either but I'll try to answer your questions:
"If contamination occurred from citrate-eaters was identified by the flasks becoming cloudy, how did the researchers ensure that there wasn't also contamination by other bacteria that don't conveniently provide visual presence?" They did determine that the resulting E. coli were able to in fact digest citrate. They confirmed that these were E. coli.
"Could it be that there were citrate-eaters present, in a population too small for detection, in the flask, at the time it was frozen? In other words, is it possible that the last frozen sample was in some cases already itself contaminated?" This is unlikely, since they were able to essentially take the frozen flasks and rerun the experiment. They found(as I understand it. The paper still does not seem to be generally accessible) that the when one reran the experiment with the frozen flasks they sometimes evolved citrate digestion and sometimes did not.
"If the E coli can develop the ability to eat citrate by acquiring plasmids from citrate-eaters, is there perhaps another mechanism by which they could have acquired this ability? Since we know that contamination by foreign bacteria DID occur, I don't see how this can be ruled out." It is possible but unlikely given the evidence that it appeared to take multiple mutations. Hopefully followup work will find the specific genes responsible for this in which case we will be able to tell pretty clearly if these are pre-existing E. coli genes or not.
Posted by: Joshua Zelinsky | June 4, 2008 12:07 PM
Amazing article reminds me of how fascinated I am with science and biology.
Posted by: Cale | June 4, 2008 12:18 PM
Clear as Mud,
I am completely pro-science. That's why I said what I did. I work in a lab doing research. What do you do? Did you read the article?
"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."
So, I was simply pointing this out that while the bacteria were now able to uptake citrate they were losing other capabilities. I was also simply trying to limit the wrong extrapolations on both sides. Science by definition cannot prove the existance or non-existance of God, whether that God is Jehovah, Ala, or Vishnu. Also, data can only support or reject hypothesis, it cannot prove anything. So, I should have said this data supports the idea of evolution through mutation on a micro scale. Is that a correct statement or not? This is a fascinating discovery and I look forward to reading the paper.
Posted by: Nate | June 4, 2008 1:35 PM
Sterling report. Thanks, James
Posted by: James E. Tribble | June 4, 2008 1:42 PM
Ah yes. Small steps over 20 years are feasible, but small steps adding into significant changes over millions of years are completely unreasonable.
Posted by: Ray | June 4, 2008 2:19 PM
wow the immediate thing that strikes me is that the cultures differ in exposure to light based on their placement in the stack.
the energy of light especially certain type of fluorescent bulbs can strike gene molecules and cause mutation.
the mutation rates should be plotted based on exposure to the outside (more lite part ) of the stacks
Posted by: George Watson | June 4, 2008 3:17 PM
George,
I think the movie is of what was done with the plates after they were used in the experiment, and not of an experiment itself. The experiments were probably done in a light-free incubator, anyway.
Mel
Posted by: Mel | June 4, 2008 3:47 PM
a useful reminder that one-in-a-billion is only a synonym for "not happening" on a human scale
Statistically speaking, a "one in a billion" chance of something on a human scale gives you six to seven people with that something in the world. So anybody who's using it as a synonym for "not happening" needs to reboot their cliche server.
Posted by: Interrobang | June 4, 2008 4:52 PM
My first thought after reading about this experiment was, wow think what would happen if this population of bacteria was exposed to a multitude of different environments for a few hundred million years. Imagine what might develop.
Posted by: Bill | June 4, 2008 6:46 PM
Or when the dealer shuffles the cards, the deck will have ~ 1:10^68 chance of that order. [If the shuffle is perfect; there is no such thing of course.] I would say that anybody who's using it as such a synonym needs to reboot their math server.
Posted by: Torbj�rn Larsson, OM | June 4, 2008 6:46 PM
From a scene in Judgement Day: Intelligent Design on Trial
Posted by: James F | June 4, 2008 8:41 PM
Finley, you'd get farther by practicing your religion (and mine) of loving your neighbor as....Never knew anybody to be persuaded by such vitriol as yours. Breathe man, God can handle this His way not yours.
Posted by: Faith | June 4, 2008 9:34 PM
Interrobang: Statistically speaking, a "one in a billion" chance of something on a human scale gives you six to seven people with that something in the world.
And similarly, per Paul C, this may well have been a one-in-a-trillion chance, but they had 40 trillion bacteria!
... needs to reboot their cliche server. LOL!
Josh: Actually, it was critical to this experiment, that they were in fact hoarding their horde!
Posted by: David Harmon | June 4, 2008 9:48 PM
Reading this I was taken back to the book 'Artificial Life' by Steven Levy where the very same thing was observed through computer generated evolution. A recommended read for those interested.
