This Week in Evolution

Return of the viruses

2009-11-16T15:51:09Z

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.

Experimental evolution of bet hedging

2009-11-11T19:42:04Z

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.

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.

LITERATURE CITED
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

2009-11-11T16:38:54Z

"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 trade some of our potential reproduction for longevity (Ratcliff et al., 2009).

I usually 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.

You know how evolution-deniers 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. Next, 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 (as we had predicted, based on evolutionary theory), has been cited over 100 times and is probably my best-known contribution to science, so far.

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. As long as the National Science Foundation keeps giving me grants, life is good.

Our most important recent paper, which began with an idea from grad student Will Ratcliff, explains increased longevity with dietary restriction (or with a diet containing toxins plants make to defend themselves against insects), based on the evolutionary benefit of delaying reproduction when the gene pool is shrinking.

I am writing a book, "Darwinian agriculture: where does nature's wisdom lie?" which is intended for an intelligent but nonspecialist audience. It should be published late in 2010, by Princeton University Press. When progress on the book is slow, I sometimes neglect this blog.

R. Ford Denison

Most significant publications:

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.

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., and B.L. Harter. 1995. Nitrate effects on nodule oxygen permeability and leghemoglobin. Nodule oximetry and computer modeling. Plant Physiol. 107:1355-1364.

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., S. Hunt, and D.B. Layzell. 1992. Nitrogenase activity, nodule respiration, and O2 permeability following detopping of alfalfa and birdsfoot trefoil. Plant Physiol. 98:894-900.

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., and R.S. Loomis. 1989. An Integrative Physiological Model of Alfalfa Growth and Development. Univ. Calif. Div. Agr. Nat Res., Publ. 1926, 73 pp.

Denison, R.F., and P.S. Nobel. 1988. Growth of Agave deserti without current photosynthesis. Photosynthetica 22:51-57.

Denison R. F., P. R. Weisz, and T. R. Sinclair. 1988. Oxygen supply to nodules as a limiting factor in symbiotic nitrogen fixation. Pages 767-775 In R. J. Summerfield, editor. World Crops: Cool Season Food Legumes, Kluwer Academic Plublishers, Dordrecht.

Weisz, P.R., R.F. Denison, and T.R. Sinclair. 1985. Response to drought stress of nitrogen fixation (acetylene reduction) rates by field-grown soybeans. Plant Physiol. 78:525-530.

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.

Experimental evolution meets genomics

2009-11-05T21:37:57Z

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.

Experimental evolution of sex (revised)

2009-10-23T18:29:31Z

"I show that a similar cost of sex exists when asexual mutants arise... but not when the species is a self-fertile hermaphrodite.... Although individual fitness (expected reproductive success) is assumed to be equal for sexual and asexual females, the heritability of fitness is... twice as high in asexual females" -- Richard Michod, Darwinian Dynamics

I should be working on my book, but a paper that just came out in Nature got me thinking about sex. A population with half males and half females will grow only half as fast as one consisting only of females that self-fertilize or clone themselves. So, many people have asked why sex evolved.

That's an interesting question, but I'm not sure about the rationale. As noted by Michod, a population of self-fertilizing hermaphrodites doesn't have any intrinsic growth advantage over a population of hermaphrodites that mostly cross-fertilizes. So is the problem sex, or males?

Evolutionary changes in gene frequency over generations depend on whether individuals with a given gene survive and reproduce more than other members of their population, not on the consequences for overall population growth. (Individuals can move between populations.) So we really have two related questions:
1) why do genes for producing male offspring persist? and
2) why do genes for cross-fertilization persist in species that can self-fertilize?

From an individual perspective, it's not apparent that producing male offspring is always a bad idea. Do couples with two sons have fewer descendants than those with two daughters? It can depend on the sex ratio in the population. If a human couple produces one offspring of whichever sex is in the minority, their offspring may have an easier time finding a mate.

But what about cross-fertilization? If a female cloned herself, her offspring would have all of her genes, rather than just half of them. So the frequency of genes for self-fertilization would tend to increase, unless individuals resulting from cross-fertilization were more likely to survive and reproduce. An offspring with half as many of one's genes, but a 2.1-fold better chance of survival (maybe because a sexual partner contributes different disease-resistance genes) gives a greater increase in fitness. So, one key to understanding the evolution of sex (cross-fertilization) is to measure the survival of individuals with one parent versus two, under conditions that plausibly occurred at critical points in a species ancestry.

