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November 25, 2009

Not so fast!

I always enjoy Olivia Judson's columns in the New York Times, but today's post on evolution "failing" left out an important point. She referred to a paper published last year from Richard Lenski's long-term evolution experiment, showing that a bacterial population took 31,000 generations to evolve the ability to use citrate. Furthermore, although she didn't mention this, this trait has only evolved, so far, in one of their twelve replicate populations. If evolution is too slow to keep up with the changes we humans are making in the environment, then species that might evolve and survive if changes were slower will instead go extinct.

I agree that this is a significant problem, but I wouldn't assume that it would take polar bears, for example, 31,000 generations to evolve adaptations to warmer temperatures. The bacteria that Lenski's group studies don't have sex. So if one cell has a mutation that would allow it to use citrate, but only in combination with a second mutation found in another cell, they don't have any way to combine the two mutations in one citrate-using individual. If cells with only one mutation or the other have no advantage over cells with neither, then lineages with the first mutation will usually die out before acquiring the second mutation. A lineage could die out, for example, because the next mutation is gets is one of the many lethal ones, rather than one of the few beneficial ones.

Bacterial populations can sometimes evolve rapidly (with significant changes in only a few days) because their generation times are so short and because their large population sizes include many mutants. Evolution requiring a series of steps isn't a problem so long as each step is an improvement. But when a mutation is neutral or negative, except in the context of a second mutation, sexual species can evolve faster. Not necessarily fast enough to save the polar bears, though.

Celebrating "The Origin of Species" everywhere

Poster advertising Darwin symposium in Beckley, West Virginia, where I was a USDA researcher for several years.

Yesterday, I'm told, was the 150th anniversary of the publication of The Origin of Species. In honor of this occasion, and of the 200th anniversary of Darwin's birth, 12 February 1809, there were major symposia at the Universities of Cambridge and Chicago, and minor ones all over; I wasn't the only one to make a commemorative cake, although I thought mine was more scientific than most, but probably not as tasty as if it had evolved, with selection imposed by human preferences.

November 23, 2009

Off-topic: Jam Hound helps musicians improve their skills

When I was a grad student, I used to enjoy weekly play-along "jam sessions", where a group of people would get together and play old-time, bluegrass, or Celtic music. The better musicians were mostly pretty patient with us beginners, but I sometimes wished I could practice a bit beforehand, learning songs at my own speed. I could usually do fairly well on penny whistle, but could never keep up on banjo or hammer dulcimer. What I needed was Jam Hound, a free website set up by my brother, Glenn, a mandolin and guitar player and computer genius.

So far, the site includes:
* Rhythm Track Generator
* Ear Training
* Fingerboard Tutors
...mainly intended for musicians, including beginners, playing folk songs and fiddle tunes.

If you're interested, have a look and leave a comment if you have any suggestions for improvements.

Are ants' fungus gardens a source or sink for nitrogen?

This week's paper, Symbiotic Nitrogen Fixation in the Fungus Gardens of Leaf-Cutter Ants, has already been discussed by Ed Yong, whose blog is among my favorites, and by the always-interesting Susan Milius of Science News. When she interviewed me, I endorsed the main conclusions of the article but expressed skepticism on one point.

The paper clearly shows that the fungus "gardens" cultivated by leaf-cutter ants contain bacteria that extract nitrogen from the air. The part I wondered about was their statement that:

We estimate that a single mature leaf-cutter ant colony may contribute as much as 1.8 kg of fixed N per year into neotropical ecosystems (see SOM text for details).
The ant colonies are part of the ecosystem, so I guess nitrogen the colony contributes to itself is a contribution to the ecosystem, just like profits made by currency speculators are a contribution to the economy. But are the ant colonies a source of nitrogen for neighboring plants, or are they taking nitrogen from those plants?