Posted by: someone | June 5, 2008 1:38 AM
Very interesting article. Maybe we need to conserve the population of bacteria same as we conserve the flora and fauna.
Posted by: fazlinnazli | June 5, 2008 2:04 AM
Matt @ #8 -- prokaryotes like E. coli don't, as a rule, have introns. They have a single, circular chromosome which is extremely compact and generally has overlapping genes on both strands; no introns, and probably not much alternate splicing of gene products, either, to the best of my knowledge. Bacterial genomes are so small and compact that they simply don't have room for a lot of non-coding, non-control region junk -- rule of thumb is that there is a high selection pressure to keep their own size within certain hard limits, so there is at least that much selection pressure to keep their main chromosome's size down, too. The difference between the human genome and a bacterial genome isn't just size; the structural differences and differences in degree of functionality are also immense.
There are also small snippets of independent genetic material passed along through prokaryotic lines as plasmids, which can be (and often are) readily swapped between different species, however. These are not part of the main chromosome, however, and travel independently. It would have been possible -- though it looks like it has been controlled for -- that mutations which allowed the use of citrate were picked up in plasmids from contaminating bacteria.
@clear_as_mud -- "Species" is, as I understand it, an even more nebulous concept when it comes to high-mutation-rate, asexual critters like bacteria; which is why I've heard microbiologists refer to "species clouds" of bacteria which are not so much still all the same species, but are still very closely related and not really anything else. You can't name every single mutated strain a new full taxonomic name, which is why you end up with designations like E. coli O157:H7.
Posted by: Luna_the_cat | June 5, 2008 8:03 AM
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?
Posted by: Andrew Conkling | June 5, 2008 9:37 AM
Great experiment. Apologies for the rantings of some of my well-meaning but scientifically illiterate Christian friends.
Over on the ASA list (ASA is an organization of scientists who are also Christians) we have also been commenting on this experiment. ASA may be found at www.asa3.org -- we have a talk group which anyone may join.
Burgy
www.burgy.50megs.com/effect.htm
( a world of the really strange -- quantum mechanics)
Posted by: Burgy | June 5, 2008 10:18 AM
Andrew did read how many generations we are talking about here? 44,000 generations of E. coli since 1988. Human generations we think of around 25 years. Can't think in terms of human time scales. Evolution is happening all around all the time (not to mention on us and within us). Most of life on this planet isn't multicellular. Singled celled organisms and viruses are the norm, while we (humans and other multicellular eukaryotes) are the oddity. Look at HIV and drug resistance. Look at the flu. Evolution is very observable over what we humans consider "short" periods of time.
Posted by: ponderingfool | June 5, 2008 10:28 AM
Bridging a couple of points. At last year's "Wistar Retrospective",
Well, it seems that Lenski's bacteria have evolved a new structure, one for the consumption of citrate. I wonder if Behe will acknowledge this important challenge to his whole black box theory.I'm also reminded that at the same conference, pro-ID biologist Ann Gauger discussed an experiment she conducted that did not result in the emergence of the cell structures she anticipated. Reporter Daniel Brooks noted:
Wagner is a leading professor of evolutionary biology at Yale University.Vedddy Interesting.
Both of these can be found in this article at The Panda's Thumb
Posted by: Elf M. Sternberg | June 5, 2008 11:26 AM
Andrew: Evolution of bacteria happens constantly since they have several generations per day. This is why we constantly need new and more expensive research into antibiotics: most common bacterial threats have evolved resistance to most of the antibiotics 40 years old, and some (like MRSA) are resistant to almost everything we have today.
Posted by: Elf M. Sternberg | June 5, 2008 11:28 AM
@Andrew Conkling: we have also observed evolution in
--plants (for example, Spartina anglica, originated as a fertile species as the result of a polyploid mutation around 1870),
--algae (the green alga Chlorella vulgaris made the leap from being a unicellular organism to a multicellular colony organism in the lab, as a random-mutation-strongly-selected-for response to sustained protist predation, around 1988-89),
--insects (for example, the speciation of Culex so-called molestus -- there is a taxonomic conflict for that name which has not been resolved, hence the "so-called" -- from Culex pipiens, in the 100 years since Culex pipiens followed workers underground as they built the London subway system),
--and mice (a possible 6x speciation of Mus musculus in Madeira over the last 500 years, and a more recent drastic morphological and behavioral change on Gough Island within the last 150 years, although the extent of genetic differences in the Gough Island mice aren't known yet).
In the normal run of things, we do not observe full speciation events, since full species separation tends to take time. That does not mean that we have not observed evolution leading to speciation, however, or that we have *never* observed speciations. It's one of those wonderful situations of, now that we have some idea of what to look for and how to look for it, the more we look the more we find.