This week's paper, "Mutation load and rapid adaptation favour outcrossing over self-fertilization", set out to "recapitulate the evolutionary process under the specific conditions predicted to favour either selfing or outcrossing." Levi Morran, Michelle Parmenter, and Patrick Phillips used the nematode, C. elegans, which consists of males and hermaphrodites. (This mix, and the lack of pure females, suggests there can be individual benefits to maleness, whatever the consequences for the population as a whole.) They used genetic manipulation to make populations that only self-fertilized or never self-fertilized, exposed them to high mutation rates or to a bacterial pathogen, and let them evolve.

]]> Their hypothesis was that cross-fertilization would limit the accumulation of bad mutations: if two individuals with two different bad mutations mate, some of their offspring will get both mutations and die, but some will get neither, whereas self-fertilizing populations may not have any mutation free individuals. Sure enough, mutations accumulated in the self-fertilizing population, resulting in decreased fitness. Cross-fertilization was also beneficial to the populations exposed to the pathogen: the population made to cross-fertilize evolved resistance, perhaps because they could combine good mutations from different parents.

As discussed above, however, just because some trait benefits the population as a whole doesn't guarantee that it will evolve. So a more interesting results used populations where the amount of cross-fertilization was allowed to evolve. An increase in mutation rate caused two different strains to evolve more cross-fertilization. Pathogen exposure seemed to have a similar effect, although there was a lot of variability.

Previously, it was thought that even the low rate of natural cross-fertilization in this species was enough to provide most of the benefits, but they saw improvements with additional cross-fertilization. This was achieved by increasing the percentage of males, which they suggested would provide additional benefits via sexual selection. If males fight over females and the healthiest males win, or if females choose the healthiest males, maybe we aren't so useless to our populations after all.

Evolving resistance to cheaters

2009-10-16T00:01:29Z

This week's paper, "Cheater-resistance is not futile" was published in Nature. It describes experimental evolution of the social amoeba Dictyostelium, whose propensity to cheat other members of its species was discussed by Will Ratcliff in a recent guest post titled "Sneaky slime molds."

When two Dictyostelium strains are mixed in a reproductive structure, cheaters contribute fewer cells to the stalk that holds up the reproductive spores. Could the presence of such cheaters select for cheater-resistance genes, just as the presence of owls or hawks selects for mouse genes that make their coats match the soil color?

]]> To find out, the researchers started with a genetically diverse population (the raw material for natural selection) and added a cheater. By definition, the cheater would tend to increase in frequency over cycles of reproduction, but they prevented that by using a cheater they could kill after it had had its effect on the relative reproduction of the other strains.

They did this several times, and each time one or two cheater-resistant genotypes took over the selected population. For example, starting with a population that made less than 40% of the spores when mixed 50:50 with the cheater, they evolved a population that made about 50%. (The cheater-resistant strain didn't push its advantage, apparently!)

In at least some cases, they identified the specific mutation that let their mutant hold its own against the cheater. The gene "has no annotated homologues in other organisms", so it's probably not a universal anticheater gene. In fact, it didn't even work against all Dictyostelium cheaters. Still, it would be interesting to know how it works at the molecular level.

Meanwhile, cooperators take heart. It's possible to keep cheaters under control, without becoming a cheater yourself.

Darwin at the Smithsonian

2009-10-12T18:29:06Z

I recently had two or three hours to spend at the Smithsonian, en route to the airport. I hadn't been to the natural history museum for awhile, and was interested to see how they were celebrating Darwin's anniversaries this year. Pretty well, it turns out. Banners outside advertised a Darwin exhibit and "Plants and butterflies: partners in evolution." Inside, there was apparently an organized "Evolution Trail", which I didn't have time to follow.

The Darwin exhibit is off the entrance hall with the elephant and has a mix of biographical and scientific exhibits. My main criticism was their definition of "co-evolution" as being limited to evolution for mutual benefit. Evolutionary arms races (e.g., between hosts and parasites) are also coevolution. The entrance hall on the other side, where I came in, has two display cases of Darwiniana.

The butterfly exhibit was dominated by a live butterfly room inside a larger room with displays on the coevolution of plants and butterflies, with fossils labeled "examine the evidence." I was happy to pay $6 admission to the butterfly room since I wanted to make a donation anyway and enjoyed having a frittilary land on my nose.