Page 14 of the Supplementary Material presents estimates from a paper by Wirth and colleagues showing that the ants harvest leaves containing 18 grams of nitrogen each day, and discard 12 grams of nitrogen (used-up leaves, etc.) in refuse piles. They estimate that 4.9 grams of that discarded nitrogen comes from the nitrogen-fixing bacteria in the ants' fungus garden, but so what? They are still taking 6 grams more nitrogen from the plant community each day than they are returning.

Before we can decide whether ant colonies are a source or a sink of nitrogen, we need to know what happens to the 6 grams of nitrogen that apparently disappears into the ant colony each day. When ants defecate away from home, that could return some nitrogen to the plant community, a contribution not included in the calculation above. Nitrogen that accumulates within the fungus garden may eventually become available to plant roots when the nest is abandoned. But some nitrogen in the ant colony may be permanently lost from the ecosystem. This includes gaseous losses as ammonia or nitrogen oxides. Nitrate nitrogen can move down into the soil with percolating water; some of this leached nitrogen may be recaptured by roots before it gets too deep in the soil, but the rest will be lost, eventually reaching a river or ocean.

Until we have more information on these processes, all we can say is that the colony appears to take more nitrogen from the plant community than it returns to them, despite the fact that the ants get some of their nitrogen from nitrogen fixation rather than importing all of it in harvested leaves.

Furthermore, the nitrogen they do return is distributed, not for maximum benefit to the plant community, but for the convenience of the ants. This reminds me of a feed lot that takes in grain-protein nitrogen from a large area, then dumps manure nitrogen in a small area at higher rates than plants can use.

There is also an interesting evolutionary question here. Why do the bacteria in the ant gardens fix nitrogen? Symbiotic rhizobium bacteria in the root nodules of legumes fix much more nitrogen than they need for their own growth and give most of it to their plant hosts. We showed that they do this because nodules that fail to provide their hosts with nitrogen are subject to sanctions that reduce the reproduction of rhizobia inside (Kiers et al. 2003); this prevents such "cheaters" from becoming too common. But I don't see how ants could impose sanctions on different bacterial genotypes based on how much nitrogen they fix. So my guess is that these bacteria only make as much nitrogen as they need for their own growth, and release it mainly when they die. Or, perhaps, when they are killed.

Kiers, E.T., Rousseau, R.A., West, S.A. & Denison, R.F. (2003) Host sanctions and the legume-rhizobium mutualism. Nature, 425, 78-81.

R. Wirth, H. Herz, R. J. Ryel, W. Beyschlag, B. Holldobler, Herbivory of leaf-
cutting ants. A case study on Atta colombica in the tropical rain forest of
Panama, Ecological Studies (Springer, Berlin, Heidelberg, 2003), pp. xvi, 230.

November 16, 2009

Return of the viruses

I just read a disturbing post on the amusingly-titled serious-science blog "Mystery Rays from Outer Space", discussing two examples of human pathogens that apparently escaped from laboratories. The key evidence, in each case, is evolution... or rather, lack of evolution....

The most recent example is from PLoS-One: a dengue virus now infecting people in Brazil and Columbia is almost identical, genetically, to a virus last seen in Asia twenty years ago. An earlier example was published in Nature in 1978, reporting an H1N1 flu virus whose closest genetic match was from 1950 version.

Why do we think that these viruses escaped from (or were released from) laboratories? Couldn't they have been living in some isolated human population in a remote valley, or perhaps in some wild species? No. Over a twenty-year period, the viruses would have evolved, through some combination of random mutation, nonrandom natural selection (like that imposed by the immune systems of its hosts), and random genetic drift (changes in the frequency of different genotypes due to chance). As the 1978 Nature paper put it, the only way the virus wouldn't have evolved over the course of 20 years is if it were "frozen" somewhere.

A laboratory freezer seems the most likely culprit. Under that hypothesis, scientists must have thawed an old sample, presumably for research purposes, and then carelessly infected themselves and then others. It is possible, however, that the virus was frozen somewhere else, like in the frozen body of a mountain climber recovered from a glacier after twenty years.

