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August 29, 2009

Peacock comment

Most of the "comments" I get on older posts are commercial spam, which I delete. But if you're interested in a creationist comment on Dave Wisker's guest post on peacocks, here it is. It seemed to be original rather than cut-and-paste, so I approved it, but did add some comments of my own.

August 27, 2009

Are antibiotics a weapon or a signal?

(Guest blog by my PhD student, Will Ratcliff)

If we get a nasty bacterial infection, we all know to go to the doctor for antibiotics. Few of us stop to think of where these antibiotics come from, which is too bad, because their origin is rooted in the stuff of a James Bond film: bloodsport and espionage. Scientists put a few different microbes on a Petri plate, let them duke it out, and then steal the chemical secrets of the victorious strain. Antibiotics are thus considered by most microbiologists to be pure weaponry, honed by natural selection for the most effective killing (or disabling) of competitors at the lowest cost.

But some recent papers suggest a new hypothesis: antibiotics are actually signaling molecules that happen to be toxic at high doses (Mlot 2009). As evidence for this view, researchers note that microbes exposed to antibiotics at sublethal concentrations don't simply shrug off the insult and go about their business: they react. Some bacteria turn on their SOS response, some make biofilms, some fail to make biofilms, some get less virulent (Shank and Kolter 2009), and yet others more virulent (Linares et al. 2006). These responses appear to vary among species without a general pattern.

So are antibiotics serving as a weapon or a signal?

Let's start at square one: what do they mean by signal? Many of the papers in this literature seem to use signal to mean "molecule produced by species A that elicits a response in species B other than death". But to evolutionary biologists, it matters why species A produces the signal and why species B reacts as it does....

According to Steve Diggle et al. (2007), communication can be divided into three categories depending on the fitness consequences to each party :
The defining feature of a signal is that it has evolved because it increases the fitness of both the producer and the receiver. So we arrive at the central evolutionary problem with signaling: when is it beneficial to expend energy to provide another organism (perhaps of another species) with information that will increase its fitness?

A few scenarios I've thought up -- I'm sure there are more -- are A) when this reduces chances that you or your kin will be injured or eaten (e.g. I'm poisonous and if you eat me we'll both regret it) B) when this deters potential competitors from inhabiting the same area as you or your kin (e.g. I'm already halfway done with the food, and am not inclined to share, so you should probably go somewhere else), or C) when it is necessary for the initiation or maintenance of a mutualistic interaction, like the a legume root nodule by rhizobia. For cases A or B, at least, the sender may benefit from sending this message even if it is false, an example of coercion (or at least manipulation) analogous to Viceroy butterflies or back-arching cats that appear larger than they really are.

Before we can state with any confidence that an antibiotic is a signal, we need to know if producing and responding to a sublethal dose of the antibiotic produces benefits for both the producer and the receiver. Benefits like 'not dying from the antibiotic' don't count, nor does 'going into a biofilm preadapts a microbe to unexpected protozoal grazing '. These are questions that will probably be answered as microbial ecology moves forward.

If sublethal doses of antibiotics aren't signals, how do we explain their effect? Biofilm formation by bacteria exposed to antibiotics may increase their antibiotic tolerance, increasing their fitness at the expense of the antibiotic producer. From our previous definitions, the antibiotic would be a cue, not a signal. Similar arguments could be concocted for the production of detoxifying enzymes like β-lactamases or turning on the SOS response. An even simpler hypothesis is that some of the observed responses are not behavioral, but are the observable impact of an injury. Mucking about with a bacterium's ribosomes may not kill it, but it will likely leave some measurable impact.

Finally, antibiotics may simultaneously act as both a weapon and a signal. Assume that the concentration and effectiveness of an antibiotic drops off with distance from a producing microbe. Low concentrations of antibiotic may be an ineffective weapon, but can still effectively signal that any further encroachment on the antibiotic producer's turf is dangerous. Note that avoiding the killing zone of an antibiotic increases the exposed microbe's fitness (it does not die) and that of the producer (competition from other microbes is reduced). Right now this is pure speculation, but I wouldn't be surprised to find out that it's true.