Near the Oceans exhibit was a display of Burgess Shale fossils I hadn't seen before, including Pikaia, a tiny 500-million-year-old chordate. We chordates have evolved a lot since then. Nearby were some fossil stomatolites.

The mammal room was great, focusing on adaptations in everything from bats to giraffes (splaying front legs to drink, with an explanation of adaptations to limit blood flow to head) to pangolins with termite mounds. Right in the middle of the floor was a window down to fossil hominid footprints.

I wish I could have stayed longer. One problem with a quick visit to the Smithsonian is that post9/11 hysteria has closed most of the bag-check rooms. You can't bring your luggage into the museum and if you leave it somewhere, they'll try to detonate it. (Luggage made of sapient pearwood can defend itself, but I wouldn't recommend bringing it to Washington!) But here's a secret tip for my regular readers only: the 4th St. entrance to the National Gallery still has a check room, complete with x-ray machine. Don't tell too many people, or they'll probably close it.

Coming up in March: the Hall of Human Ancestors!

Local TV new blows Ardipithecus story

2009-10-02T15:32:13Z

If you don't believe in evolution, you might not want to listen to this next story. Scientists reported this week on a new fossil, possibly a human ancestor, older than Lucy. The good news is, we're not descended from chimps after all. The bad news is, chimps and humans are descended from the same ancestor.

That's a paraphrase of how our local TV news covered Ardipithecus ramidus, the fossil hominid discussed in a series of papers in this week's issue of Science. Read all about it on Carl Zimmer's blog. The TV anchor didn't say which scientists claimed we are descended from chimps, perhaps because no scientist has made that claim. Chimps have evolved over the six million years or so since our last common ancestor, including their split with bonobos. Can we expect the story below on the TV soon?

Startling breakthrough in human genetics! You aren't descended from brother after all, or even from your cousin. You and your brother still have the same parents, and you and your cousin have the same grandparents, though. I hope that doesn't upset you too much.

We don't know for sure that present-day humans are descended from Ardipithecus . It's a reasonable hypothesis, but any hypothesis is, by definition, subject to possible disproof. For example, if we found another fossil that was clearly much more similar to modern humans, dating from the same time or earlier, then we'd conclude that Ardipithecus probably has no surviving descendants.

But this species probably isn't too far from the direct line of descent between our common ancestor with chimps and modern humans. Suppose you wanted to know what your great grandmother looked like, but there was no surviving picture of her. If you had pictures of her sister or her daughter, that would give you some idea, even if all her living descendants are descended from a son.

Of course, much of what we know about our ancestors now comes from analyzing DNA in humans and closely related species. We can figure out when vitamin C synthesis was lost or adult lactose tolerance gained, for example. But we don't yet understand development enough to predict height, foot shape, etc., from inferred DNA sequences of ancestral species. So keep those fossils coming!

Off topic: Frank view of blasphemy

2009-09-30T15:53:03Z

A couple of months ago, I read this New York Times article by economist Robert Frank, suggesting that Darwin's ideas may be a better guide to economics than (popularized versions of) Adam Smith's ideas. I was impressed and have been reading his books with considerable interest.

Many of his economic ideas parallel ideas I'm exploring in my book on Darwinian Agriculture. A singer, runner, or lawyer who's only 1% better may make ten times as much money, just as a leaf that's only 1 mm above the leaf of a competing plant may have ten times the photosynthesis. "Arms races" among humans -- working overtime will let you afford a house that is more expensive than average, so that your kids can go to a better-than-average school, but if everyone works overtime half the population still sends their kids to below-average schools -- parallel arms races among plants -- being taller than your neighbor means more photosynthesis and so more seed production, but if every plant grows taller that doesn't increase total photosynthesis and wastes resources on tall stems. And so on.

But today, in honor of Blasphemy Day, I want to summarize an interesting idea from his book, Choosing the Right Pond.

Freedom of speech is often presented as an "inalienable right", perhaps granted by (though never actively protected by) some hypothetical Creator. Frank suggests an alternative origin, based on freedom of association and economies of scale....

]]>
Although migration in and out of most countries is somewhat restricted, a sufficiently motivated person can often evade those restrictions. Mobility within countries is typically even less restricted. So freedom of association is, to some extent, a truly inalienable right.