November 11, 2009

Experimental evolution of bet hedging

Will headshot.jpg
Guest blogger: Will Ratcliff

This week's paper, "Experimental evolution of bet hedging" by Hubertus Beaumont, Jenna Gallie, Christian Kost, Gayle Ferguson and Paul Rainey, published in Nature, shows that a trait that initially evolves for non bet hedging purposes can be maintained in the population through bet hedging.

The theory of bet hedging was first mathematically developed by Daniel Bernoulli (yes, the Bernoulli we all learned about in high school physics) in 1738. Because the basic idea is so simple - uncertain future conditions make conservative strategies beneficial - it is likely that folk wisdom advising bet hedging long predates Bernoulli's maths. The phrase "Don't put all your eggs in one basket" is one example of a widespread but anachronistic reminder to spread risk. Before we dive into this week's paper, I want to briefly cover the theory of bet hedging.

Like investing in the stock market, evolution is a multiplicative process, not an additive one. Steve Stearns (2000) illustrates this well....

"If a genotype has reproductive success that is twice the [population's] average in this generation and three times the average in the next, then its fitness [measured, as usual, relative to the population average] over those two generations is six times (2 × 3), not five times (2 + 3). If each of two children has three grandchildren, then there are six, not five, grandchildren."

This means that the correct way to measure average returns is the geometric mean, not the arithmetic mean. The geometric mean is fairly easy to find: just multiply a genotype's fitness in generations 1 through n, and then take the nth root of that number. For example, the geometric mean of 3, 2, and 4 is the cube root of 24 (3x2x4), or about 2.88. Key properties of the geometric mean are:

1) It is always lower than the arithmetic mean. For example, the arithmetic mean of 3, 2, and 4 is 3, which is greater than 2.88. The amount that it is lower depends on how variable fitness is during the period in which it is measured. The more variable fitness is, the lower the geometric mean is relative to the arithmetic mean.

2) Genotypes with the highest geometric mean fitness will dominate the population over the long-term. Natural selection thus optimizes the geometric mean, not the arithmetic mean (though in the short-term this is not always true: see this recent paper that I really should blog about).

So, what does this all have to do with bet hedging? Qualitatively, bet hedging is defined as a trait that spreads risk, trading-off some potential short-term benefit for a long-term benefit. "Trading off" implies that a bet hedging trait is one that reduces arithmetic mean fitness but increases geometric mean fitness. Let me illustrate with an example: assume that for an annual plant, March 23rd is the single best day for its seeds to germinate. However, there is a small risk that there will be a severe frost that kills 95% of the seedlings that germinated that day. This event is rare enough to have little effect on the arithmetic mean, but it has a big effect on the geometric mean. A plant genotype that produces seeds which all germinate on March 23rd will have the highest fitness in the population until the year that early frost hits, but then that lineage will decrease drastically. If a plant were to leave seeds that germinate from March 15-30th, it is giving up some potential arithmetic mean fitness because many of its seeds are germinating at suboptimal dates, but by spreading risk it reduces variation in fitness and increases geometric mean fitness. This would be bet hedging.

Thus we arrive at the central problem with empirical bet hedging research: how do we know if a putative bet hedging trait evolved for the purposes of bet hedging? Simply observing that a trait is unexpectedly variable provides no evidence for bet hedging. One needs to show that the trait decreases arithmetic mean fitness, but increases geometric mean fitness. As stated by Andrew Simons (2009, see Ford's blog post on this paper) "It is because of difficulties in characterizing the fitness effects of environmental variance over appropriate time scales that so little empirical work on bet hedging exists." A more subtle variation on the above question has to do with evolutionary dynamics: might a trait evolve for reasons other than bet hedging, then be maintained as a bet hedging strategy when conditions change?
If only we had the complete history of an organism's evolution of bet hedging! Then we could actually answer the questions above...

