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.
June 3rd, 2008 at 12:32 am
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.
June 3rd, 2008 at 12:57 am
Pure awesome.
June 3rd, 2008 at 3:03 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.
June 3rd, 2008 at 3:06 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).
June 3rd, 2008 at 6:06 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.
June 3rd, 2008 at 8:23 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…
June 3rd, 2008 at 8:50 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.
June 3rd, 2008 at 11:16 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?
June 3rd, 2008 at 1:27 pm
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!
June 3rd, 2008 at 3:48 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!
June 3rd, 2008 at 3:51 pm
Thanks, Baka. Very exciting stuff.
June 3rd, 2008 at 3:52 pm
creationist “yeah, but it’s still just a bacteria. Let me know when a bacteria evolves into a dog or a cat.” /creationist
June 3rd, 2008 at 4:29 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
June 3rd, 2008 at 5:29 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.
June 3rd, 2008 at 7:08 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?
June 3rd, 2008 at 9:10 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?
June 3rd, 2008 at 10:22 pm
Thank you, thank you, thank you. This has made my evening, and reinvigorated my love for and interest in biology.
Brian
June 3rd, 2008 at 10:30 pm
horde not hoard
June 4th, 2008 at 6:45 am
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.
June 4th, 2008 at 9:20 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.
June 4th, 2008 at 9:21 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.
June 4th, 2008 at 9:30 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.
June 4th, 2008 at 9:50 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.
June 4th, 2008 at 10:07 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.
June 4th, 2008 at 10:20 am
Sorry, there is no substitution for the Holy Bible! Word!
JT
http://www.FireMe.To/Udi
June 4th, 2008 at 11:03 am
@Nate
In terms of fitness in their environment it is of course a step forward.
June 4th, 2008 at 11:05 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.
June 4th, 2008 at 11:59 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.
June 4th, 2008 at 12:07 pm
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.
June 4th, 2008 at 12:18 pm
Amazing article reminds me of how fascinated I am with science and biology.
June 4th, 2008 at 1:35 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.
June 4th, 2008 at 1:42 pm
Sterling report. Thanks, James
June 4th, 2008 at 2:19 pm
Ah yes. Small steps over 20 years are feasible, but small steps adding into significant changes over millions of years are completely unreasonable.
June 4th, 2008 at 3:17 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
June 4th, 2008 at 3:47 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
June 4th, 2008 at 4:52 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.
June 4th, 2008 at 6:46 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.
June 4th, 2008 at 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.
June 4th, 2008 at 8:41 pm
From a scene in Judgement Day: Intelligent Design on Trial
June 4th, 2008 at 9:34 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.
June 4th, 2008 at 9:48 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!
June 5th, 2008 at 1:38 am
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.
June 5th, 2008 at 2:04 am
Very interesting article. Maybe we need to conserve the population of bacteria same as we conserve the flora and fauna.
June 5th, 2008 at 8:03 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.
June 5th, 2008 at 9:37 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?
June 5th, 2008 at 10:18 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)
June 5th, 2008 at 10:28 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.
June 5th, 2008 at 11:26 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
June 5th, 2008 at 11:28 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.
June 5th, 2008 at 12:14 pm
@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.
June 5th, 2008 at 2:45 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.
June 5th, 2008 at 3:47 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!
June 5th, 2008 at 4:50 pm
Aw, man. You’re right, Elf, I completely dropped the ball on that one.
I guess I got stuck at the mice…..
June 5th, 2008 at 5:50 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:
June 5th, 2008 at 5:52 pm
Or perhaps viruses:
June 5th, 2008 at 6:08 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?
June 5th, 2008 at 6:11 pm
The post says they checked for the presence of plasmids and found none.
June 6th, 2008 at 12:59 am
wow
… thnax for this great report.i am a chemist bzsed here in saudi
June 6th, 2008 at 4:59 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.
June 6th, 2008 at 3:12 pm
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.
June 9th, 2008 at 4:35 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
June 9th, 2008 at 5:32 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.
June 9th, 2008 at 9:33 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.
June 10th, 2008 at 6:12 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 1×1^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
June 10th, 2008 at 10:24 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.
June 10th, 2008 at 10:30 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.
June 10th, 2008 at 11:57 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 are several mechanisms for this, but the most important is probably natural selection acting on a pool of inheritable variability.
How do you measure information? One common mutation is the duplication of a strand of genetic material. If this happens, another mutation can occur in a duplicate section. How is this not information, by your use of the word?