Often, people would prefer to associate with those who share their views on particular issues. But no two people agree on everything. The larger the group, the more areas of disagreement. You may be able to find a small country where most people share most of your views, but any large country is likely to include many people with different, perhaps deeply offensive, views.

Now, add economies of scale. There are many advantages to living in a larger country. Trade within countries isn't hampered by borders or tariffs. Bigger countries have more influence on international agreements. And so on. If you want the advantages of living in a larger country, you have to accept (in some sense) sharing it with those with different views.

Back to blasphemy. Hearing or seeing their religion (Islam, Christianity, Gaea/group-selection, whatever) or national/tribal symbols insulted often upsets people. Frank argues that blasphemy may sometimes actually harm people, in the same sense that noise or smog does, even if the only physical effect is an increase in stress hormones. This was a new idea for me, but I think he may have a point. But, he continues, preventing people from speaking their mind also causes stress.

You can imagine a market-based approach to this problem, where religious zealots and aspiring blasphemers discuss how much money to exchange, and in which direction, to compensate zealots for not having to hear blasphemy or to compensate nonbelievers for restricting their freedom. But the transaction costs would be huge, particularly in a large (and hence inevitably diverse) country, where one person's blasphemy is another's dogma.

A better solution is to classify hearing offensive speech as one of the costs of living in a large country. You may object to noise ordinances that limit your right to hold late-night parties or you may think you pay more than your share of taxes. Of course you can work to change those laws, but no large group is going to agree with you on everything. Get used to it.

Or move to some tiny country whose laws are more consistent with your views. But be prepared for disappointment. Northern Ireland, Bosnia, Iraq, and the Palestinian Territories apparently aren't small enough to ensure unanimity. I bet Quebec wouldn't be either.

Happy Blasphemy Day!

Off topic: Sears spied on customers

2009-09-25T21:07:29Z

Sears tricked customers into installing software that recorded:

"the contents of shopping carts, online bank statements, drug prescription records, video rental records, library borrowing histories, and the sender, recipient, subject, and size for web-based e-mails. The software would also track some computer activities that were not related to the Internet."

The Federal Trade Commission asked them to destroy the data and to be more honest about their plans next time they do something like this. I wonder whether that is a strong enough punishment to deter similar activities by other companies?

I hadn't seen anything about this in the news before reading about it on Bruce Schneier's blog. Why isn't he in charge of Homeland Security?

Guest Blog: Sneaky slime mold

2009-09-21T17:22:27Z

Slime molds allocate less to costly public goods when sharing then when alone.

(Special Guest Blogger: Will Ratcliff )

The slime mold Dictyostelium discoideum ('dicty' for short) spends most of its life alone, hunting soil bacteria and yeast. But when food runs out, tens of thousands of individuals aggregate into a mobile slug (cool youtube video) which crawls to an advantageous place and differentiates into a ball of spores on top of a long stalk. Individual dicty either become a dead stalk cell or a reproductively viable spore.

© Copyright, Mark Grimson and Larry Blanton

What possible incentive could there be for a dicty to sacrifice its life (become a stalk cell) for the benefit of those that become spores? If you answered 'there is no direct advantage to dying for others', you're right! Nonetheless, kin selection can lead to this type of self-sacrifice if a) the dicty in the stalk are highly related to the dicty that form spores (so are highly likely to have the same "unselfish genes"), and b) spores benefit from being higher off the ground (better chance of dispersal?).

But what happens when slugs are composed of more than one genotype? Here stalk formation becomes a 'tragedy of the commons' in which it is in each clone's interest to cheat, letting the other clone form a greater fraction of the stalk. So do dicty cheat? If so, how do they do it?

The short answer, as reported by Buttery et al. in the paper Quantification of Social Behavior in D. discoideum Reveals Complex Fixed and Facultative Strategies recently published in Current Biology is that:

Yes, dicty cheat; they cheat like crazy.

There are two ways in which a dicty clone in a mixed slug could cheat, producing less stalk and leaving more spores than its competitor....

]]> First, the dicty clone could have a higher intrinsic frequency of spore formation. In some clones, most cells become part of the stalk, putting their spores high up in the air, while others favor shorter stalks and thus produce more spores. When mixed together, a clone that forms many spores might automatically cheat a clone that forms a lot of stalk, benefiting from the tall stalk while contributing relatively little to its construction. Second, a dicty clone may sneakily increase its frequency of spore formation when in a mixed slug, relative to what it would do alone, letting the other strain make most of the stalk.