Enter this week's blog post. Paul Rainey's group works with the bacterium Pseudomonas fluorescens, which is well-known for experimental evolutionary studies on adaptive radiation. A new niche for these bacteria can be created simply by letting a flask of nutrient media sit still on a bench. Mutants capable of making a surface biofilm (and getting access to oxygen, a limiting nutrient when the flask is still) have a large fitness advantage and quickly invade. Shaking the flask removes this niche and the biofilm formers are quickly outcompeted by non-biofilm formers.

The authors created an environment that fluctuated frequently by transferring bacteria from static to shaking flasks. Further, they waited to make the transfer until a new genotype evolved in the flask with a different colony shape, transferring only this rare genotype to the next flask (Figure 1). This transfer strategy sets the fitness of the common genotype to 0. In order to maximize geometric mean fitness (or even have it greater than 0 after two transfers), a single genotype must produce variation in colony morphology faster than a different genotype with novel colony morphology can arise through mutation and selection.
Thumbnail image for bet-hedge.jpg
Figure 1- Pseudomonas transfer regime

Beaumont et al. found that in 2 out of 12 replicate selection lines, a single genotype evolved that stochastically switched the expression of a gene that encapsulated the bacteria on and off. As a result, this single genotype formed two distinct colonies, depending on whether or not the cell that founded the colony was encapsulated or not. Unlike all the other non-switching genotypes, this genotype was able to persist in the selection experiment through many transfers.

So is this bet hedging? In the context of our definition of bet hedging above, the genotype that generates new colony morphologies at a high rate (thereby increasing geometric mean fitness) must come at a cost to growth rate within a single flask, relative to a non-switching genotype (thereby reducing arithmetic mean fitness). This is not what happened.
The mutation leading to switching was totally beneficial relative to the immediate ancestor. Within a single flask, it actually grew faster than the immediate ancestor, possessing a relative fitness of ~1.18. As a result, this mutation increased both arithmetic and geometric mean fitness, so did not originally evolve because of bet-hedging.

Although the initial evolution of this trait doesn't meet our definition of bet hedging, the persistence of this genotype in the experiment can be attributed to bet hedging. No non-switching genotypes were able to invade the population, and thus be passed on to new flasks, because the switching genotype generated variation in colony morphology so quickly. This illustrates that the switching genotype had the highest geometric mean fitness of any strain tested. But further experiments showed that the switching genotype did not always possess the highest arithmetic mean fitness.

When the switching genotype was used to found a population that was then transferred in bulk from flask to flask (without choosing a single colony to found the next flask), new mutants were eventually able to invade the population. Some of these invaders had lost the ability to switch phenotypes. These new genotypes thus possessed higher growth rates, and if the environment did not change, would have both higher arithmetic and geometric mean fitness. But under the original rules of the selection experiment (Figure 1), these non-switching genotypes would not be transferred to the next flask and would thus possess a geometric mean fitness of 0, which is lower than the switching strain. The switching strain thus trades growth rate in a constant environment (and reduced arithmetic mean fitness) for growth rate in a fluctuating environment (and increased geometric mean fitness). We can conclude that the persistence of the switching genotype in the environment was thus due to bet hedging.

This work provides a beautiful view of the evolutionary dynamics of bet-hedging. While it does not change our theoretical understanding of how natural selection maximizes fitness in a fluctuating world, it does demonstrate that bet-hedging can evolve through co-option of a trait that originally evolved for non-bet hedging reasons.

Beaumont H. J. E., J. Gallie, C. Kost, G. C. Ferguson, and P. B. Rainey. 2009. Experimental evolution of bet hedging. Nature 462:.
Simons A. M. 2009. Fluctuating natural selection accounts for the evolution of diversification bet hedging. Proceedings of the Royal Society B: Biological Sciences 276:1987-1992.
Stearns S. 2000. Daniel Bernoulli (1738): evolution and economics under risk. Journal of Biosciences 25:221-228.

About "This Week in Evolution" and R. Ford Denison

See my Google Scholar page for an up-to-date list of publications.
Or, see "recent publications and publicity" for news and commentary.