“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.”
No, as I describe in the example above. Don’t you feel better about this conundrum now that you know it was a silly misunderstanding?
“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.”
Well, by mutation. Most mutations are neutral. Some are beneficial, some are harmful. If by higher life forms you mean sexually dimorphic critters like humans, the beneficial mutations tend to spread pretty rapidly. The harmful ones, of course, are those genes which are expressed as traits that are reproductively disadvantageous, and so of course tend to disappear from the gene pool.
“Thus, Evolution never gets past the single celled organisms.”
******************************************************
From: http://www.talkorigins.org/faqs/faq-speciation.html
Boraas (1983) reported the induction of multicellularity in a strain of Chlorella pyrenoidosa (since reclassified as C. vulgaris) by predation. He was growing the unicellular green alga in the first stage of a two stage continuous culture system as for food for a flagellate predator, Ochromonas sp., that was growing in the second stage. Due to the failure of a pump, flagellates washed back into the first stage. Within five days a colonial form of the Chlorella appeared. It rapidly came to dominate the culture. The colony size ranged from 4 cells to 32 cells. Eventually it stabilized at 8 cells. This colonial form has persisted in culture for about a decade. The new form has been keyed out using a number of algal taxonomic keys. They key out now as being in the genus Coelosphaerium, which is in a different family from Chlorella.
*****************************************************
So a single-celled organism adapted to a threat by becoming a colony organism (the simplest of multi-celled).
“Of course they have no explanation for how such a cell “appears” in the first place.”
Irrelevant to how evolution worked to produce the diversity of life, after the first cells showed up. There are folks who are doing serious work on how abiogenesis happened. We’ll get back to y’all when we get it figured out.
“In short step 0 no cells they have no explanation”
Sometimes the answer is ‘we don’t know’.
“Step 1 1 celled organisms we have some cool bacteria
Step 2 2 celled organisms we have no explanation for higher forms”
Sure we do. I showed you how a first step to multi-celled life was observed just a few years ago.
“Step 1×1^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.”
You are seriously confused, lad. We have a very good understanding of how recent evolution occurred. (Which doesn’t mean we don’t have a lot more yet to learn.) Mutation is a change in the genes passed on to the next generation; most mutations are neutral. You have about 100 mutations yourself, as do I. Bad mutations (genes expressed in reproductively disadvantageous ways) do not get passed on very well. Why on Earth would harmful genes accumulate?
And what *do you mean by “information” in this context?
June 11th, 2008 at 6:33 am
OMG, this is still hopping here.
I see the two biggest anti-evolution lies are active.
1) “Mutations are all bad, evolution can’t use it”
2) “Nothing in the universe confers “INFORMATION ™” to help evolution. No don’t ask me what “INFORMATION ™” means! I haven’t thought it through enough!”
thus, all of science is wrong.
Another annoying tendency by these folks:
1)Demand a complete explanation of every minute event from the beginning of time to today, whether or not enough research has ever happened.
2)Deny every point, anyway, because you don’t believe anything scientists say.
3)If there is even the tiniest uncertainty, though, it absolutely proves all of science is LYING!
(Man, life is so easy this way… you’re right no matter how wrong you really are!)
June 11th, 2008 at 4:32 pm
You keep saying some mutations are good bad indifferent. whether that statement is right has no bearing on the discussion. You can’t get DNA from NO DNA its blatant ignorance to say otherwise.
For a single cell to exist it must
1) have a cell wall
2) Ways to pass food/waste through cell wall
3) Digest said food
4) Differentiate Between what is good and waste to get rid of waste
5) Replicate itself.
If any of the above do not exist all at the same time you never get to single celled organisms.
Evolutionists still have the problem that once said cell with its 400 genes(simplest single celled organism we know of) exists it has to gain more genes. Mutations don’t add Genes to DNA strands. They change what is there. Changing of 400 gene DNA strands trillions of times won’t make DNA strands with 401 genes. There is no process to INCREASE the amount of information inherent in the single celled organisms.
Fact is, for people to believe evolution you must show the steps otherwise you are simply believing that evolution is true.
Fact, evolutionists believe by faith that the universe spontaneously appeared with no scientific supporting evidence and plenty against it.
Fact, evolutionists believe by faith that a single celled organism spontaneously appeared.
Fact, Evolution is Faith
Brian
June 11th, 2008 at 4:54 pm
Brian, you are a right moron. I won’t even touch the other things you mentioned because they are irrelevant. But you should know better than to equate abiogenesis with evolution. Unless you skipped that section of the pamphlet they were handing out in Sunday School.
