Tag Archives: Research Blogging

When does a beneficial mutation fail to benefit?

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Beneficial mutations, according to Hollywood, include the superpowered ability to make San Francisco Bay foggy. Photo via Comics Contiuum.

ResearchBlogging.orgEvery time a cell divides is an opportunity for mutation, creating new genetic variation that may be beneficial, may be harmful, or may make no difference at all. In sexually reproducing species, the fate of a useful new mutation is relatively straightforward. If it overcomes the vicissitudes of genetic drift, the mutation will spread through the population as recombination swaps it into different genetic backgrounds, so that on average the mutation spreads or disappears on its own merits.

In asexual species, though, things are less straightforward. This is because new mutations are stuck with the genetic backgrounds in which they first appear—whether they spread of disappear depends not only on the fitness benefits they might provide, but on how beneficial the variation in the rest of the genome is, too. A new beneficial mutation in an asexual population is like a race car driver who can’t change cars—she might be an ace at the wheel, but if she’s stuck in a Yugo, she’s probably not going to win.

So what happens to a new beneficial mutation in an asexual population is largely dependent on random factors: genetic drift and mutation. That randomness means that in order to know how new useful mutations behave in general, the only robust solution is to watch lots of new useful mutations in lots of otherwise identical populations.

In other words, it’s a question best approached using experimental evolution. That brings us to a study just released in advance of print by the journal Genetics, in which a team headed by Greg Lang uses some clever methods to track the origin and fate of beneficial mutations in yeast.

The first clever thing about the project is that its authors knew in advance where to expect a beneficial mutation. Yeast cells reproduce both sexually and asexually—if the experimental populations are maintained in conditions that keep them reproducing asexually, mutations that turn off the costly cellular machinery necessary for sexual reproduction provide a measurable benefit.

Electron micrograph of budding yeast cells. Image from Microbe World.

By using a strain of yeast engineered to produce fluorescent protein in the course of sexual reproduction, the authors could check for the presence of permanently asexual mutants by taking a sample from the population, prompting it to mate and measuring the sample’s total fluorescence. Lower fluorescence would mean that more cells had lost the ability to reproduce sexually; if samples from a population were to become less and less fluorescent over time, the beneficial mutation would be spreading through the population.

Lang and his coauthors then set up the kind of experiment that you can only do with single-celled critters: they started 592 populations of yeast evolve for 1,000 generations of asexual reproduction. Each population started out from a single genetic strain, so differences between populations started from the same strain were purely due to differences in the random processes of mutation and drift. (The full experimental design used two different strains of yeast, and kept the population size at either 100,000 or 1,000,000 cells, for a total of four treatments.)

You might expect that the loss-of-sex mutation would reliably emerge and spread until it dominated each replicate population. In fact, that only occurred in a small fraction of the replicates. In many more cases, the loss-of-sex mutation showed up and started to spread, but was then overwhelmed by yeast that could still reproduce sexually—presumably because other, more beneficial mutations had arisen elsewhere in the population. This phenomenon, clonal interference, is widely expected to happen in competition among clonal strains.

What determined the success or failure of the loss-of-sex mutation? The authors found a considerable range of variation in the rate at which loss-of-sex strains increased in the experimental populations, suggesting that variation elsewhere in the genome contributed to the fitness of the yeast strain carrying the loss-of-sex mutation. Since every replicate population started as a genetically identical clone, that meant that mutations built up quite early in the course of experimental evolution. That variation corresponded to differences in the fitness of strains within the population—and the success or failure of the loss-of-sex mutation depended on whether it turned up in a strain that was already pretty fit to begin with.

Without recombination to mix up the genome, a beneficial mutation is bound to genetic variants at many, many other loci that may boost the benefits from that mutation, or cancel them out. In a clonal population, each genome succeeds or fails as a unit—a single useful mutation simply cannot do it alone.

References

Lang, G., Botstein, D., & Desai, M. (2011). Genetic variation and the fate of beneficial mutations in asexual populations. Genetics DOI: 10.1534/genetics.111.128942

Lang, G., Murray, A., & Botstein, D. (2009). The cost of gene expression underlies a fitness trade-off in yeast. Proc. Nat. Acad. Sciences USA, 106 (14), 5755-60 DOI: 10.1073/pnas.0901620106

Released from predators, guppies reshape themselves—and their environment

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A (domestic) male guppy. Photo by gartenfreuden.

ResearchBlogging.orgConsider a population of guppies living in the Aripo River in Trinidad. They have a happy existence, as far as guppies can be happy, but their lives are shaped by the constant threat of larger, predatory fish. The river runs clear over a colorful gravel bed, and guppies who stand out against that background are eaten quickly. Even guppies whose coloration helps them blend in have to be ready to make a break for it if a predator shows up. All in all, a guppy’s chances of surviving to mate depends most on its ability to hide from bigger fish, and to swim quickly when it can’t hide.

Then one fine day a biologist comes along, scoops up a couple hundred guppies, and moves them to a pool in a tributary of the river. The pool is separated from the mainstream by a series of waterfalls, so larger fish can’t swim up—the guppies are now free from their most dangerous predators. They can be fruitful and multiply. In this new habitat, camouflage and evasive maneuvers don’t matter so much. What does matter is finding enough food to make some babies in the midst of a whole bunch of other guppies who are also not particularly worried about predators.

John Endler started the experiment I’ve just described back in 1976 to see whether guppies’ coloration helps them hide from predators [PDF]. The guppies he moved to a predator-free stream have continued to evolve, though, and three decades later, new studies are showing how release from predators changed the guppies—and how those changed guppies could be changing the living community around them.

Since the 1976 introduction, Endler and other biologists have tracked the Aripo River guppies’ response to the change in natural selection he created. Release from predators is considered one of the classic sources of ecological opportunity that can free a population to evolve new traits and behaviors, and explore new ways of making a living. At the same time, a sudden lack of predators means that competition within the population can become stronger.

Points of measurement for guppy body and head shape, illustrated on a stained specimen. Image from Palkovacs et al, fig. 1.

In one study just published by PLoS ONE, Eric Palkovacs and two colleagues compared the body shape of guppies from the experimental population with guppies from the source stream. (Endler had noted changes in body shape along with changes in coloration in his original paper.) First, Palkovacs and his coauthors gauged how rapidly female guppies taken from each site snapped up standardized food. Then they killed the test fish, treated them with stain, and measured their body and head shape. Fish from the site with lower predation ate faster, and they had bigger mouths and deeper bodies than fish from the site with more predators.