Posted by: Luna_the_cat | June 5, 2008 12:14 PM
Nate #31
So, I was simply pointing this out that while the bacteria were now able to uptake citrate they were losing other capabilities.
Well, no, you were asserting (without evidence) that this involved the loss of other capabilities. I think it's clear that you are involved in worldview defense here. You don't like the idea of useful mutations, so you assert that they have other strongly negative side-effects. I think this is fairly clear from your series of comments. First, you being with some uncertainty:
#22: I would like to know what all the tradeoffs were in these bacteria as well.
Then, later, make an assertion without evidence:
#27: If it is proof for anything is seems fairly obvious that it's proof that an organism cannot gain a capability through mutations without losing several others.
But back to your comment #31:
I was also simply trying to limit the wrong extrapolations on both sides.
On both sides? No, you're simply attempting to limit conclusions on the evolutionary side.
Science by definition cannot prove the existance or non-existance of God, whether that God is Jehovah, Ala, or Vishnu.
You're right about this one. Although many people (including you, apparently) feels the need to undermine scientific results because it's important to carve out a "science can't explain it" explanation in order to preserve a place for your God in the universe. Obviously, the evolution of bacteria (or macroevolution, more generally) cannot disprove the existence God, but many theists seem to act like it does and, thus, attack evolutionary evidence as if they are defending God. [sarcasm]I suggest that you widen your attack against all natural explanations, because all of them might erode belief in God. For example, maybe you should complain about the (naturalistic) theory of gravity - which is obviously meant to remove God from the job of pushing us down on the earth's surface. Attempts to claim that gravity happens naturalistically are obviously attacks on God himself.[/sarcasm] More seriously, you don't need to undermine evolution or gravity to maintain a belief in God.
Posted by: tinyfrog | June 5, 2008 2:45 PM
Luna, how could you forget the Mrcaru lizards, as well reported by SB's own GrrrlScientist? In barely 30 generations the lizard population shifted from an all-insect diet and to a plant-matter-heavy diet, requiring fundamental morphological changes to their gut to acheive that.
But such fundamental changes so quickly show that those lizards already had the potential for such structures in their DNA!
Posted by: Elf M. Sternberg | June 5, 2008 3:47 PM
Aw, man. You're right, Elf, I completely dropped the ball on that one.
I guess I got stuck at the mice.....
Posted by: Luna_the_cat | June 5, 2008 4:50 PM
More so as their respective populations apparently is best characterized by ecological niches:
I think that happens to viruses as well. And there it seems one can compare asexual and sexual population spread directly:
Posted by: Torbj�rn Larsson, OM | June 5, 2008 5:50 PM
Or perhaps viruses:
Posted by: Torbj�rn Larsson, OM | June 5, 2008 5:52 PM
Impressive!
It's exactly the same, depending on the pH: the salts of the citric acid are the citrates.
Not "while". Long before. Tens of thousands of generations before.
I also don't see what mechanism you imagine that somehow recognizes a mutation as leading to a "capability" and that somehow destroys "capabilities" to keep their number constant, or something. I recommend an introductory university course into genetics, or for that matter a highschool biology book.
I thought it's called C. molestans?
How do they show that?
Posted by: David Marjanović | June 5, 2008 6:08 PM
The post says they checked for the presence of plasmids and found none.
Posted by: David Marjanović | June 5, 2008 6:11 PM
wow
... thnax for this great report.i am a chemist bzsed here in saudi
Posted by: kenjebz | June 6, 2008 12:59 AM
@David Marjanović -- No, I'm pretty sure the fight is over the name molestus. And yeah, on re-reading I am indeed sure they eliminated the possibility that the E. coli had picked up plasmids from anything else.
It is an interesting paper -- what I really want to know, though, is what IS the necessary sequence of mutation which preceded Cit+ along that Ara-3 line? What do those mutations do? I would love to know more detail.
Posted by: Luna_the_)cat | June 6, 2008 4:59 AM
Thanks to Carl for such a great synopsis of the Lenski long-term lines. I'm a graduate of the Lenski lab and am happy to answer some of the more specific questions about trade-offs. I hope Zachary Blount (the first author on the most recent paper featured on this blog) chimes in to provide a few more specifics.
One of the papers we wrote on these trade-offs in the Lenski lines IS in fact open-access and can be found here:
http://www.biomedcentral.com/1471-2148/2/12
A few others are here: http://cooperlab.wikidot.com/publications
and here:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=298728
To summarize, we found that the first few beneficial mutations that took over these populations were pleiotropic , that is, they affected many phenotypes. In some cases, these reduced the ability of the evolved E. coli to grow in other environments. In one notable case, an entire set of genes required for growth on the sugar ribose were deleted. The end results were faster-growing E. coli on glucose, but at the expense of growing elsewhere.