This renders your point of evolution requiring faith moot and unfounded since evolution does not entail what you claim it does.
June 11th, 2008 at 6:10 pm
I notice you never even bothered to answer my DNA point for increasing DNA strand length, just started name calling… Still waiting for a rational explanation of that one…
Did you even read what you wrote ChrisD? Abiogenesis is the base of evolution and those who want to claim there is no God.
Did you miss the simple logic card passed out at the latest atheist rally?
Step 1 life came from non life? Followed by Step 2 life obtaining more complex DNA somehow…
Brian
June 11th, 2008 at 9:24 pm
Actually, gene duplication is a common mutation. They are not quite as common as point mutations, which is what you’re babbling on about, but they do happen.
Basic genetics for dummies:
http://scienceblogs.com/pharyngula/2008/04/basics_how_can_chromosome_numb.php
June 11th, 2008 at 9:27 pm
And of course, once a gene has duplicated, it can then undero mutations which can in turn provide… a new feature:
The Evolution of Trichromatic Color Vision by Opsin Gene Duplication in New World and Old World Primates
http://www.genome.org/cgi/content/abstract/9/7/629
June 11th, 2008 at 9:33 pm
[Mutations don’t add Genes to DNA strands. They change what is there. Changing of 400 gene DNA strands trillions of times won’t make DNA strands with 401 genes. There is no process to INCREASE the amount of information inherent in the single celled organisms.]
Can you prove that with 100% certainty? I don’t think so. I know there has been at least 1 documented case of genetic mutation which has fused 2 genes into 1 in the human genome (via researching using alleles on said gene which were found not only at the ends, but also in the middle). Why would it be impossible for a mutation to not create an extra? Improbable? Perhaps. Impossible? No. It may have already happened and just not been a beneficial mutation that was passed along.
June 11th, 2008 at 9:47 pm
No, it follows as an inference from biochemistry. We are ignorant of the process, but no one — certainly not a ignoranimus like you — has ever shown as a biochemical fact that it is impossible.
To do so, you would need to examine every single organic chemical compound and combination of compounds, in every possible environment, exposed to every possible combination of energy inputs.
You, on the other hand, would have trouble adding vinegar to baking soda unsupervised.
Fixed.
Fixed.
Fixed.
June 11th, 2008 at 11:09 pm
Creationsits should understand that the writing by various personages from biblical times were more reporters of the news of the time, while science tries to give a step-by-step of how things seem to go together and work. A sort of book of direction on how to fix things.
I see no great divide between belief in God and accepting the information of how provided by science. It all fits rather nicely. Because a thing is not explained in the Bible does not prevent it from being or happening.
June 12th, 2008 at 8:38 am
Well if you don’t want to be called names then quit fitting the definition of those names so well. How can I argue with you since what you are saying with regard is wrong on a factual level as it relates to evolution?
Evolution has nothing to say about the origin of life, but states that once the ball got rolling (in whichever method suits your emotions best), evolution by natural selection is what lead to the diversity we see today. Period. No speculation about which unmoved mover diddled what diddley where to get the ball rolling - it’s irrelevant.
June 12th, 2008 at 8:39 am
Correction to the above: Omit “with regard”.
June 12th, 2008 at 11:39 am
Owlmirror: I’ll take your gene duplication event and raise you one
Saccharomyces (baker’s yeast) seems to have duplicated its entire genome at some point in the past:
http://web.mit.edu/manoli/www/publications/Kellis_Nature_04.pdf
Brian: Usually we talk about mutations as if they were simple “letter” changes. This –> Thus —> Thug etc. Sometimes the machinery that duplicates DNA screws up; sometimes some outside “insult” damages the DNA (radiation, or a chemical). If that were the only way mutations arose, it would make sense that the number of genes wouldn’t change. But as the pharyingula link points out, the machinery that duplicates DNA can screw up in other ways too. Sometimes when it’s copying DNA, it copies the same part twice. This gives two identical copies of a stretch of DNA. If there were genes in that stretch, now there are two copies of each one. Often, that can be a harmful thing: some proteins have to be in a cell at specific levels, and if there’s two copies of a gene creating a protein, that can be bad. On the other hand, sometimes there’s a lot of flexibility built in to the system, and a cell can cope with this.