Palkovacs and his coauthors also observed that the guppy populations at the experimental site were denser—without predators thinning them out, the fish are probably most limited by their food supply. A study published last year in PNAS suggests that this denser guppy population might reshape its own environment. The paper’s authors created artificial ponds stocked with algae and small invertebrates, then introduced guppies from the high-predation source site or from the low-predation experimental site. They also controlled for the differences in guppy population density associated with predator pressure, maintaining the fish at either the high density observed with low predation, or the lower density observed with high predation.

Where the guppies came from made a significant difference in the artificial ecosystems, and these differences were in some cases exaggerated by the increased population density caused by predator release. Guppies from the “released” site ate less selectively than guppies from the site experiencing higher predation, who favored invertebrates over algae. As a result, guppies from the released site were associated with less algae growth, and higher invertebrate population density. Probably because they ate more plant matter, guppies from the released site also excreted less nitrogen, reducing the nutrient’s availability for plant growth.

These results echo a study I discussed last year, which used a very similar approach to show that speciating sticklebacks can change their environment. It’s another reminder that evolutionary change can feed back to change the environmental conditions that prompted change in the first place—that natural selection operates in the midst of continuous change.

References

Bassar, R., Marshall, M., Lopez-Sepulcre, A., Zandona, E., Auer, S., Travis, J., Pringle, C., Flecker, A., Thomas, S., Fraser, D., & Reznick, D. (2010). Local adaptation in Trinidadian guppies alters ecosystem processes. Proc. Nat. Acad. Sciences USA, 107 (8), 3616-21 DOI: 10.1073/pnas.0908023107

Endler, J. (1980). Natural selection on color patterns in Poecilia reticulata. Evolution, 34 (1), 76-91 DOI: 10.2307/2408316

Palkovacs, E., Wasserman, B., & Kinnison, M. (2011). Eco-evolutionary trophic dynamics: Loss of top predators drives trophic evolution and ecology of prey. PLoS ONE, 6 (4) DOI: 10.1371/journal.pone.0018879

Deprived of pollinators, flowers evolve to do without

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Who needs pollinators? Not monkeyflowers—at least not after a few generations of evolution. Photo by Brewbooks.

ResearchBlogging.orgThe loss of animal pollinators poses a potentially big problem for plants. However, many plant species that rely on animals to move pollen from anther to stigma have the capacity to make due if that service goes undone—and, as a new study released online early by the journal Evolution demonstrates, such plants can rapidly evolve to do without pollinators [$a] if they must.

The paper’s authors, Sarah Bodbyl Roels and John Kelly, demonstrate this using a simple greenhouse experiment with the monkeyflower Mimulus guttatus, a wildflower native to western North America, and a member of a genus rapidly developing into a major model system for studying the evolution of ecological isolation and floral evolution.

Mimulus species vary in their reliance on animal pollinators—some grow minimalistic flowers, with the anther so close to the stigma that pollen transfers without any assistance. In natural populations, M. guttatus is usually pollinated by bees, but individual plants vary in the distance between anther and stigma, and this variation has a genetic basis. So a population of M. guttatus deprived of pollinators would have the raw material to evolve a solution—natural selection would favor plants that are better able to self-pollinate. As the population evolved to be more self-fertilizing, it might also evolve to look more like self-pollinating Mimulus species, losing the bright petals that attract pollinators.

To see whether this could actually happen, Bobdyl Roels and Kelly challenged an experimental population of Mimulus guttatus to do without pollinators, and tracked its response.

The authors raised seeds derived from a natural wild population of Mimulus guttatus in greenhouses under two trial conditions: control populations were provided with hives of bumblebees to pollinate them when their flowers were ready for servicing; and experimental populations were left to produce what seed they could without pollinators. The authors collected the seeds produced by each population, and planted them to form the next generation.

A bumblebee digs for nectar in flowers of Mimulus moschatus. Photo by Mollivan Jon.

Early on in the experiment, the experimental populations deprived of pollinators fared badly. Without pollinators, the average plant produced two seeds or fewer by the end of the generation, compared to eight or ten seeds per plant in the population provided with bees. By the fifth generation, however, this was starting to improve—plants in both populations without pollinators were producing more seeds, and one of the two experimental populations produced nearly as many seeds as the control plants.

Examining the traits of plants produced by this final generation (actually, the grand-offspring of the fifth generation, to control for effects of inbreeding), the authors found that the average distance between the pollen-producing anther and the pollen-receiving stigma had shrunk significantly in plants from the experimental population. Across all the treatments, plants with a shorter distance between stigma and anther produced more self-pollinated seeds. There was no evolved change in other floral measurements, however—plants in the no-pollinators treatment had petals as big and showy as plants evolved with bumble bees.

In a natural population of Mimulus guttatus, the drop-off in seed production created by loss of pollinators should have much the same effect as in this experiment, creating a strong selective advantage for individual plants that can make more seeds on their own. The fact that the experimental plants did not evolve reduced petals could mean that in the cushy conditions of a greenhouse, there wasn’t much need to stop spending resources making showy flowers. Or maybe, when the major source of natural selection is the need to make any seeds at all, selection to save resources on flower production is relatively weak and correspondingly slow-acting.

As the authors point out, one of many changes humans are making to natural communities around the world is to disrupt pollination relationships. In a sense, experiments like theirs are being carried out worldwide, on hundreds of plant species—and each species will adapt, or fail to adapt, in its own way.

Reference

Bodbyl Roels, S., & Kelly, J. (2011). Rapid evolution caused by pollinator loss in Mimulus guttatus. Evolution DOI: 10.1111/j.1558-5646.2011.01326.x

How can you tell if a plant is carnivorous? Feed it!

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A Venus flytrap closes on an unfortunate spider. Photo by cheesy42.

ResearchBlogging.orgPlants that eat animals offend our trophic sensibilities. Those of us who can move independently are supposed to eat those of us who can make sugar from sunlight—that’s just the way the food chain works, right?

Well, not really. From a certain perspective, plants prey on animals all the time, using the sneaky strategy of just waiting us out—when we animals stop moving for good, we’re fertilizer. And there are quite a few plants that aren’t so patient. Venus flytraps, sundews, and pitcher plants have been recognized as carnivores since before Charles Darwin devoted a book to their ecology and anatomy. They all have structures—fly-trapping leaves, or sticky hairs, or deep pitfalls full of water—that are uniquely good at catching wayward insects. All of them also grow in particularly nutrient-poor soils, such as bogs, where the nitrogen from trapped insects makes a big difference.

The vast majority of plants lack either adaptations for trapping, or the same kind of need for nitrogen—they either don’t grow where they can’t get the stuff, or they hire symbiotic bacteria to help fix it. Yet there is a third category of plants, which are not exactly carnivorous, but which might just “eat” the occasional stray fly anyway. Many plants have hairy surfaces that can catch insects, or leaf structures that trap water and create pitfalls—and some of these plants can take advantage of the critters caught in these proto-traps.

