Making themselves at home: Spider mites disable plant defenses, then spin their own

Tomatoes, one of many plants that play unwilling host to red spider mites. Photo by sylvar.

ResearchBlogging.orgPlant-eating insects must overcome some of the cleverest weaponry in the living world—from poisonous latex to sticky hairs—just to find a meal or a place to lay eggs. Many deal with their host plants’ toxic defenses by digesting them or sequestering them safely for personal use, but the red spider mite Tetranychus evansi simply turns them off.

Tetranychus evansi eats a wide range of plants, from tomatoes to potatoes. One female mite can eat enough to lay 50%-70% of her weight in eggs every day, and while that isn’t much on the scale of a single, miniscule red mite, it adds up quickly when colonies build into dense clusters on host plants, sucking them dry and covering them in webs of spun silk.

Most host plants respond to such an onslaught by ramping up production of chemicals that make them unpalatable to herbivores, or that interfere with the mites’ ability to digest plant tissue. However, a team of Dutch and Brazilian biologists recently found that T. evansi somehow short-circuits this response [$a].

The team, whose senior author is the Dutch biologist Arne Jannsen, discovered that mites raised on leaf tissue from tomato plants previously attacked by T. evansi survived longer and laid more eggs than mites raised on tissue from plants that had never been attacked. Analsyis of RNA from tomato leaves attacked by the mites revealed that they were producing fewer of the signalling proteins associated with responding to insect damage than leaves damaged by another, related mite species—and one protein was produced at lower rates than in undamaged leaves!

Mites, up close. Photo via AgroLink.

In other words, the mites were not just preventing the host plant from boosting its defences in response to a mite attack—they were suppressing the defenses below what they would be without an immediate threat. Like a burglar cutting the power to a home security system, T. evansi can somehow prompt a hostile host to become more hospitable.

This raises another problem, however. With its defenses down, the host plant is also more hospitable to other insect herbivores, which could reduce the plant’s value to T. evansi, or even activate the alarms the mites have managed to suppress. A second study by the same team suggests that this may be part of the function of the webs T. evansi spins as it consumes its host.

In this second round of experiments, the group returned to the closely related mite Tetranychus urticae, which was used to stimulate plant defenses in the first study. Earlier work had found that some strains of T. urticae can tolerate or suppress host plant defenses [$a], though not nearly as effectively as T. evansi. That earlier work found that non-suppressing mite strains could benefit from living on the same plant as a suppressing strain, and the new study first demonstrated that this effect is even stronger when T. urticae shares a plant with T. evansi.

A whole lot of (presumably happy) mites. Photo via AgroLink.

In contrast, T. evansi colonies fared worse in the presence of the non-suppressing mites, whether fed leaves that had already been attacked by T. urticae, or placed on a mite-free leaf of a plant with another leaf infested by the non-suppressing species. All else being equal, T. urticae benefits from the defense-suppressing activity of T. evansi, but reduces the value of the host plant to T. evansi.

Faced with this freeloading competitor, T. evansi apparently replaces the disabled plant defenses with webbing. The team found that even though T. urticae thrived when given evansi-chewed tomato leaves, the non-suppressing mites had difficulty colonizing leaves covered in T. evansi webs. Moreover, T. evansi introduced onto a plant with the non-suppressing mites spun more webbing than when introduced onto a mite-free plant; but they didn’t ramp up web-spinning when sharing a plant with another colony of their own species, suggesting that the mites can respond to competition by building up their defenses.

So not only does T. evansi possess the means to turn off its hosts’ biological security system, it erects its own defenses to protect the plant from one competitor that might try to take advantage of the situation. How, exactly, the mites interfere with plants’ defensive responses will be an interesting future line of study. I’d also be very interested to see whether other herbivorous insects—things larger than other mites, and not so easily put off by some silk security fencing—also preferentially attack plants disabled by T. evansi. ◼


Kant, M., Sabelis, M., Haring, M., & Schuurink, R. (2008). Intraspecific variation in a generalist herbivore accounts for differential induction and impact of host plant defences Proc. Royal Soc. B, 275 (1633), 443-52 DOI: 10.1098/rspb.2007.1277

Sarmento, R., Lemos, F., Dias, C., Kikuchi, W., Rodrigues, J., Pallini, A., Sabelis, M., & Janssen, A. (2011). A herbivorous mite down-regulates plant defence and produces web to exclude competitors. PLoS ONE, 6 (8) DOI: 10.1371/journal.pone.0023757

Sarmento, R., Lemos, F., Bleeker, P., Schuurink, R., Pallini, A., Oliveira, M., Lima, E., Kant, M., Sabelis, M., & Janssen, A. (2011). A herbivore that manipulates plant defence. Ecology Letters, 14 (3), 229-36 DOI: 10.1111/j.1461-0248.2010.01575.x


Flowers stay open for pollinators, not daylight

A honeybee explores the depths of a dandelion, one of the species used in Fründ et al.‘s experiments. Photo by je-sa.