Mixed up in all this is a general misunderstanding of the processes that natural selection optimizes. Linares et al. (2006) stated that:

"We thus could start to envisage a Copernican turn-about for the role of antibiotics in nature: from weapons involved in microbial struggle for life to collective regulators of the homeostasis of microbial communities."
This is essentially an old-school, group-selection argument, positing that individual species have evolved mechanisms to regulate the broader community because communities that are regulated do better. However, since the rate at which communities reproduce and die is slow relative to that of individual microbes, and their species composition is highly fluid, individual selection and kin selection swamp community-level selection. It is very unlikely that individuals would evolve mechanisms for the regulation of the community as a whole.

The bottom line: Simply observing that bacteria respond to sublethal antibiotic exposure does not provide any evidence that antibiotics evolved for the purpose of signaling or have been appropriated as a signaling agent. Indeed, even if antibiotics act only as a weapon, we expect bacteria exposed to sublethal antibiotic concentrations to respond either by being injured, or by acting to minimize injury (antibiotics acting as a cue). While we know that antibiotics can act as a weapon, we don't have any clear evidence that antibiotics act as a signal. Until we have these data, I wouldn't give the signaling hypothesis much weight.

Diggle S. P., A. Gardner, S. A. West, and A. S. Griffin. 2007. Evolutionary theory of bacterial quorum sensing: when is a signal not a signal? Philosophical Transactions of the Royal Society 362: 1241-1249
Linares J. F., I. Gustafsson, F. Baquero, and J. L. Martinez. 2006. Antibiotics as intermicrobial signaling agents instead of weapons. Proceedings of the National Academy of Sciences 103:19484-19489.
Mlot C. 2009. Antibiotics in nature: beyond biological warfare. Science 324:1637-1639.
Shank E. A., R. Kolter. 2009. New developments in microbial interspecies signaling. Current Opinion in Microbiology 12:205-214.

August 25, 2009

Vertical farms: a pyramid scheme?

I hate to bash the New York Times twice in one week, but this is such a stupid idea that I hardly know where to start. Some guy thinks we should build multistory skyscraper "farms" in New York City. He claims that:

For every indoor acre farmed, some 10 to 20 outdoor acres of farmland could be allowed to return to their original ecological state (mostly hardwood forest). Abandoned farms do this free of charge, with no human help required.
What about the abandoned farmers? But I'm not really worried about them, because this is not going to happen, at least not on a scale that poses an economic threat to many farmers.

If hydroponics is as wonderful as claimed in this article, do you wonder why most farmers still grow stuff in soil, rather than covering their fields with hydroponic tanks? Hint: it's not because they're stupid.

Growing plants on the roof of a building -- a "green roof" -- poses various challenges, but at least a roof can get the same amount of rain and sunlight as a ground-level garden would, assuming no shading by nearby buildings. With a multilevel "vertical farm", however, water and light must somehow be divided among the levels. OK, if the tower is taller than anything nearby, it can get some sunlight coming in sideways, but consider the geometry...

NYC is a bit more than 40 degrees (latitude) north of the equator. We can simplify our calculations, and bias our results slightly in favor of vertical farms, by calling it 45. Then, between the equinoxes (Mar. 21-Sept. 21, when noontime sun is vertical at the equator), the noontime sun over NYC is always at least 45 degrees above the horizon. If you don't want any part of a one-acre "field" (about 200x200 ft) to be shaded by the next floor above, with the sun is at 45 degrees, then the next floor would need to be 200 feet up. (To take full advantage of the solar radiation that a farmer gets for free, you would actually need 400 ft spacing for when the midsummer, noontime sun reaches 60 degrees above the horizon. When the sun is below 45 degrees, closer spacing would do, but then the light is spread so thin that you don't get much photosynthesis.)

How tall a building are we talking about? To suspend 20 acres of growing area over 1 acre of land, your 200x200 ft square tower would need to be 4000 ft tall, more than three times the height of the Empire State Building, with the sun at 45 degrees, or 8000 ft (more than a mile) if you want to capture all that midsummer noonday sun. What if the building were only 100 feet square? Then you could get 20 floors (but only 5 acres) in a building 2000 (or 4000) ft tall. But, the shorter the building, the farther it needs to be from any other buildings that might shade it.