Sticky purple geranium can trap insects on its sticky leaves, and seems to get some nutrition out of them. Photo by jby.

One such plant is the sticky purple geranium (Geranium viscosissimum), which grows on dry Palouse hillsides around my current hometown of Moscow, Idaho. As its name implies, sticky purple geranium is sticky—its leaves are velvety with tiny glandular hairs, which leave a gummy residue on your hands if you brush against them. These hairs make it difficult for small insect herbivores to get to the leaves—but they also trap some of those insects.

Back in 1999, a biologist in my department at the University of Idaho, George Spomer (who left the department before my arrival), showed that sticky purple geranium leaves would digest a protein film pressed against them, somewhat like the leaves of a sundew. When Spomer placed protein labeled with carbon-14 on geranium leaves, he found elevated levels of carbon-14 elsewhere in the plant, suggesting that geranium leaves could absorb protein as well as digest it [$a].

Spomer demonstrated that the plants he studied could digest and absorb insects caught on their leaves, but his data can’t tell us whether that ability is of any particular use to a geranium growing in a natural population—whether, that is, geraniums actually need the nutrients they might get from trapped insects. A more recent study of another possibly carnivorous plant gets closer to answering that question.

Water collected in the leaves of a teasel plant forms a death trap for insects, and a source of nitrogen for the plant. Photo by HermannFalkner/sokol.

The plant in this second study is fuller’s teasel, Dipsacus fullonum, a widespread European wildflower that has been introduced into North America. The leaves of many teasel plants form catchments (pictured above) that can collect water and form a makeshift pitfall, which catches and drowns small insects. It has been speculated that, like sticky purple geranium, fuller’s teasel can absorb nutrients from these catchments full of rotting insect corpses. British biologists Peter Shaw and Kyle Shackleton set out to test this hypothesis not by tracking protein from trapped insects, but by determining whether teasel plants benefit from the trapping.

To do this, Shaw and Shackleton experimentally manipulated the number of insects trapped in the catchments formed by teasel plants’ leaves. In one treatment, they watched experimental plants and removed insects as soon as they were trapped; in the other, they “fed” the experimental plants an extra bluebottle maggot at set intervals. They compared both treatments to a group of plants that were left un-manipulated as a control. The “fed” plants didn’t necessarily grow bigger or produce more seeds, but they did produce more seeds as a proportion of their total biomass. That is, fuller’s teasel plants that trap more insects can devote more of their resources to making seeds.

Does this make fuller’s teasel carnivorous? Maybe, but probably not in the same sense that a Venus flytrap is. Teasels tend to grow in better soil than carnivorous plants do in general—they like open fields and stream banks, in my experience. Furthermore, we don’t have any evidence that teasels actively attract insects, as most carnivorous plants do. On balance, it seems far more likely that what Shaw and Shackleton found is not carnivory as we usually know it, but plants making sure that a handy source of nitrogen doesn’t go to waste.

Fuller’s teasel relies on insects for pollination—but does it also rely on them for nutrition? Photo by gynti_46.

References

Darwin, C. (1875.) Insectivorous plants. Google Books link.

Shaw, P., & Shackleton, K. (2011). Carnivory in the teasel Dipsacus fullonum — The effect of experimental feeding on growth and seed set. PLoS ONE, 6 (3) DOI: 10.1371/journal.pone.0017935

Spomer, G. (1999). Evidence of protocarnivorous capabilities in Geranium viscosissimum and Potentilla arguta and other sticky plants. Int. J. Plant Sci., 160 (1), 98-101 DOI: 10.1086/314109

Moths that pass in the night: Reproductive isolation due to pickiness, or just bad timing?

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ResearchBlogging.orgOn a summer night in a Florida corn field, a female armyworm moth emerges from her underground cocoon and spreads her wings to dry in the humid air. Over the next few weeks, she will fly miles away in search of a mate, and a likely-looking patch of host plants on which to lay her eggs.

Her brief adult life will be shaped in many ways by the life she led as a larva, feeding on domestic corn. She could easily find other grasses to feed her offspring, but she’ll probably seek out another cornfield. She may encounter armyworm males who were raised on many other grasses, but the odds are that the males she accepts as mates will also have grown up eating corn. This is so likely to be the case that it has left a mark on the genetics of her species [PDF].

At night in a cornfield, moths mate nonrandomly. Photo by K e v i n.

Yet it isn’t clear how much of this isolation between armyworms from corn (the “corn strain”) and armyworms from other grasses (called the “rice strain”) arises because moths from the different host plants actively prefer mates from their own larval food plant, or because they just don’t encounter moths from the other food plants as frequently. Like many moths, armyworms of both sexes deploy pheromones to attract and woo mates—so maybe armyworms from the same food plant smell better to each other. On the other hand, corn-strain armyworms do more of their mate searching early in the evening (although they’ll keep hunting all night), while rice-strain armyworms wait to search till the last few hours of nighttime.

Disentangling which of these two sources of isolation—preference versus timing—maintains the genetic differences between host plant strains of the armyworm takes some careful experimental work. As in many biological questions, the answer might well be not one or the other, but a little of both [$a].

In a study published in the latest issue of The American Naturalist, a team of entomologists at the Max Planck Institute for Chemical Ecology took on the question of what keeps the armyworm host strains separated. They performed two mating experiments with laboratory-reared moths of both sexes from both strains.

Fall armyworm adult. Photo via Wikimedia Commons.

First was a “no-choice” experiment in which moths were kept in a chamber with a single member of the opposite sex from their own strain, or the other strain. The test was repeated over three nights in a row. On the first night, females from the corn strain were less likely to mate with males of the rice strain than males of their own, and when they did accept rice-strain males, it wasn’t till later in the night. The second and third nights, though, corn-strain females mated about equally with males of both strains. Rice-strain females mated with males of both strains at about equal frequency all three nights, although they did so late in the night.

In the second round of experiments, moths were introduced into flight cages with one member of the opposite sex from each of the two host strains, so they could choose between them. To control for the differences in timing of mate searching between the two strains, the team repeated the experiment twice—in one version, the choosing moth had the entire length of the night to pick a mate, and in the other, the moths were only put into the same cage for the last four hours of the night, when the grass strain prefers to mate.

Fall armyworm larva. Photo by agrilifetoday.

In the all-night experiment, corn-strain males and females were both more likely to choose a mate from their own strain than the other. Rice-strain moths of both sexes mated with moths of both strains about equally—but rice-strain females were less likely to choose any mate at all. On the other hand, when the research team waited till the end of the night to introduce the test moths to their possible mates, rice-strain moths of both sexes mated much more frequently overall, and rice-strain females strongly preferred rice-strain males. Corn-strain males were basically indiscriminate in the late-night experiment, and corn-strain females were also less choosy.