The authors tested 6 natural isolates that varied substantially in their intrinsic frequency of spore formation, and made all possible combinations of two-genotype mixed slugs. What they found is that 5 out of 6 genotypes cheated facultatively, forming more spores when in a mixed slug then when alone. Surprisingly, strains that formed more spores in mixed slugs were also able to keep the competitor strain from doing the same to them . This is a really cool result, demonstrating that evolutionary conflict over stalk production has led to this humble slime mold's ability to measure social context and preferentially cheat nonrelatives.

But here's the catch: while facultative cheating was rampant, it seemed to have little overall impact on fitness (here measured as spore number alone, ignoring the potentially important but unknown effects of stalk size) under test conditions. The fitness rank order of the 6 strains in mixed sporangia was almost completely determined by each strain's intrinsic spore:stalk allocation.

The evolutionary persistence of genes for facultative cheating suggests that it was sometimes important to these strains ancestors in the wild, but that remains to be shown. This is great work, but is hampered by the current black-box status of this microbe's ecology. Stalks are presumed to be beneficial, otherwise natural selection would have long ago eliminated them, but the quantitative benefit of greater stalk height is currently unknown. As a result, the authors had to define fitness only in terms of the number of spores formed. Their 6 strains that varied in spore:stalk ratio therefore differed greatly in 'fitness', but each might have the stalk:spore ratio that maximizes fitness in its source environment, if the benefits of greater stalk size are considered. If this were the case, mixed slugs in the wild would usually form between strains with similar stalk:spore ratios. Once differences in that ratio are taken out of consideration, the fitness consequences of facultative cheating may in fact be quite large.

How to maybe possibly get a grant

2009-09-18T17:41:09Z

I'm not doing a paper-of-the week (although I'm expecting a guest post) because I'm too busy reading a bunch of proposals for a grant panel. I can't give any details, of course, but here are some general observations that may be of interest to people who apply for or fund grants.

So far, every proposal I've read has seemed worth funding. This was not true the last time I served on a similar panel. Maybe the word has gotten out that grant funding is highly competitive, so few people bother sending weak proposals? This makes it easier to understand why some of my own recent proposals were rejected, often for what seemed like minor problems.

Unfortunately, we can only fund a small fraction of the proposals submitted. Of course, we could fund more proposals if we gave each group less money. There might be some merit in that approach, but I'll leave that topic for another time.

For those who are writing or thinking about proposals, here are some generic tips:

]]> You need a good idea (typically, an important question and a plausible way to answer it) or a few related good ideas and (at least in biology) some preliminary data showing your idea might work. If you don't already have a grant, it may be hard to get those preliminary data. Someone should do something about this problem, but you need to realize that you're competing with proposals that do have preliminary data.

Given the strength of the competition, research that "may be relevant to" something important (a question that lots of people want the answer to, or a solution to some important practical problem) is probably going to rate lower than research that will actually answer the important question or solve the important problem. If you can't reasonably promise that from your current proposal, can you at least show how it's an essential (rather than optional) step towards that goal?

To be competitive, you need to have published something related to the proposed work. If you've published one or two relevant papers each of the last 2-3 years, I'll be pretty confident that you'll publish your results from a new grant promptly. Unpublished results are much less likely to get used, even if you tell a few people about them at a meeting or something, so don't expect public funding if you don't publish. Maybe we shouldn't expect as many publications from people without past grant support; I'll have to get the grant program's guidance on that.

Make life easy for reviewers! Author-year citation (Adams, 1979) is better than numbers (42); if I already know the paper, it saves time; if I don't, and I look it up (maybe just the abstract), it's easier to remember. Avoid acronyms nonspecialists don't know. If there are one or two you need to use repeatedly, define and use. Otherwise, it's better to spell it out or use a plain-English substitute: "the sensor" [described when first referred to], rather than WTFIANAEE. Both of these suggestions cut into the space you could otherwise to repeat vague claims for how important your work is or provide details on how many microliters of master mix you plant to use. Do explain once why your work is important (preferably to people beyond your subspecialty) but data showing that a method works in your lab is more convincing than minuscule detail of what you plan to do. That's my opinion, anyway.