Either way, the building would cost much more than the 5 to 20-acre farm it is intended to replace. My brother makes a living from a 20-acre organic vegetable and fruit farm, but he's not making payments on the world's tallest building. Of course, you could put the floors much closer together if you used artificial light, but then we're talking about lots of hardware and electricity. (The drawing the accompanies the article shows floors roughly twice as far apart as they are across, but uses half of that height for solar panels. Assuming 5% efficiency, these could provide enough electricity to do nothing much, again assuming no shading by nearby buildings.)

What about some other shape? A pyramid might be good. The outer edge of each floor would get natural light and could be used to grow crops, while the inside of the pyramid could be artificially-lit office space. You still couldn't increase your growing area much above the footprint of the building, without the shading problem discussed above, but it might be pretty. I suspect, however, that the author has a different kind of pyramid in mind. He writes:

(Disclosure: I've started a business to build vertical farms.)

Let me guess: the business model doesn't depend on income from selling farm products, but on franchise fees or grants from governments and foundations for "demonstration projects" that demonstrate how gullible they are.

There's probably an evolutionary angle to this story somewhere.

August 21, 2009

Are these the same evolutionary biologists who advised Hitler?

Actually, Hitler drew on preDarwinian sources like Martin Luther as well as on people who may have been influenced by people who were influenced by a German mistranslation of the Origin of Species. But I want to discuss a less-serious case of falsely attributing incorrect ideas to evolutionary biologists.

"Evolutionary biologists, the experts on the theory of aging, have strong reasons to suppose that human life span cannot be altered in any quick and easy way. But they have been confounded by experiments with small laboratory animals, like roundworms, fruit flies and mice. In all these species, the change of single genes has brought noticeable increases in life span."
This confounded quotation is from Nicholas Wade's recent New York Times article. Actually, "the change of single genes" isn't so "quick and easy" in humans yet. Even so, I don't know who these unnamed evolutionary biologists are who claim human lifespan can't be altered easily. Swimming with crocodiles usually works.

But perhaps Wade meant "increased" rather than "altered." Increasing lifespan doesn't seem to be that hard either. Exercise and protection from infectious disease (vaccines, clean water supplies, antibiotics) both seem to help. Where are the evolutionary biologists who supposedly deny this? What evolutionary biologists have said is that there are trade-offs between potential longevity and potential reproduction, most recently confirmed for macaques.(1) George Williams' classic paper on these tradeoffs(2) is discussed here by John Dennehy.

The relative importance (i.e., fitness benefit) of current reproduction vs. longevity allowing later reproduction depend on whether population size is increasing or decreasing.(3) If population is increasing, offspring produced later contribute genes to a larger gene pool, where they will have proportionally less effect. Conversely, if population is likely to decrease, forgoing current reproduction may increase fitness, if it significantly increases the chances of reproducing later. This is because each offspring produced later will be added to a smaller gene pool, thereby having a greater evolutionary effect. We recently suggested that many species have therefore evolved the unconscious ability to predict population declines and delay reproduction, thereby increasing longevity.(4) Our hypothesis explains some otherwise-puzzling results:

1) soft drinks with artificial sweeteners are just as likely to cause metabolic syndrome as those with sugar(5,6) - "food is plentiful, so population will increase, so I should reproduce now, so adjust insulin levels etc. accordingly, whatever the long-term consequences"
2) food odors reverse the longevity increase otherwise seen with food deprivation(7) - "even though I'm not eating, someone nearby is, so population isn't likely to decrease after all; cancel plans to sacrifice current reproduction to increase longevity"
3) many plant toxins improve health in low doses, a phenomenon known as "hormesis"(8) - "if I'm eating these bitter leaves, there must be a famine in progress; this will lead to population decrease, so I should switch the reproduction/longevity switch to the longevity position; I'll wait until after the famine, when the gene pool is smaller, to reproduce"

A key point is that delaying reproduction can increase fitness even without increasing the number of offspring produced. This is because fitness is a relative measure, with increasing per-offspring impact in smaller populations.

If our hypothesis is correct, what are the practical implications for increasing human longevity?