With two copies, a cell gains a certain “freedom.” If you owned one car, you might be reluctant to tinker with it, since it’s the only car you have. With a second car, you might feel more free to “pimp” one car a bit, since now you have a spare if you somehow damage the first car beyond repair. In my example, of course, there’s a conscious decision involved. In the case of cells, this simply means that a cell doesn’t *care* what happens to the extra copy of the gene. Sometimes it acquires a harmful mutation. Cells can usually safely ignore this, now, since they never needed that copy of the gene in the first place. Indeed, the human genome is littered with examples of “pseuodgenes” which no longer do anything, but which seem to have arisen as copies of genes which DO have functions. But sometimes, this tinkering creates something new. It doesn’t even take a LOT of tinkering. In Owlmirror’s example, a gene whose product helps detects light duplicated, and then changed so that it was senstitive to a different color of light. In this way, you can go from “black-and-white” light sensitivity to color vision (I know, I’m simplifying a bit). There’s a ton of other examples of a duplicated copy of a gene being altered to have a new function. In biology, we often talk about “gene families” in which a single gene was duplicated over and over until you have sometimes dozens of related genes which all do different things. Often, you can identify these duplicate genes because they’re located near the original gene (in one species you find a single copy; in another species you find two), though over time, genes can shuffle themselves around.
The point in all of this, though is that even if you start with 400 genes, there are a number of mechanisms for increasing the number of genes over time.
June 12th, 2008 at 1:17 pm
Hi, my name is Zachary Blount. I am the first author on the paper this posting describes. I am sorry I am late coming to the party here, but I was traveling when it came out, and just now got home to regular internet access. If anyone is still checking this comment section, I would be happy to answer in as timely a fashion as I can anyone’s questions that would help clarify the research described in the paper.
June 12th, 2008 at 3:17 pm
Zachary Blount said,
There is not just this comment section — hundreds of comments about your research are on the New Scientist magazine website, the Panda’s Thumb blog, the Uncommon Descent Blog, Ed Brayton’s Dispatches from the Culture Wars blog, and possibly other places. Michael Behe wrote a response to your research results. Links to these websites (except Ed Brayton’s blog) are on my following blog post:
http://im-from-missouri.blogspot.com/2008/06/lenskis-e-coli-bacterial-microevolution.html
BTW, all of the blogs mentioned except mine practice arbitrary censorship of comments and commenters and so may be unreliable.
The following comment is excerpted from the above post on my blog:
The mutations appear to have occurred at two or even three stages — the first — or preliminary — mutation at around the 27,000th generation (around the 20,000th generation according to some sources), the second at around the 31,500th generation, and possibly a third around the 33,000th generation.
Question: To what extent did the first mutation spread through the population, if it spread at all, considering that it apparently conferred no advantage?
There were around 44,000 generations in 20 years, or about 2,200 generations per year. So assuming that the first mutation occurred at 27,000 generations and the second occurred at 31,500 generations, that would be about 2 years from the first mutation until the second mutation. That seems to mean that the second mutation is rare — however, on the other hand this second mutation appears to be common because it was repeated numerous times by starting with the unfrozen samples of previous generations. So how could the second mutation be both rare and common at the same time? Maybe the second mutation is really quite common but is rarely expressed because there are relatively few individuals with the first mutation, which confers no advantage.
Carl Zimmer says in the original post,
The original post gives the following explanation for the preceding observations:
Actually, the rise and fall at 31,500 and 33,000 generations respectively is not what indicates that the citrate-eating trait is not just a one-mutation affair, because — as noted above — it appears that an essential preliminary mutation occurred at around 27,000 generations (around 20,000 according to some sources).
Also, in a sense the citrate-eating bacteria are not really competing with the glucose-eating bacteria, because the two kinds of bacteria have different food sources.
The citrate-eaters were initially getting quite good at competing with the glucose-eaters, rising to 19% before nearly vanishing and then becoming dominant. The opening post does not adequately explain why the citrate-eaters nearly vanished.
Also, the original post said,
As I calculated above, there is an average of about 2,200 generations per year, so if a new population was started each day with a sample from an old population, then there were about 6 generations per population. With only 6 generations, there might be a significant possibility — depending on the size of the sample — that a mutation occurring in an old population would not be collected in the sample used to start the next population, particularly if the mutation occurred in one of the last generations of the old population. The populations should of course be well-stirred before collecting the samples to start the next populations — the original post says that he flasks full of E. coli were placed on a “gently rocking table”, and I presume that means that the populations were well-stirred before collecting the samples.