In short, when mating during their usual activity periods, females of both strains were choosy about their mates; but when offered mates at the wrong time, they didn’t discriminate as much. The authors suggest that these mistimed matings were less discriminating because they were more likely to be initiated by the males, who showed relatively weak preferences even during their own usual mating times.

So the genetic differentiation between armyworm host strains is probably due to both timing and mate choice, and the two isolating factors affect males and females differently. Females, particularly rice-strain females, are quite picky about mating with a male of their own strain. Males, on the other hand, seem mainly to be prevented from pursuing females of the other strain by the fact that their respective schedules don’t line up. As the study’s authors conclude, all these individual rejections and missed connections, added up across entire armyworm populations, bring these moths a little bit closer to speciation.

References

Prowell, D., McMichael, M., & Silvain, J. (2004). Multilocus genetic analysis of host use, introgression, and speciation in host strains of fall armyworm (Lepidoptera: Noctuidae). Annals Entomol. Soc. America, 97 (5), 1034-44 DOI: 10.1603/0013-8746(2004)097[1034:MGAOHU]2.0.CO;2

Schöfl, G., Dill, A., Heckel, D., & Groot, A. (2011). Allochronic separation versus mate choice: Nonrandom patterns of mating between fall armyworm host strains. The American Naturalist, 177 (4), 470-85 DOI: 10.1086/658904

In which I try to explain why “heritability” is not quite the same thing as “heritable”

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ResearchBlogging.orgRobert Kurzban responds in the ongoing “adaptive” homophobia kerfuffle (henceforth, the O.A.H.K.) with continued confusion about how biologists identify possible adaptations and test to see whether natural selection is responsible for them. He notes that one effect of natural selection is to remove heritable variation in traits under selection, so that many traits which are probably adaptations—arguably, sometimes the best-adapted traits—actually have zero heritability.

This is true. But it’s important to note that a trait having zero heritability, or no genetic variation, is not the same thing as that trait not being heritable, or having no genetic basis. If the trait has zero heritability, the observed variation in the trait may not be heritable, but the trait still may be. Kurzban’s confusion over this distinction may be a fault of the terminology, as was pointed out to me in a couple independent conversations following the last round of the O.A.H.K.

That aside, reduced heritable variation in a trait—relative to appropriate standards for comparison, like other traits in the same species or the same trait in closely related species—is sometimes used to infer that selection has acted on that trait in the past. This is what my lab has done in the case of Joshua tree and its pollinators, which Kurzban cites. This sort of approach provides only indirect evidence of natural selection’s activity—but it’s often the best you can do when your focal species isn’t amenable to growing in a lab or greenhouse within the span of a single grant cycle.

The two varieties of Joshua tree, because apparently these are part of the discussion now. Photo by jby.

The comparison to other traits or to other species is the critical point here. Without it, you can’t determine whether a lack of genetic variation is due to strong selection, or due to the fact that there is no genetic basis for the trait. In isolation, the observation that there is no heritable variation for a single trait or behavior in a single species doesn’t tell you much except that natural selection cannot currently be acting on the observed range of variation in that trait. If there’s no genetic basis for the trait at all, then it cannot have been under selection in the past, either.

Forming hypotheses versus testing them

Regarding Kurzban’s broader point about how biologists identify adaptations:

Futuyama’s textbook, which Yoder cites for the discussion of heritability, indicates the following: “Several methods are used to infer that a feature is an adaption for some particular function” (p. 261), and lists the criteria that evolutionary psychologists rely on, including complexity, evidence of design, experiments, and so on. From the material I quoted in my prior post, it seems to me that by indicating the two kinds of evidence that are necessary for inferring a feature is an adaptation, Yoder is rejecting Futuyama’s claim that one can infer adaptation from its form, complexity, and so on.

Here Kurzban is confusing how we initially infer that a trait or behavior might be an adaptation with how we actually demonstrate that a trait or behavior is an adaptation. Forming a hypothesis is not the same thing as testing it, as Jon Wilkins explained so well. If Kurzban is accurately representing evolutionary psychology’s standards of evidence, then he’s confirmed Wilkins’s accusation that evo psych usually doesn’t go beyond the step of forming a plausible hypothesis to collecting the data that can test it.

Demonstrating that an adaptive hypothesis is well supported by data is, as I’ve previously said, a lot of work—usually enough for more than one scientific article. Depending on what is easiest to do, building the case that a trait is an adaptation might start with a paper that merely demonstrates a trait’s function—but that trait has not been conclusively shown to be an adaptation until we know that its demonstrated function is selectively important, and that the trait itself has a genetic basis.

While familiar to anyone who reads the evolutionary biology literature, this maybe isn’t so obvious to non-biologists. This may be because popular science accounts don’t always differentiate between hypotheses with good scientific support and those with none. Walk through a zoo or a natural history museum, and you’ll read nothing but adaptive hypotheses all day—but you’ll rarely see good, deep discussion of how well they’re supported.

This is why, since I started graduate school, I’ve became rather tiresome company on trips to museums and zoos. But one of the great things about popular writing by working scientists (from my perspective as a scientist) is that it lets specialists explain exactly such finicky details of our fields directly to the public. Doing so clearly and accessibly is challenging, to be sure, but naïve, uncritical endorsements of unsupported hypotheses—about the adaptive values of human behavior, or anything else—are available in just about every major media outlet. If scientists don’t do better than that in our own science communication, what value do we have to add to the discussion?

And now something new: relevant data

Your reaction to this image might be in your genes, but the evidence is that it can change, too. Photo source unknown, presumed public domain.

Which brings us back to evaluating Gordon Gallup’s “adaptive” homophobia hypothesis. Kurzban also points to evidence (ye gads! data!) that natural selection actually could have something to work with in the case of attitudes towards homosexuals. A 2008 Australian twin study, which finds a genetic component of variation in responses to a questionnaire about attitudes towards homosexuality.

This is indeed, as Kurzban suggests, preliminary data in support of the idea that natural selection could operate on homophobia. As Neuroskeptic pointed out in the comments on my last O.A.H.K. post, it also means that natural selection could be operating on tolerance of homosexuals. It’s an interesting and important question, actually, why the authors of that study chose to frame their results as showing the heritability of intolerance, rather than the heritability of tolerance.