"Can you tell me, in lay language, what makes this achievement significant?"
"I can try", said Denison, cautiously.
-- The Gods Themselves (Asimov)
Ford Denison explains why eating more kale and less meat may trigger physiological changes that sacrifice some potential reproduction but increase longevity (Ratcliff et al., 2009).

Podcast interview with Carl Zimmer on "Darwinian Agriculture."
Short audio story
on our host-sanctions research, produced by AAAS.

About this blog:
Time permitting, I discuss one scientific journal article per week, presenting new data on past evolution or ongoing evolution. My interests in the evolution of cooperation and in agriculture make me include more papers on microbes and plants than some other blogs with an evolutionary focus. I occasionally discuss other topics.

About me:
You know how evolution-denialists sometimes claim that they "used to believe in evolution", as if one person's changed opinion trumped the thousands of scientific articles on evolution published each year? For what it's worth, I didn't start as an evolutionary biologist. I earned a PhD in crop science from Cornell in 1983 and was a US Department of Agriculture researcher for several years, before becoming a professor of agronomy at UC Davis in 1993. There, I taught crop ecology, directed a major field experiment on agricultural sustainability (LTRAS), and did research on cover crops that get nitrogen from symbiotic rhizobium bacteria in their root nodules.

My interest in evolutionary biology developed gradually. I wanted my teaching to explain as many facts as possible, using a framework of universal principles, rather than jumping randomly from one fact to another. The universal principles that explained the most crop-ecology-related facts turned out to be conservation of energy, conservation of matter for each chemical element, and evolution by natural selection. The Selfish Gene, by Richard Dawkins, helped clarify my thinking and introduced me to the work of George Williams, John Maynard Smith and especially Bill Hamilton on the evolution of cooperation and, more recently, aging.

Their evolutionary ideas spread to my research, as I tried to answer a question few people had even asked: why do rhizobia invest their resources in taking up nitrogen from the atmosphere and giving it to their host plants, rather than using those resources for their own reproduction? Our 2003 paper in Nature, showing that soybean plants impose fitness-reducing sanctions on rhizobia that fail to fix nitrogen answered that question (although we are still working out some details), and is probably my best-known contribution to science, so far. But our less-cited paper on Darwinian Agriculture, also published in 2003, has generated more speaking invitations and a book contract with Princeton University Press.

In 2005, I took early retirement from UC Davis and a grant-supported adjunct position at the University of Minnesota, in order to live with my horticultural-scientist wife, after many years working in different cities. Here, I have been collaborating with Mike Sadowsky on legume-rhizobia symbiosis and with Mike Travisano on experimental evolution of multicellularity, a project he initiated with Will Ratcliff, who did his PhD with me. I am also trying to develop an experimental system to test our explanation for why certain stresses increase longevity. I provide occasional advice to groups concerned with food security and agricultural sustainability. As long as the National Science Foundation keeps giving me grants, life is good.

R. Ford Denison

Favorite publications through 2011 :
(Google Scholar maintains an up-to-date list, with citations and links, here.

Ratcliff,W.C., R.F. Denison. 2011. Alternative actions for antibiotics. Science 332:547-548.

Denison, R.F., E.T. Kiers. 2011. Life histories of symbiotic rhizobia and mycorrhizal fungi. Current Biology 21:R775-R785.

Oono, R., C.G. Anderson, R.F. Denison. 2011. Failure to fix nitrogen (N2) by nonreproductive symbiotic rhizobia triggers host sanctions that reduce fitness of their reproductive clonemates. Proceedings of the Royal Society B 278:2698-2703.

Denison, R.F. 2011. Past evolutionary tradeoffs represent opportunities for crop genetic improvement and increased human lifespan. Evolutionary Applications 4:216-214.

Ratcliff, W.C., R.F. Denison. 2010. Individual-level bet hedging in the bacterium Sinorhizobium meliloti. Current Biology 20:1740-1744.

Oono,R., R.F. Denison. 2010. Comparing symbiotic efficiency between swollen versus nonswollen rhizobial bacteroids. Plant Physiology 154:1541-1548.