June 12th, 2008 at 6:20 pm
Michael Behe wrote of the Lenski-Blount-Borland study,
I agree with Behe. Even though I think that the second mutation in the Lenski-Blount-Borland study is fairly common (because it often re-appeared in populations that descended from frozen samples of the 27,000th — or 20,000th according to some sources — generation or later), it took approx. 4,500-11,500 generations or approx. 2-5 years for the second mutation to be expressed at approx. the 31,500th generation, and I think that was because there was a scarcity of bacteria with the preliminary first mutation because the preliminary first mutation alone conferred no advantage in survival. So if more mutations are needed, the chance of getting all the right ones in one bacterium grows exponentially worse, as Behe said.
I wonder if there is any data on how quickly the second mutation was re-expressed in the populations descended from the unfrozen populations of 20,000-27,000 generations or later.
June 13th, 2008 at 7:57 am
I know I’m days late to the party but I just wanted to chime in to direct people’s attention to a really cool and conceptually related paper on the evolutionary robustness of genetic coding schemes:
The Rate of Compensatory Mutation in the DNA Bacteriophage {phi}X174
(
Bacteriophages are viruses that eat microbes and there’s ~10 of them for every bacteria on the planet and they’re a huge driver behind evolution. Everyday, bacteriophage kill in the ballpark of a third of the bacteria on the planet. They can steal genes from their hosts, mess around with them for their own ends for generations, and insert them into other hosts. This makes them (1) potential generators of genetic novelty, (2) potential mechanisms for lateral gene transfer (like plasmids, which keep being brought up) and (3) predators of bacteria that can potentially drive bacterial evolution through red queen dynamics. If you want to maximize the number of “independently selectable copies” of a protein that might jump around and mutate in crazy ways, bacteriophage aren’t a bad place to look.
)
Anyway, the article I wanted to direct people’s attention to gets quantitative with bacteriophage evolutionary issues in a cool way:
=====ABSTRACT START======
A compensatory mutation occurs when the fitness loss caused by one mutation is remedied by its epistatic interaction with a second mutation at a different site in the genome. This poorly understood biological phenomenon has important implications, not only for the evolutionary consequences of mutation, but also for the genetic complexity of adaptation. We have carried out the first direct experimental measurement of the average rate of compensatory mutation. An arbitrary selection of 21 missense substitutions with deleterious effects on fitness was introduced by site-directed mutagenesis into the bacteriophage {phi}X174. For each deleterious mutation, we evolved 8 - 16 replicate populations to determine the frequency at which a compensatory mutation, instead of the back mutation, was acquired to recover fitness. The overall frequency of compensatory mutation was ~70%. Deleterious mutations that were more severe were significantly more likely to be compensated for. Furthermore, experimental reversion of deleterious mutations revealed that compensatory mutations have deleterious effects in a wild-type background. A large diversity of intragenic compensatory mutations was identified from sequencing fitness-recovering genotypes. Subsequent analyses of intragenic mutation diversity revealed a significant degree of clustering around the deleterious mutation in the linear sequence and also within folded protein structures. Moreover, a likelihood analysis of mutation diversity predicts that, on average, a deleterious mutation can be compensated by about nine different intragenic compensatory mutations. We estimate that about half of all compensatory mutations are located extragenically in this organism.
======ABSTRACT END=======
Basically it’s good to remember that the longer the descendants of a single isolated strain “hang out” the more chances for harmful mutations that are subsequently compensated for. It’s likely that over time, you’ll get a “halo” of genomes with genetic differences (with different potentials for positive mutations) that are nonetheless reasonably stable as far as gross phenotype goes. And the bigger the disaster the better chance there’s a way to compensate for it…
A lot of quantitative/theoretical issues with “multiple steps to find a positive mutation” are ameliorated when you remember this. Genomes might be simply that robust. Instead of “two improbable steps” it might be more plausible to imagine “twenty damage/repair cycles that eventually open up a new path”.
–
It would be keen to see if different prophages (bacteriophages laying dormant in a bacterial genome) are lurking in any of the involved strains.
A lot of times they pop out just by exposing a culture to bit of DNA damage (the phages detect the DNA damage and you get a “rats fleeing a sinking ship” effect as bacteria start to die from viruses) so it’d be cheap to try for a clear positive sign that phages might be involved before going to the trouble of sequencing anything. If the phages pop out you could sequence just the phages, rather than the whole genome. Bacteriophage genomes are frequently less than a hundred kilobases.
(Apologies if some of the bacteria have already been sequenced or otherwise checked for phages, I couldn’t get the full paper because I don’t have academic library access right now.)