However, as I noted all the way back at the beginning of the O.A.H.K., we also know that homophobic attitudes can change considerably over the course of an individual’s lifetime. It’s hard to say how survey responses taken at a single point in time relate to what natural selection would actually have to work with, if homophobic attitudes or lack thereof somehow shape an individual human being’s expected reproductive fitness. Even if there is some solid genetic basis to homophobia, we still don’t have data that can rigorously determine whether or how natural selection might act on that variation.

References

Godsoe, W., Yoder, J.B., Smith, C.I., Drummond, C., & Pellmyr, O. (2010). Absence of population-level phenotype matching in an obligate pollination mutualism Journal of Evolutionary Biology, 23 (12), 2739-2746 DOI: 10.1111/j.1420-9101.2010.02120.x

Verweij, K., Shekar, S., Zietsch, B., Eaves, L., Bailey, J., Boomsma, D., & Martin, N. (2008). Genetic and environmental influences on individual differences in attitudes toward homosexuality: An Australian twin study. Behavior Genetics, 38 (3), 257-265 DOI: 10.1007/s10519-008-9200-9

In which several evolutionary psychologists still don’t understand evolution

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ResearchBlogging.orgJesse Bering has responded to criticism—by me, Jon Wilkins, and P.Z. Myers, among others—of his post about Gordon Gallup’s hypothesis that fear of homosexuals is favored by natural selection, in the form of an interview with Gallup. The result is informative, but probably not in the way intended.

To recap: Gallup proposed that homophobia could be adaptive if it prevented gay and lesbian adults from contacting a homophobic parent’s children and—either through actual sexual abuse or some nebulous “influence,” making those children homosexual. In support of this, he published some survey results [$a] showing that straight people were uncomfortable with adult homosexuals having contact with children.

I pointed out that all Gallup did was document the existence of a common stereotype about homosexuals—he presents no evidence that believing this stereotype can actually increase fitness via the mechanism he proposes, or that it is heritable.

Homophobia. And, um, everyone-else-phobia, too. Photo by yksin.

So now Gallup and Bering have responded, although they have not, I think, improved their case. There’s a lot for me to address here, so I’ll try to break it up into sections, and follow the order of the interview.

In which Gordon Gallup is not a homophobe

In the response post, Gallup (and Bering, who contributes quite a lot to the argument in his role as interviewer) takes issue with the collective objections of working biologists, but manages not to actually address those objections. Bering starts the conversation on the moral high ground:

BERING: Let’s address the elephant in the room. It’s embarrassing for me to even ask this of you, since the answer is so obviously “no” to me. Is your theory a justification of your own homophobia?

GALLUP: A lot of people think that if a person has a theory it’s a window unto their soul. I have lots of theories. (See CV (pdf).) I have a theory of homophobia, I have a theory of homosexuality, and I have a theory of permanent breast enlargement in women, just to mention a few. So that would make me a homophobic, homosexual who is preoccupied with women’s breasts.

Neither I, nor any of the other critics I’ve seen have called Gallup a homophobe. He may be uniquely bad at understanding how societal homophobia nullifies his interpretation of his survey results, but that doesn’t make him a homophobe. Thanks for clearing that up, though, guys.

Gallup then demonstrates that he either hasn’t actually read any of the latest criticism, or has missed the point entirely:

… It is interesting how my critics tip-toe around the fact that my approach is based on a testable hypothesis, and how they go out of their way to side-step the fact that the data we’ve collected are consistent with the predictions. Whether it is politically incorrect or contrary to prevailing social dogma, is irrelevant. In science, knowing is preferable to not knowing. Minds are like parachutes, they only function when they’re open. If I were a homosexual, I’d want to know about these data.

I certainly didn’t tiptoe around the testability of Gallup’s hypothesis—I wrote that (1) the data he presented do not test his hypothesis, and (2) the data we do have regarding the probable fitness benefits of homophobia and its heritability contradict his hypothesis. I’m entirely prepared to revise my conclusions given new data, but Gallup doesn’t have any.

In which at least one of us doesn’t understand heritability

In his next question to Gallup, Bering accuses me of “bungling” the definition of heritability, linking to evolutionary psychologist Rob Kurzban, who says that my brief definition of heritable as “passed down from parent to child more-or-less intact” is wrong because heritability is actually “the extent to which differences among individuals are due to differences in genes.”

Wow, dude. You are aware that what you just said means exactly the same thing as what I originally said, right?

Let’s go to the textbooks that Kurzban says I’m contradicting. Here’s the passage on heritability from Douglas Futuyma’s gold-standard undergraduate textbook Evolution (page 209):

One way of detecting a genetic component of variation, and of estimating VG [trait variation attributable to genetic differences] and h2 [the proportion of total trait variation explained by genetic variation], is to measure correlations* between parents and offspring, or between other relatives. For example, suppose that in a population, the mean value of a character in the members of each brood of offspring was exactly equal to the value of that character averaged between their two parents (the MIDPARENT MEAN) (Figure 9.20A). So perfect a correlation clearly would imply a strong genetic basis for the trait. [Bold text and bracketed notes mine; otherwise sic.]

The asterisk in that quote leads to a footnote pointing out that regression, rather than correlation, is more typically used. This is the definition of heritability that I learned in my undergraduate and graduate courses. It’s also the definition I’ve just helped teach to a class of third- and fourth-year undergraduate biology students in my capacity as a teaching assistant on a course in population biology.

In non-statistical terms (the kind I try to use on this blog), a positive regression between a parent’s traits and those of their offspring means, in fact, that the parent’s traits are passed on to their offspring, um, more-or-less intact.

Parent-offspring regression is widely used to estimate heritability [PDF], but you can also do similar analyses using trait measurements for siblings, or multiple generations on a pedigree. In all of these cases, known parental or sibling or familial relationships are proxies for genetic similarity—you can estimate heritability without knowing anything about specific genes. (In fact, sometimes biologists use genetic data to reconstruct pedigree relationships, then estimate heritability from the pedigree.) As implied in the quote from Futuyma’s textbook, this approach is statistically equivalent to showing that there is a significant portion of trait (phenotype) variation explained by genetic variation—which is where Kurzban seems to have become confused.

Wild parsnip, mostly here to break up the wall of text. Photo by Bas Kers.

Here’s a specific example near and dear to my field of study, species interactions: To determine whether parsnip webworms could be under natural selection to resist nasty chemicals produced by their food plant, the wild parsnip, May Berenbaum and Arthur Zangerl estimated the genetic component of variation [$a] in the worms’ capacity to choose food with lower levels of the toxins, and to tolerate the toxins they did eat. To do this, they raised webworm larvae of known parentage in the lab, and tested them on controlled diets. Their actual statistical analysis tested for an effect of the worms’ sibling relationships (parentage) on their ability to avoid toxins and survive them.