Posted by: Vaughn | June 6, 2008 3:12 PM
One Major quibble.
You state they controlled for plasmids to make sure the batch was "pure". There is no nice easy way to check for plasmids unless you check each E. coli cell. Its physically impossible to do the gene sequencing that fast.
Besides their control is stated in the article... They looked at it and if it was cloudy they tossed it. The ol' eyeball control method isn't exactly "foolproof"
Please lets stay with the scientific facts and let others argue philosophy.
In this case the scientific facts show that they never had a real control at all except what they could see. On top of this little fact is that it has already been documented elsewhere that E. coli, certain strands, already had the ability to move citrates across its membrane to eat.
Until they do the gene sequencing to actually check for contamination or mutation we are all barking in the wind. If we hear nothing more on this subject the conclusion will be that it was contamination. If they provide a gene sequencing paper that is verified by others, then yes, he probably will get the Nobel Prize. Certainly not until then though.
Brian
Posted by: Brian Foote | June 9, 2008 4:35 PM
Ummmmm........ what is with the Bull crap about this proving evolution? Let me break it down to you. Mutation is the opposite of evolution, meaning it becomes flawed. This whole article is pointless.
Posted by: jake | June 9, 2008 5:32 PM
That was a very interesting article.
@Jake:
Mutations are not the opposite of evolution - mutation along with natural selection is what makes up evolution. (From my limited knowledge of biology) A mutation is simply a change in the DNA sequence, and yes, it can be harmful(which most mutations are), and so making the organism "flawed", or it can be neutral, or beneficial.
Posted by: Ralph | June 9, 2008 9:33 PM
Evolution is that lower life forms somehow gain information. Bacteria can "gain info" from bacteria, nothing higher than that.
Once you are above the bacteria stage, then there really is no Mutation that gains information. Mutation of DNA/RNA as a process for gaining information is a dead starting position. It cannibalizes/destroys some information to display its mutation in another direction. For higher life forms you must show how one GAINS INFORMATION. MUTATION NEVER ADDS information it changes what EXISTS. THey never show how such information comes into being in the first place.
Thus, Evolution never gets past the single celled organisms. OF course they have no explanation for how such a cell "appears" in the first place.
In short step 0 no cells they have no explanation
Step 1 1 celled organisms we have some cool bacteria
Step 2 2 celled organisms we have no explanation for higher forms
Step 1x1^nth celled organisms we really have no explanation because everything we do see is decreasing in Genetic complexity, increasing in bad mutations being passed to their children.
Brian
Posted by: Brian Foote | June 10, 2008 6:12 PM
Sorry, Brian Foote, you are making a lot of claims to truth, but they're only assumptions meant to buttress your own view that evolution can't work.
Evolution is that lower life forms somehow gain information.
Oh, okay, so you're saying that mutations can't produce information.
Once you are above the bacteria stage, then there really is no Mutation that gains information.
Wait - above the bacterial level, no mutation can add information? So which is it? Mutations can't produce information (as you claim in your first statement), or mutations can create information in bacteria but not higher organisms? You're being inconsistent.
Mutation of DNA/RNA as a process for gaining information is a dead starting position.
You need to think more about mutation, probability, and realize that mutations are very capable of (at the very least) optimizing genes. In fact, in order to make the statement that mutations can never produce information, you have to assume that mutations deliberately and mysteriously avoid causing any change that could improve an organism. For example, if a gene has a pre-existing harmful mutation, then you have to claim that all possible mutations to that gene will avoid changing it back to its normal form. You have to claim the absurd position that mutations *know* not to reverse a pre-existing harmful mutation.
Posted by: tinyfrog | June 10, 2008 10:24 PM
"Ummmmm........ what is with the Bull crap about this proving evolution? Let me break it down to you. Mutation is the opposite of evolution, meaning it becomes flawed. This whole article is pointless."
See, now don't all you scientists feel foolish? Each of you, having studied for tens of thousands of hours, schooled for years, and thousands of such scientists as you, working for decades... and Jake here is able to destroy all of your work and theories with just a couple of sentences typed between handfuls of cheetos.
Posted by: craig | June 10, 2008 10:30 PM
Brian@64 "Evolution is that lower life forms somehow gain information. Bacteria can "gain info" from bacteria, nothing higher than that."
Wow. Where did you get this silly idea? Evolution is a change in alleles in a population over time. There