Denison, R.F., J.M. Fedders, B.L. Harter. 2010. Individual fitness versus whole-crop photosynthesis: solar tracking tradeoffs in alfalfa. Evolutionary Applic. 3:466-472.

Oono,R., I. Schmitt, J.I. Sprent, R.F. Denison. 2010. Multiple evolutionary origins of legume traits leading to extreme rhizobial differentiation. New Phytol. 187:508-520.

Oono R., R. F. Denison, and E. T. Kiers. 2009. Tansley review: Controlling the reproductive fate of rhizobia: how universal are legume sanctions? New Phytologist 183:967-979.

Ratcliff W. C., P. Hawthorne, M. Travisano, and R. F. Denison. 2009. When stress predicts a shrinking gene pool, trading early reproduction for longevity can increase fitness, even with lower fecundity. PLoS One 4:e6055.

Sadras, V.O., R.F. Denison. 2009. Do plant parts compete for resources? An evolutionary viewpoint. New Phytologist 183:565-574.

Ratcliff, W.C., R.F. Denison. 2009. Rhizobitoxine producers gain more poly-3-hydroxybutyrate in symbiosis than do competing rhizobia, but reduce plant growth. ISME Journal 3:870-872.

Kiers E. T., R. F. Denison. 2008. Sanctions, cooperation, and the stability of plant-rhizosphere mutualisms. Annual Review of Ecology, Evolution, and Systematics 39:215-236.

Ratcliff, W. C., S. V. Kadam, and R. F. Denison. 2008. Polyhydroxybutyrate supports survival and reproduction in starving rhizobia. FEMS Microbiology Ecology 65:391-399.

Mitchell, A.E, Y.J. Hong, E. Koh, D.M. Barrett, D.C. Bryant, R.F. Denison, and S Kaffka. 2007. Ten-year comparison of the influence of organic and conventional crop management practices on the content of flavonoids in tomatoes. J. Agric. Food Chemistry 55:6154-6159

Kiers, E.T., M. Hutton, R.F. Denison. 2007. Human selection and the relaxation of legume defences against ineffective rhizobia. Proceedings of the Royal Society B 274: 3119-3126.

Denison, R.F., D.C. Bryant, and T.E. Kearney. 2004. Crop yields over the first nine years of LTRAS, a long-term comparison of field crop systems in a Mediterranean climate. Field Crops Research 86:267-277.

Martini E. A., J. S. Buyer, D. C. Bryant, T. K. Hartz, D. Barrett, and R. F. Denison. 2004. Yield increases during the organic transition: improving soil quality or increasing experience? Field Crops Research 86:255-266.

Okano, Y., K.R. Hristova, C. Leutenegger, L. Jackson, R.F. Denison, B. Gebreyesus, D. LeBauer, and K.M. Scow. 2004. Effects of ammonium on the population size of ammonia-oxidizing bacteria in soil -- Application of real-time PCR. Applied and Environmental Microbiology 70:1008-1016.

Kiers E. T., R. A. Rousseau, S. A. West, and R. F. Denison. 2003. Host sanctions and the legume-rhizobium mutualism. Nature 425:78-81.

Denison R. F., E. T. Kiers, and S. A. West. 2003. Darwinian agriculture: when can humans find solutions beyond the reach of natural selection? Quarterly Review of Biology 78:145-168.

Denison R. F., C. Bledsoe, M. L. Kahn, F. O'Gara, E. L. Simms, and L. S. Thomashow. 2003. Cooperation in the rhizosphere and the "free rider" problem. Ecology 84:838-845.

Kinraide T. B., R. F. Denison. 2003. Strong inference, the way of science. American Biology Teacher 65:419-424.

West, S.A., E.T. Kiers, E.L. Simms & R.F. Denison. 2002. Sanctions and mutualism stability: why do rhizobia fix nitrogen? Proceedings of the Royal Society 269:685-694.