In all of Gallup’s lengthy response to Bering’s question about heritability, he doesn’t say a word about this kind of data with regard to homophobia. That’s because it doesn’t exist, and, as far as I can tell from the interview, he has no intention to try and collect it. To be completely fair, it’s harder to collect heritability data on humans than on webworms—but it’s hardly impossible. As Gallup notes, there are studies documenting heritability for, of all things, human grip strength [PDF].

Kurzban’s critique is correct in one very specific regard, which Bering doesn’t touch on. It is relatively difficult, both for logistic and resource-related reasons, to estimate a trait’s heritability and determine whether natural selection is acting on it within the same study. (Although there are plenty of exceptions—here’s one example [$a] pulled at random from my reference library.) That’s why I said, in my original post, that biologists expect evidence for heritability or fitness benefits in support of an initial claim that a trait or behavior is adaptive. The study I cited as an example of support for adaptation—which shows that horned lizards’ horns prevent predator attacks [PDF]—demonstrates fitness benefits, but not heritability. This point should be familiar to anyone who regularly reads the evolutionary biology literature.

Grip strength: known to be heritable. Homophobia: not so much. Photo by West Point Public Affairs.

So, again, Gallup has no data on the heritability of homophobia. The rest of his interview shows that he still doesn’t have any data to demonstrate fitness benefits for it, either.

In which evidence of fitness benefits also remains absent

Gallup then comes to the question of whether a child who would otherwise be straight can be “converted” to homosexuality by early same-sex sexual contact.

As detailed in my 1996 reply to Archer, we’ve collected data from male homosexuals that show that most gay males don’t report getting a clear sense of their homosexual orientation until they have their first same-sex postpubertal sexual experience.

Most gay men don’t know for sure that they’re gay until they’ve actually, you know, tried gay sex? Quelle surprise. This is absolutely classic mistaking of correlation for causation, and it suggests that Gallup doesn’t know much about the actual experience of sexual minorities. When you grow up surrounded by straight people, it often takes very direct evidence to convince you that you’re attracted to people of the same sex. If same-sex activity shortly after puberty can cause homosexuality, wouldn’t parents be most concerned about homosexuals having contact with teenagers? At the risk of sounding like a broken record, this is yet another thing we can’t tell from Gallup’s survey data—he asked about pre-pubescent children, and in one case 21-year-old children, but not children who have just passed puberty.

Finally, Gallup deals with the relative risk that homosexuals will molest children. He does this by moving the goalposts for pedophilia:

There is also evidence that shows that the propensity to have sex with minors is positively correlated with promiscuity among homosexual males. Unlike heterosexual pedophiles, homosexuals who have sex with minors target young postpubertal victims.

That’s not pedophilia Gallup is talking about—that’s violation of age-of-consent laws. The comparison between heterosexual-identified pedophiles, who target children, and homosexuals who have sex with post-pubertal teens under the age of consent is, frankly, intellectually dishonest. By definition those are two different groups. The comparison to make is that between all homosexuals who have had sex with minors and all heterosexuals who have had sex with minors. I would imagine that, as Gallup basically admits in his next sentence, those two groups look much more similar.

So that’s where we stand: still no evidence that homophobia is heritable, and still no evidence that it provides a fitness benefit by preventing the homophobe’s children from becoming homosexuals. Gallup’s only data are still, over fifteen years after his initial publication, a set of survey responses that are consistent with any number of hypotheses for the origins of homophobia. Claiming that those data demonstrate an adaptive function for hatred of homosexuals doesn’t just fail the standards of evidence for evolutionary biology, it’s bad scientific reasoning.

In which we come to a conclusion of sorts

In a coda to the interview, Bering accuses me and his other critics of failing to engage with Gallup’s results. I think my previous discussion, and Bering’s response to it, speak for themselves. Bering has demonstrated to me that he doesn’t understand undergraduate-level biology, and that, as Will Wilkinson suggested, he’s more interested in ginning up controversy than scientific rigor. (On which point he wins, I suppose. D&T’s visit count went through the roof when P.Z. Myers linked here.)

Bering also makes some conspicuously uninformed speculations about my own experience and motivations. I won’t dignify that with a response except to say yes, Jesse, I’m gay, and you don’t know the first thing about what I have or haven’t encountered in the way of “palpable disapproval.” First and foremost, though, I’m a scientist. Contrary to what you seem to think, I love a good counterintuitive, paradigm-shifting hypothesis, but I also expect it to be supported with data.

Bering, however, is convinced that he’s established himself as a hard-nosed scientific iconoclast in opposition to all us stodgy, dogmatic, evidence-demanding biologists. He concludes,

So, I’ll continue to dredge up any old theory, no matter how meager the supporting data …

Clearly, Jesse, I can expect nothing more of you.

References

Arden, N., & Spector, T. (1997). Genetic influences on muscle strength, lean body mass, and bone mineral density: A twin study. Journal of Bone and Mineral Research, 12 (12), 2076-2081 DOI: 10.1359/jbmr.1997.12.12.2076

Berenbaum, M., & Zangerl, A. (1992). Genetics of physiological and behavioral resistance to host furanocoumarins in the parsnip webworm. Evolution, 46 (5), 1373-84 DOI: 10.2307/2409943

Young, K. (2004). How the horned lizard got its horns. Science, 304 (5667) DOI: 10.1126/science.1094790

Campbell, D. (1996). Evolution of floral traits in a hermaphroditic plant: Field measurements of heritabilities and genetic correlations. Evolution, 50 (4), 1442-53 DOI: 10.2307/2410882

Futuyma, DJ. (2005). Evolution. First ed. Sunderland, MA: Sinauer Associates. Google Books.

Gallup, G. (1995). Have attitudes toward homosexuals been shaped by natural selection? Ethology and Sociobiology, 16 (1), 53-70 DOI: 10.1016/0162-3095(94)00028-6

Mousseau, T., & Roff, D. (1987). Natural selection and the heritability of fitness components. Heredity, 59 (2), 181-97 DOI: 10.1038/hdy.1987.113

Parasitism of a different color

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ResearchBlogging.orgThe common cuckoo is such a lazy parent that brood parasitism—laying its eggs in the nests of other birds—is built into its biology.

No bird will willingly adopt cuckoo chicks, which usually out-compete, and sometimes kill, their adoptive siblings. Given any hint that one of the eggs in her nest isn’t hers, a bird will eject the intruder. So cuckoos have evolved eggs that mimic the coloring of their hosts’ eggs—dividing the species into “host races” that specialize on a single host species, and lay eggs that mimic that host’s.

Cuckoo eggs (indicated by arrows) in the nests of three different host species. Illustration via The Knowledge Project.