June 13th, 2008 at 10:43 am
Larry F: Why would you not assume that a given mutation can spread even though it does not confer an advantage? A mutation can be neutral, and thus, the chance of a given mutation spreading is in some ways like the chance of someone winning the lottery. It happens every time they run a lottery that someone wins! (But you and I are not going to). This is basic probability.
June 13th, 2008 at 11:07 am
Just to add to what Greg said, neutral mutations actually have a very good chance of spreading through the gene pool. This mechanism is called genetic drift and is especially probable in small populations such as these.
June 13th, 2008 at 11:08 am
Thank you, Larry. I’ve been really puzzled by the basic concepts behind some ID lines of thought, but your comment made one of them absurdly clear.
Who (besides Behe) suggested that only mutations that confer a direct advantage get passed on? In fact, the only mutations that are likely not to get passed on are the radically nonadaptive–the rapidly fatal ones, those that prevent reproduction, etc. Everything else, barring accident or unfitness unrelated to the mutation, will get around a bit. I mean, really, if the tendency to store fat in such a way as to create a beer belly is still with us….
June 13th, 2008 at 11:15 am
I think part of the confusion is the conflation that happens all the time among creationists between day to day population genetics and selection.
Try it. Recite this mantra several times a day for several days:
“Evolution is not real. It is not possible to achieve the complexity we see in life from mere random chance. An aardvark cannot be assembled when the tornado hits the junkyard.”
After a while you will conflate selection and mutation as one process. That can lead to the benighted confusion we see above (and generally in everything Larry F. writes or says. And Behe.)
June 13th, 2008 at 11:22 am
Stephanie,
My beer belly isn’t adaptive? What about as a source of energy to keep me warm in winter?
*sigh*
June 13th, 2008 at 11:46 am
@ponderingfool, Elf M. Sternberg, Luna_the_cat, and PirateHooker (via my blog for some reason): Thanks for the comments; makes sense, I just didn’t know that.
June 13th, 2008 at 11:48 am
@Zachary
I’m not a biologist, so forgive me if this sounds ignorant. Will the evolved E. coli be sequenced so that the actual gene changes can be located? Also, the other populations which did not evolve this capability, would they also be sequenced to find if they carried a neutral change? I’m just ecstatic about this research, it is cool beyond cool.
June 13th, 2008 at 11:49 am
Who left the door open on Larry’s cage? How many times do I have to say it, when you get done poking him with the stick, MAKE SURE TO CLOSE AND LOCK THE DOOR!
June 13th, 2008 at 11:56 am
Arguing with Larry is as smashing your head into a brick wall. Don’t worry folks. As Larry the Omnipotent told us on the Florida Citizens for Science webpage If he wasn’t taught it in high school (1960s) then it is not valid!
June 13th, 2008 at 12:02 pm
What are the ODDS against that happening!!
Goddidit!
Just kidding.
June 13th, 2008 at 12:07 pm
Just skimmed this thread and am a bit time pressed today.
Lots of questions about this paper. For the cognescienti, if they will.
1. IIRC, Lenski et al. found 1/3 of their lines picked up mutator phenotypes. Are these the ones that evolved cit+?
2. What do you/they think of the various adaptive mutation theories which have some experimental support floating around. e.g. the work of Hall, BG and so on?
3. The cit+ cultures seem to require 3 mutations. I realize the nature of all 3 probably aren’t known, but what info do you have? One of my wild guesses would be a mutator, followed by a permease specificity change, and maybe upregulation of the permease and/or the enzymes that metabolize citrate, the TCA cycle. TIA.
June 13th, 2008 at 12:28 pm
Awesome, fascinant, overwhelming to say the minimum, the educative power of it is beyond imagination and I wonder if to raise the collective knowledge and wisdom of our species
a similar endevour could be run with entities we use to call “creationists” in order to explore the possibilities that our species could ever become, collectively, scientifically aware of itself and its surroundings in logical and rational terms and so left behind the misleading viral concept of God that unfortunately long ago Plato set up so absurdly but disguised as logical.
June 13th, 2008 at 12:41 pm
I love Larry. He, with his bizarrely ill-informed opinions on law, biology, history and, well, pretty much everything encapsulates our narcissistic, self-important Country’s mind-set better than any textbook could ever hope to achieve.
Plus, Larry has a rock-solid function in life. I equate Larry to the South Pole of a magnet, wherever he points, you can find the truth in the oppo