Denison R. F. 2000. Legume sanctions and the evolution of symbiotic cooperation by rhizobia. American Naturalist 156:567-576.

Hasegawa, H., D.C. Bryant, and R.F. Denison. 2000. Testing CERES model predictions of crop growth and N dynamics, in cropping systems with leguminous green manures in a Mediterranean climate. Field Crops Research 67:239-255.

Jacobsen K. R., R. A. Rousseau, and R. F. Denison. 1998. Tracing the path of oxygen into birdsfoot trefoil and alfalfa nodules using iodine vapor. Botanica Acta 111:193-203.

McGuire, A.M., D.C. Bryant, and R.F. Denison. 1998. Wheat yields, nitrogen uptake, and soil moisture following winter legume cover crop vs. fallow. Agron. J. 90:404-410.

Denison R. F., R. Russotti. 1997. Field estimates of green leaf area index using laser-induced chlorophyll fluorescence. Field Crops Research 52:143-150.

Denison R. F., T. B. Kinraide. 1995. Oxygen-induced depolarizations in legume root nodules. Possible evidence for an osmoelectrical mechanism controlling nodule gas permeability. Plant Physiology 108:235-240.

Denison R. F., J. F. Witty, and F. R. Minchin. 1992. Reversible O2 inhibition of nitrogenase activity in attached soybean nodules. Plant Physiology 100:1863-1868.

Denison R. F., D. B. Layzell. 1991. Measurement of legume nodule respiration and O2 permeability by noninvasive spectrophotometry of leghemoglobin. Plant Physiology 96:137-143.

Denison R. F., B. Caldwell, B. Bormann, L. Eldred, C. Swanberg, and S. Anderson. 1976. The effects of acid rain on nitrogen fixation in western Washington coniferous forests. Water Air and Soil Pollution 8:21-34. My first publication, funded by my first grant, funded by the National Science Foundation's since-abandoned Student Originated Studies program, when I was an undergrad at The Evergreen State College.

November 5, 2009

Experimental evolution meets genomics

Richard Lenski and colleagues have been monitoring evolution of the bacterium Escherichia coli in his laboratory for 40,000 generations. Their latest paper, "Genome evolution and adaptation in a long-term experiment with Escherichia coli" was recently published in Nature.

One nice thing about E. coli is that they can freeze samples of their evolving populations every few thousand generations, for later analysis. So they were able to compare the fitness of different generations by competing each against a thawed ancestor. They also found the complete DNA sequence for many of these strains....

This wouldn't have been possible when their evolution experiment began. It would have been impossibly expensive even a few years ago, but DNA sequencing has been getting cheaper, as Richard Dawkins predicted in his essay, "Son of Moore's Law."

They found that their bacterial populations accumulated genetic changes at a fairly constant rate over the first 20,000 generations. This is what you would expect, if they were randomly accumulating "neutral" mutations, with no effect on fitness. But random neutral mutations would include "synonymous" mutations that change DNA sequence without changing the corresponding protein, whereas they found mostly protein-changing mutations. Those should have some real effect and apparently a positive one.

Over the same period, fitness increased relative to the ancestral strain. But the increase in fitness showed a different pattern from total changes in DNA sequence. While DNA sequence changes accumulated at a fairly constant rate, fitness increased very rapidly over the first 1000 generations or so. Since then, fitness has continued to increase, but much more slowly. This later increase could be roughly linear, but there's enough noise in their data that it's hard to be sure. One possible explanation for this pattern is that the early genetic changes had wide-ranging effects, even if the DNA-level changes were small. This is what you would expect if the changes involved regulatory systems, for example. Those early changes were clearly positive, on balance, but they may have had some negative side effects. The slow-but-steady improvements since then may involve a large number of genes, each with a small beneficial effect, possibly reducing some of those negative side-effects.

Fellow microbial evolutionary biologist Paul Rainey has a commentary on the paper in the same issue. Rainey himself has published a very interesting paper even more recently, which Will Ratcliff has promised to write about.