As you can see from this illustration, the match is often extremely good—the cuckoo egg is really only obvious when the hosts’ eggs are visibly smaller. In fact, a new study by Mary Caswell Stoddard and Martin Stevens shows that this matching is often even better than it looks to the human eye [$a].

Birds see the world differently than humans—where we have three kinds of color-sensitive cells in our eyes, they have four. This allows them to see colors in the ultraviolet range, which is invisible to us. Birds’ eyes also have an additional class of sensory cell that may help them perceive and discriminate among textures. So to study the match between cuckoo and host eggs, Stoddard and Stevens first had to figure out what each egg looked like to a bird.

A reed warbler feeds the cuckoo chick that has taken over its nest. Photo via Wikimedia Commons.

To do this, they developed a mathematical model of each host species’ vision. The model estimated how similar two eggs should look to a bird, given raw data about what colors of light the eggs reflect and the specific colors the bird can detect. Using the model, Stoddard and Stevens could then calculate the “overlap” between the colors and patterning of a host egg and the egg of a cuckoo specializing on that host species.

Stoddard and Stevens then applied the vision model’s measure of similarity to museum specimens of eggs from the cuckoo-parasitized nests of eleven European bird species. They found that cuckoo eggs matched their hosts’ quite well overall, but the match was best for cuckoos specialized on especially vigilant hosts. For each host, the authors looked up studies of egg rejection behaviors to calculate the probability that each species would eject eggs that didn’t look like their own. Species with higher ejection probabilities were parasitized by cuckoo host races whose eggs were better mimics.

That suggests host rejection behavior exerts strong natural selection on cuckoos, which makes sense given that successfully fooling a host is essential to cuckoo reproduction. In light of evidence that cuckoos can also exert selection on their hosts, it looks as though brood parasitism is a truly coevolutionary interaction between cuckoos and their hosts—one that can cause both to evolve greater diversity.

Reference

Stoddard, M., & Stevens, M. (2011). Avian vision and the evolution of egg color mimicry in the common cuckoo. Evolution DOI: 10.1111/j.1558-5646.2011.01262.x

An adaptive fairytale with no happy ending

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ResearchBlogging.orgThe evolution of human traits and behaviors is, as I’ve noted before, a contentious and personal subject. This is enough of a problem when there’s some data to inform the contentiousness. In the absence of meaningful data, it’s downright dangerous.

Take, for instance, Jesse Bering’s recent post about the evolution of homophobia, which Steve Silberman just pointed out to me.

A grim fairy tale indeed. Photo by K Wudrich.

When evolutionary biologists say a trait or behavior is “adaptive,” we mean that the trait or behavior is the way we see it now because natural selection has made it that way. That is, the trait or behavior is heritable, or passed down from parent to child more-or-less intact; and having it confers fitness benefits, or some probability of producing more offspring than folks who lack the trait. Lots of people, including some evolutionary biologists, speculate about the adaptive value of all sorts of traits—but in the absence of solid evidence for heritability or fitness benefits, such speculation tends to get derided as “adaptive storytelling.”

Evolutionary biology wasn’t always so rigorous, once upon a time. Then Stephen Jay Gould and Richard Lewontin buried adaptive storytelling under an avalanche of purple prose in their landmark 1979 essay “The Spandrels of San Marco” [PDF]. Norman Ellstrand made a similar point with better humor in a satirical 1983 article for the journal Evolution proposing adaptive explanations for why children always start life smaller than their parents [PDF]. Nowadays, when evolutionary biologists want to, say, argue that horned lizards’ horns are an adaptation for defense against predators, they have to demonstrate the claimed fitness benefit [PDF].

Evolutionary psychologists, however, seem not to have gotten the memo.

Bering’s post focuses on a series of studies by the evolutionary psychologist Gordon Gallup. Gallup was interested in the question of whether there might be an adaptive explanation for homophobia—which, given the fact that many (although far from all) human cultures treat homosexuality as a taboo—is a fair question for research. He hypothesized that treating homosexuality as taboo helped to prevent homosexual adults from contacting a homophobic parent’s children, which would reduce, however slightly, the prospects of those children growing up to be homosexual, and ensure more grandchildren for the homophobe.

Gallup supported this adaptive hypothesis with … evidence that straight people were uncomfortable about homosexuals coming into contact with children [$a]. Here’s the opening sentence of that paper’s abstract:

In a series of four surveys administered either to college students or adults, reactions toward homosexuals were found to vary as a function of (1) the homosexual’s likelihood of having contact with children and (2) the reproductive status (either real or imagined) of the respondent.

If you’ve noticed that this doesn’t mention evidence of heritability or a fitness benefit to homophobia, that’s not because I left it out—that’s because Gallup’s work contains no data to support either.

What this amounts to is arguing that homophobia is an adaptation favored by natural selection because homophobia is a thing that exists.

Could a complex behavior like homophobia have a genetic basis? Sure. Homosexuality itself is a complex behavior, and it certainly does have some genetic basis. However, the fact that attitudes toward homosexuality have shifted as far and as fast as they have in the last few decades suggests that any genetic effects underlying homophobia are pretty easy to overcome. Behaviors can be inherited culturally, too, since human children learn from their parents. But—note, again, lots of change in the last thirty years or so—cultural inheritance is more fleeting and malleable than biological inheritance.

Careful, Red Riding Hood—that wolf might be gay. Photo by crackdog.

What about Gallup’s proposed fitness benefit for homophobes? Well, that would require homophobia to, you know, actually prevent homosexuality. Gallup’s argument there hangs on two distasteful assertions. First, that gay men are more likely to be pedophiles, and second, that boys sexually abused by gay men are themselves more likely to grow up gay. In spite of Gallup’s assertions otherwise [$a], we have strong evidence from multiple studies that gay men are no more likely to be sexually attracted to children than straight men.

And there is, to my knowledge, no evidence to suggest that abuse can cause homosexuality. Bering cites a recent study that does document an association between childhood abuse and later homosexuality in men. However, the study’s authors point out that, “The reason for the connection between childhood sexual abuse and same-sex partnerships among men is not clear from our findings.”

… gay men tend, on average, to be more gender non-conforming as boys (Bailey & Zucker, 1995). This tendency could increase their appeal or conspicuousness to sexual predators, which might make them more likely to be victims of abuse (B. Mustanski, personal communication, February 11, 2008). Similarly, it is possible that boys who are developing and exploring a same-sex sexual orientation are more likely to enter situations where they are at risk for being sexually abused (Holmes & Slap, 1998). [In-text citations sic]

Why on Earth would Bering dredge up Gallup’s adaptive fairytale a decade and a half after it was published, if it was baseless to begin with and no new evidence supports it? Well, according to Bering, because he’s a hard-nosed scientist who isn’t afraid to consider uncomfortable possibilities.