"My rule of thumb is to ignore the evolutionary biologists -- they're constantly telling you what you can't think," Gary Ruvkun of the Massachusetts General Hospital remarked.
He can think whatever he wants, but the FDA should check antiaging drugs for their effects on fertility. As predicted by our hypothesis, resveratrol, a naturally occurring chemical that extends lifespan in some species, has already been shown to decrease early fecundity.(9) This wouldn't necessarily be a bad thing in humans, however.


1. Blomquist, G. E. Trade-off between age of first reproduction and survival in a female primate. Biology Letters 5, 339-342 (2009).
2. Williams, G. C. Pleiotropy, natural selection, and the evolution of senescence. Evolution 11, 398-411 (1957).
3. Hamilton, W. D. The moulding of senescence by natural selection. Journal of Theoretical Biology 12, 12-45 (1966).
4. Ratcliff, W. C., Hawthorne, P., Travisano, M. & Denison, R. F. When stress predicts a shrinking gene pool, trading early reproduction for longevity can increase fitness, even with lower fecundity. PLoS One 4, e6055 (2009).
5. Dhingra, R. et al. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation 116, 480-488 (2007).
6. Lutsey, P. L., Steffen, L. M. & Stevens, J. Dietary Intake and the Development of the Metabolic Syndrome: The Atherosclerosis Risk in Communities Study. Circulation 117, 754-761 (2008).
7. Libert, S. et al. Regulation of Drosophila life span by olfaction and food-derived odors. Science 315, 1133-1137 (2007).
8. Mattson, M. P. & Cheng, A. Neurohormetic phytochemicals: low-dose toxins that induce adaptive neuronal stress responses. Trends in Neurosciences 29, 632-639 (2006).
9. Gruber, J., Tang, S.Y., & Halliwell, B. Evidence for a trade-off between survival and fitness caused by resveratrol treatment of Caenorhabditis elegans. Annals NY Acad Sci 1100:530-542 (2007)

August 14, 2009

Mimicry based on attractive odors -- or scary ones

Bolas spiders eat male moths, luring them within range of their bolas (a blob of glue on a short throwing thread) by releasing odors similar to the sex pheromones made by female moths.(1) Some orchids are pollinated mainly by male insects, again luring them with pheromones. You might think the males would learn from their first unsatisfying encounter and switch to a different flower species, rather than taking the pollen from the deceptive orchid to another flower of the same species, but the female-mimic orchids haven't gone extinct, so apparently not.

Some insects (usually those that often have close relatives nearby) make volatile chemical alarm signals. Some wild potato plants scare aphids away by releasing odors that mimic the aphid alarm signal. To cut costs, they package the key chemicals in glandular hairs (trichomes) on their leaves, which break and release the odors only when an insect lands on the leaf.(2)

Some of the odors plants make under insect attack can attract rather than repel insects, particularly wasps that attack plant-eating insects, eating them or laying eggs in their bodies.(3) I've often wondered how this apparent cooperation between plant and wasp evolved. There wouldn't be any selective advantage to the plant from producing these odors until the wasps had evolved an interest in them. So I'm guessing that the first evolutionary step was more like eavesdropping than signaling: wasps that were attracted to the smell of wounded plants found more prey and had more offspring. Then, perhaps, plants evolved to produce more of those odors, luring wasp "bodyguards" to themselves rather than their faint-smelling competitors. Plant alarm signals that attract beneficial wasps can also attract plant pests, however, such as the Colorado potato beetle.(4)

A paper published last year shows that some orchids pollinated by wasps lure them with similar plant alarm signals, falsely promising prey insects rather than females.(5) This week, the same group reported in Current Biology that an "Orchid Mimics Honey Bee Alarm Pheromone in Order to Attract Hornets for Pollination."(6) A wounded bee is an easy meal for a hornet.

The survival of this orchid species, like that of other orchids relying on false signals, depends on their pollinators being fooled at least twice, once by the pollen donor and one by the recipient. Popular insect game show: Are You Smarter than an Orchid? Actually, that's a bit unfair. Individual orchids are presumably less intelligent than individual insects, but orchids are using DNA-programmed strategies that have been thoroughly tested by natural selection. The game should really be called: How Do Your Limited Intelligence and Limited Life Experience Stack Up Against Evolution's Time-Tested Tricks? We humans could ask ourselves the same question.