ResearchBlogging.orgIf you’ve ever stopped to admire morning glory flowers opening first thing in the morning, then noticed they’ve closed by evening, you’re at least dimly aware of one of the longest-established ideas in plant biology: that flowers open and close on a reliable daily schedule. Different species are open at different times of day, of course, but each flowering plant has its preferred open period, and it sticks to that schedule during its flowering season.

This idea led Carolus Linneaus, the father of modern biological taxonomy, to propose an Horologium florae, or “floral clock” using plantings of species with known flowering times to mark the hours. You can find his table of proposed species in the online version of Linneaus’ 1783 treatise Philosophia Botanica, if you’re not averse to Latin. Studies of flowers’ daily schedules go back to well before English was the language of international science, and continue to the present day [$a].

Yet no one seems to have spent much time considering how flowers’ schedules might respond to the activity of their very reason for being: pollinators. Flowers don’t open just to be open in a particular kind of sunlight—they’re open to attract animals that can carry pollen to another plant, and maybe leave some, too. If a flower receives enough pollen to make seeds by noon, why would it stay open until two o’clock?

According to some new experimental results, the answer to that question is that they don’t [$a].

Jochen Fründ, Carsten F. Dormann, and Teja Tscharntke set out to see whether a selection of European wildflowers adjusted their opening schedules in response to pollination, with two major experiments and a broader-scale observation project. The experiments address whether pollinator activity could change flowers’ schedules; the observations help determine how important those changes might be in studies of plant-pollinator interaction.

A floral clock in Geneva—not quite what Linneaus had in mind. Photo by aranmanoth.

In the first experiment, the team planted wildflowers—Crespis capillaris, a close relative of common dandelions—in experimental plots spaced across a field. Plots were either caged or left open to insect visitors, and Fründ et al introduced bees into some of the caged plots. So some plots had a controlled set of pollinators, some had none at all, and some had whatever pollinators were already active in the field.

The team then watched the flowers’ daily opening and closing in the experimental plots. (They had a lot of help—a long list of names in the paper’s Acknowledgements section ends with “and many others.”) Over the same period of time, flowers in the un-caged plots received more insect visitors than flowers in either other treatment, and had mostly closed by midafternoon; flowers in the caged plots with bees introduced received fewer visitors and closed hours later; and flowers in the plots with no pollinators at all stayed open till evening.

So flowers experiencing the same daylight pattern closed earlier if they received more pollinator visits. The team followed up this result by hand-pollinating flowers of C. capillaris and a handful of closely related species growing in the same field, including dandelions—and flowers of three out of four species closed more rapidly when hand pollinated. Dandelions didn’t respond to hand pollination, a result the authors explain by noting that dandelions often self-pollinate, and so don’t need to wait for animal pollinators.

Finally, the team compiled observations of plant-pollinator interactions from sites similar to their study field located across Germany, and divided them into observations taken before solar noon, when the focal flower species from the experiments above tend to be open, and after solar noon. Which pollinator species visited which flowering plants depended significantly on when the observations were made—to the extent that the apparent importance of C. capillaris and its relatives is entirely different before and after noon.

Of course, these results apply directly to only a handful of species representing a particular group of flowering plants—but it’s a group with a lot of widespread and abundant members, and the result is straightforward and striking. Animal-pollinated plants may not behave much like clocks at all. Instead, they’re more like the patrons of a singles bar: they show up at about the same time and hang around until they find someone to buy them a drink. That’s a dynamic worth keeping in mind for studies of plant-pollinator interaction, since it suggests that the partners a pollinator chooses will depend, at least in part, on whether or not it’s out after closing time. ◼


Ewusie, J., & Quaye, E. (1977). Diurnal periodicity in some common flowers. New Phytologist, 78 (2), 479-485 DOI: 10.1111/j.1469-8137.1977.tb04854.x

Fründ, J., Dormann, C., & Tscharntke, T. (2011). Linné’s floral clock is slow without pollinators – flower closure and plant-pollinator interaction webs. Ecology Letters DOI: 10.1111/j.1461-0248.2011.01654.x

von Hase, A., Cowling, R., & Ellis, A. (2005). Petal movement in cape wildflowers protects pollen from exposure to moisture Plant Ecology, 184 (1), 75-87 DOI: 10.1007/s11258-005-9053-8


Science online, urban evolution edition

Freddie Fungus and Alice Algae have no likin’ for prions. Photo by 0olong.
  • Genetically determined, except when it isn’t. The evolutionary context of misogyny.
  • Queering evolution? The new frontier for evolutionary biology may be tracking adaptation to human-built environments.
  • Mad lichen disease? Some lichens can apparently break down prions.
  • Really, where would it have gone? That big underwater plume of oil spilled into the Gulf of Mexico is still there.
  • No surprise to field scientists, I suspect. Commercial GPS systems have some downright dangerous issues with their databases for rural and wilderness areas.
  • “This was the original peer review: immediate and open” The increasing use of online platforms for post-publication peer review may be taking scientific discourse back to its Enlightenment-era roots.
  • Guess I’d better get some more gel packs. Carbohydrate supplements during exercise do, in fact, help you work longer
  • I’m sure that if/ I took even one sniff/ It would bore me terrifically, too … Pair-bonding with a mate seems to make voles less prone to amphetamine addiction.
  • Time to revise the bat “pollination syndrome.” A bat-pollinated tropical vine has leaves that collect and reflect its pollinators’ echolocation signals.