Sometimes, science can be exceedingly rude—unpalatable, even. The rare batch of data, especially from the psychological sciences, can abruptly expose a society’s hypocrisies and capital delusions, all the ugly little seams in a culturally valued fable. I have always had a special affection for those scientists like Gallup who, in investigating highly charged subject matter, operate without curtseying to the court of public opinion.

Of course, says Bering, Gallup’s work isn’t conclusive, but it sure would be interesting if someone tested it.

Except, when Gallup was forming his hypotheses about the evolutionary benefits of gay-hating—he first proposed the idea in a 1983 article—he was hardly thumbing his nose at public opinion. He was, in fact, giving natural selection’s approval to the prevailing ugly stereotypes about gay men. And, as any competent evolutionary biologist would recognize, he did it without a shred of relevant evidence.

References

Ellstrand, N. (1983). Why are juveniles smaller than their parents? Evolution, 37 (5), 1091-4 DOI: 10.2307/2408423

Gallup GG Jr, & Suarez SD (1983). Homosexuality as a by-product of selection for optimal heterosexual strategies. Perspectives in Biology and Medicine, 26 (2), 315-22 PMID: 6844119

Gallup, G. (1995). Have attitudes toward homosexuals been shaped by natural selection? Ethology and Sociobiology, 16 (1), 53-70 DOI: 10.1016/0162-3095(94)00028-6

Gallup, G. (1996). Attitudes toward homosexuals and evolutionary theory: The role of evidence. Ethology and Sociobiology, 17 (4), 281-284 DOI: 10.1016/0162-3095(96)00042-8

Gould, S., & Lewontin, R. (1979). The Spandrels of San Marco and the Panglossian paradigm: A critique of the adaptationist programme. Proc. Royal Soc. B, 205 (1161), 581-98 DOI: 10.1098/rspb.1979.0086

Wilson, H., & Widom, C. (2010). Does physical abuse, sexual abuse, or neglect in childhood increase the likelihood of same-sex sexual relationships and cohabitation? A prospective 30-year follow-up. Archives of Sexual Behavior, 39 (1), 63-74 DOI: 10.1007/s10508-008-9449-3

Young, K., Brodie, E.D., Jr., & Brodie, E.D., III (2004). How the horned lizard got its horns. Science, 304 (5667) DOI: 10.1126/science.1094790

One snout to rule them all: Does migrating help weevils win the arms race of coevolution?

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ResearchBlogging.orgNatural selection and gene flow have a sort of love-hate relationship. Natural selection acts, on average, to make a population better fit to its environment. Gene flow, the movement of individuals and their genes, can counter the optimizing effect of selection if it introduces less-fit individuals from somewhere a different environment. On the other hand, not all new immigrants are necessarily less fit—sometimes they’re better suited to their new environment than the locals.

This gets more complicated, and more interesting, when the environment in question is another living species. Then, the question is not just how movement of one species changes its response to natural selection, but how movement of the other species changes the nature of that natural selection. That’s the focus of the latest study of a Japanese weevil species and its favorite food plant. The two species are locked in a coevolutionary arms race—but who wins the arms race in any given location depends on the gene flow each species is receiving from elsewhere [$a].

Male and female camelia weevils, caught at an indelicate moment. Evidently he doesn’t find her much longer rostrum intimidating. Photo from Toju et al. (2011), figure 1.

These are camelia weevils, Curculio camelliae. As their name suggests, they like to eat camelias, at least when they’re young. Specifically, weevil larvae eat camelia seeds, which are protected by a thick layer called a pericarp. To deal with camelia pericarps, the weevils have evolved prodigious proboscises, or rostrums, which female weevils use to drill through the pericarp so they can lay their eggs inside. Note that the female in the picture above is the one with the rostrum longer than the rest of her body.

Camelias can reduce their risk of losing seeds to weevil larvae by evolving thicker pericarps; weevils can make sure they’re able to feed their young by evolving longer rostrums. Both species are constrained by costs, though—the cost of producing more pericarp tissue, or carrying around a Pinocchio-grade snout. These costs vary somewhat with climate—camelias grow thinner pericarps in cooler conditions [$a]. This means the arms race won’t proceed equally far in all camelia populations, and introduces the possibility that the way in which weevils and camelias (well, camelia seeds and pollen) move across the landscape may very well determine which species has the upper hand.

A female weevil drills into a camelia fruit. Photo from Toju et al. (2011), figure 1.

The new study sets out to see whether gene flow among populations of the two species determines how far the arms race proceeds in each population. Rather than directly track weevils and camelia seeds, the authors use genetic markers for each species—the more migrants move between two weevil (or camelia) populations, the more similar those two populations’ genetics will be. The populations in question were seven sites on a small island at the south end of the Japanese archipelago, and presumably relatively free from the influence of immigration from the larger islands.

It looks like the movement of weevils, but not camelias, affects how the arms race proceeds. As the genetic difference between weevils at two different sites increased, the difference in how far the arms race had proceeded—that is, how long the local rostrums were, and how thick the local pericarps—increased too. That suggests weevils may be prevented from evolving rostrums of the optimum length for their local camelias by the arrival of less-than-optimal migrants. On the other hand, there was no statistically significant relationship between the genetic similarity of camelia populations and their place in the arms race.

This is where the relationship between selection and gene flow gets complicated, though. Even given the relationship between weevil gene flow and how far the arms race seems to have proceeded, the genetic differences between weevil populations were consistent with very low actual rates of migration. A female weevil arriving in a population of camelias with pericarps too long for her rostrum isn’t going to contribute many offspring to the next generation of weevils at that site. So it’s not impossible that what we’re seeing is selection constricting gene flow rather than gene flow slowing down selection.

Alternatively, weevils from a population with super-long rostrums should be able to lay eggs in any population of camelias they meet. In fact, an analysis that uses the genetic data to estimate rates of immigration and emigration suggests that one of the weevil populations with the longest snouts contributes more migrants to the other sites than it receives from each of them. In arms-race coevolution, size is all that matters—and so the weevils with the longest snouts may be winners no matter where they go.

Reference

Toju, H. (2008). Fine-scale local adaptation of weevil mouthpart length and camellia pericarp thickness: Altitudinal gradient of a putative arms race. Evolution, 62 (5), 1086-102 DOI: 10.1111/j.1558-5646.2008.00341.x

Toju, H., Ueno, S., Taniguchi, F., & Sota, T. (2011). Metapopulation structure of a seed-predator weevil and its host plant in arms race coevolution. Evolution DOI: 10.1111/j.1558-5646.2011.01243.x