If your proposal isn't funded the first attempt -- this is now common, even for pretty good proposals -- assume that you may get some of the same reviewers again, but most will be new. So address pat reviewer concerns in a constructive way, without belaboring the point.

Applied Evolution Summit

2009-09-11T18:40:47Z

I've just agreed to give a talk in January at the Applied Evolution Summit: a small group of experts meeting at an island research station near the Great Barrier Reef to apply evolutionary biology to critical problems in human health, agriculture, fisheries, etc. It might surprise some evolution denialists to learn that pornography, abortion, atheism and "death panels" are not on the agenda, just science. Of course, when we talk about how global warming is affecting the coral reefs critical to some fish, we may need to go look!

I'm going to try really hard to finish my book before the meeting, which will keep me quite busy until then. I don't teach regular classes -- as an adjunct professor, I'm paid only from our grants -- but reading proposals for a grant panel, writing a paper on "spiteful solar tracking" in alfalfa for Evolutionary Applications, and helping my hard-working and brilliant grad students with methods and manuscripts can't wait until my book is done. So I may be posting only sporadically for a while.

Where do new genes come from?

2009-09-04T18:24:39Z

When a few members of a family have a gene not found in most other members, one explanation is that the gene is newly evolved, rather than inherited from the common ancestor of that family. (The other possibility is that their ancestor had it, but most descendants lost it.)

New genes often turn out to be copies of old genes, sometimes with modifications that give them very different functions. But a paper just published in Current Biology reports "Emergence of a new gene from an intergenic region", rather than duplication of an existing gene....

]]>
One definition of a gene is "a section of DNA which, if altered, has some effect on phenotype (observable traits)." Many genes are transcribed into messenger RNA and then translated into protein (perhaps an enzyme). But there is an increasing list of examples of genes whose phenotypic effects depend on activity by the RNA transcript, which may never be translated into protein. Such genes often have a regulatory function, controlling the expression of other genes.

The gene reported in this paper was detected as an RNA transcript in house mice and some of their close relatives, but not in more distant relatives like rats. Their analysis of the family tree for the gene suggests that it evolved about 3 million years ago, after the last common ancestor of mice and rats lived.

The new gene is apparently not translated into protein. Antibodies designed to detect the protein, if it is made, didn't find any. Also, evolutionary changes in the DNA sequence appear to be indifferent as to protein structure: DNA-base changes that would have no effect on protein amino acid sequence were about as common as those that would effect the protein.

There was a phenotypic effect, however, meeting our criterion for a gene. When the researchers knocked out the DNA corresponding to the transcript, sperm motility decreased. Apparently the RNA transcript had some beneficial effect on expression of other genes.

Although the DNA was in every cell, the RNA transcript was produced almost exclusively in the testis. Apparently conditions for gene expression are looser there than elsewhere, so that a variety of mutations can get a stretch of DNA transcribed. Most such mutations are presumably harmful, but the mice with beneficial mutations (like the one described in this paper) have increasing representation in successive generations.

Effective communication on preserving crop diversity

2009-09-02T14:20:48Z

This talk by Cary Fowler, on the Global Seed Vault at Svalbard, is worth watching both for the content and as a model for effective public speaking. For that reason, I've categorized it under "careers in science" as well as "agriculture." Note the lack of bullet-point slides!

[Note added 9/11: text slides can make presentations boring, but handouts of text slides help students focus on understanding rather than scribbling notes. So I'm going to cut down on text slides in talks at meetings, but not necessarily in guest lectures to undergraduate classes.]

It's worth noting that even dry, frozen seeds may lose viability in storage. (You could probably still recover DNA, but that's only of practical value for the few traits, if any, whose value can be identified from DNA sequence alone.) So it's good to take seeds out of storage and grow fresh seed periodically. Usually, you want to do this in a way that minimizes natural selection in the seed-increase environment, to avoid losing traits that were useful where the crop was grown originally. For example, you want plants far apart enough that tall plants don't shade shorter neighbors enough to keep them from producing seed. And you don't want plants that were particularly prolific in the seed-increase environment to be over-represented in your next stored sample. Preserving crop diversity is a vastly under-funded activity, although that is true of most areas of agricultural research without immediate links to short-term profit.

Although even a few stored seeds can be multiplied enough in a few years to deal with slowly developing problems, such as climate change, if there's a global wheat epidemic you need at least enough disease-resistant seed on hand that one cycle of seed multiplication will meet farmer needs for the next growing season.