1. Stowe, M. K., Turlings, T. C. J., Loughrin, J. H., Lewis, W. J. & Tumlinson, J. H. The chemistry of eavesdropping, alarm, and deceit. Proc. Natl. Acad. Sci. USA 92, 23-28 (1995).
2. Gibson, R. W. & Pickett, J. A. Wild potato repels aphids by release of aphid alarm pheromone. Nature 302, 608-609 (1983).
3. Turlings, T. C. J. et al. How caterpillar-damaged plants protect themselves by attracting parasitic wasps. Proc. Natl. Acad. Sci. USA 92, 4169-4174 (1995).
4. Bolter, C. J., Dicke, M., van Loon, J. J. A., Visser, J. H. & Posthumus, M. A. Attraction of Colorado potato beetle to herbivore-damaged plants during herbivory and after its termination. J. Chem. Ecol. 23, 1003-1023 (1997).
5. Brodmann, J. et al. Orchids mimic green-leaf volatiles to attract prey-hunting wasps for pollination. Current Biology 18, 740-744 (2008).
6. Brodmann, J. et al. Orchid Mimics Honey Bee Alarm Pheromone in Order to Attract Hornets for Pollination. Current Biology 19, 1-5 (2009).

August 7, 2009

Ants versus fungi

Ants that grow fungi for food have to control other fungi that attack their gardens, but what about fungi that attack the ants themselves? Two papers published recently reveal surprising sophistication in both ants and fungi.

Sandra Anderson and colleagues discuss "The life of a dead ant: the expression of an adaptive extended phenotype" in American Naturalist. Richard Dawkins coined the term "extended phenotype" to refer to a consistent effect of a gene inside an individual on something outside that individual. For example, it might be possible to link differences in the shape of webs made by different spiders to genetic differences among those spiders. This week's paper shows that ants infected by certain fungi show complex behavior that benefits the fungi. Ants infected by fungi with different genes would probably not show this behavior, but the genes involved have not yet been identified.

Before the fungus-infected ants die, they attach themselves (by biting) to the underside of leaves that are ideally located for fungal reproduction: on the cooler and moister north side of trees, near (but not on) the ground. The researchers showed that these locations were favorable for fungal reproduction by moving infected ants higher in the canopy or down to the ground. Ants on the ground mostly disappeared, but fungi grew abnormally in those that remained. Fungi were unable to compete their life-cycle on ants moved higher in the canopy.

I can imagine a fungus producing an ant hormone (or perhaps destroying a particular neuron) to make its ant host bite a leaf, but getting ants to bite leaves in a particular humidity and temperature range and then hold on until dying seems pretty sophisticated. It would be easier if the ants spent most of their time in that zone anyway, but the one ant colony they found was much higher, about 15 meters.

The second paper shows greater sophistication on the part of the ants. "Adaptive social immunity in leaf-cutting ants" was published by Tom Walker and William Hughes in Biology Letters. The paper is freely available on-line.

These social ants protect each other from fungal infection by grooming each other, much like meerkats or baboons. Ants exposed to the fungus got groomed about twice as long as ants exposed to a control solution without the fungus, or about three times as long if their nest had been exposed to the same fungus two days before. (Another example of learning in insects.) Ants placed in nests that were previously exposed to the fungus were twice as likely to survive for two weeks after they were inoculated.

August 5, 2009

Highly conserved, but how important?

Today Pharyngula takes a break from his exhaustive documentation of the existence of wackos and evil-doers among religious and political conservatives -- who would have guessed? -- to discuss highly conserved non(protein)coding DNA. It seems reasonable that if a DNA sequence is highly similar between humans and fish, whose last common ancestors lived way back in the good old days, then it's probably doing something important. But a paper I discussed earlier showed that highly conserved noncoding regions can sometimes be deleted without any apparent ill effects. Of course, this is also true of some protein-coding genes; we apparently have a lot of backups. Actually I'm not sure computer and circuit-board analogies are that useful.