Of mice and men, making a living in rarefied air


High-elevation populations of deer mice have evolved “stickier” hemoglobin to cope with the thin atmosphere. (Animal Diversity Web)

ResearchBlogging.orgIt’s easy to walk through the woods and fields of North America and never spot Peromyscus maniculatus, the deer mouse, but you’ve probably heard them scampering off through the leaf litter or under cover of tall grass. They’re exceptionally widespread little rodents, found in forest undergrowth and fields from central Mexico all the way north to the Arctic treeline. In all this range, they look about the same: small and brown, with white underparts and big, sensitive ears.

That apparent sameness is deceptive, however.

A big, varied range presents lots of different environmental conditions to which a widespread species must adapt. And when that big, varied range includes the Rocky Mountains, one of those environmental conditions is as basic as the air itself. At high altitudes, atmospheric pressure is lower, which means lower partial pressure of oxygen, the gas that makes life as we know it work.

The fundamental problem at high altitude is to pull more oxygen from thinner air. Natural selection is good at solving problems, and it has multiple options for adapting a mammal to thinner air at high altitudes, to the extent that these traits are heritable. Selection could favor individuals who more readily respond to thin air by breathing faster and deeper, pulling in more air to make up for its lower oxygen content. Or selection could favor individuals who produce more red blood cells, so that a given volume of blood pumped through their lungs picks up more oxygen. Or, at the most basic level, selection could favor individuals whose individual red blood cells are better at picking up oxygen, via a new form of hemoglobin, the oxygen-binding molecule that packs every red blood cell.

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Choosing your partner is only as helpful as the partners you have to choose from

Picking teammates. Original photo by humbert15.

ResearchBlogging.orgWhen you need partners for some sort of cooperative activity—say, teammates for a game of kickball—you’d probably like to have a choice among several candidates. That lets you weigh considerations about kicking strength and running speed—and who promised to give you his dessert at lunch period—to build a winning team. However, if the other team captain snaps up the good players first, the fact that you have a choice among the others might not make much difference.

Plants and animals looking for mutualists face a similar situation. Being able to choose among possible partners should allow the chooser to work with helpful partners and avoid unhelpful ones, but a new study suggests that in one widespread mutualism the process of choosing between partners can leave the chooser worse off than if it had no choice at all [$a].

Coauthors Erol Akçay and Ellen Simms focus on the effects of partner choice in the mutualism between plants and nitrogen-fixing bacteria—the interaction I’m studying in my current postdoc position, as it happens. All living things need nitrogen, but only some strains of bacteria are able to collect nitrogen from the atmosphere and “fix” it into a form that other organisms can use. Many plants, particularly members of the big and diverse bean family, have evolved to allow nitrogen-fixing bacteria to infect their roots—the plants form a nodule of root tissue around the infection and supply the tissue with sugar for the bacteria to feed on as they fix nitrogen. Eventually the nodule dries up and dies off, and the bacteria are freed into the soil, having multiplied many times over thanks to the food supply from the host plant.

A plant’s root nodules, some cut open to show the interior. Photo by pennstatelive.

To see how this choice might work in practice, Akçay and Simms construct a mathematical model of a plant with two nodules. Each nodule produces some level of nitrogen, and recieves some level of sugar from the plant. The plant negotiates with the two nodules in what’s called a “war of attrition” game: whichever partner wants a better deal cuts off the exchange of services, and holds out until the cost of losing the service it recieves is greater than the benefit it hopes to gain in the war of attrition.

Rather like ant-defended plants, plants that host nitrogen-fixing bacteria don’t seem to screen potential mutualistic bacteria before allowing them to infect their roots. However, after root nodules are established, the success of the mutualism from the perspective of both partners depends on the genetics of each [PDF], and when host plants receive supplemental nitrogen, they put fewer resources into growing nodules [PDF]. Host plants have been observed with different strains of bacteria in different nodules, and some nodules could contain diligent nitrogen fixers while others are full of freeloaders. This may be the point at which the plant has a choice of partners—it can potentially direct sugar to helpful nodules, and cut off unhelpful ones.

Because the plant has two nodules to choose from, it can potentially outlast an uncooperative nodule by relying on the other one. This works if the plant can shunt more resources to the cooperative nodule and recieve more nitrogen from it in return. However, the success of this strategy depends on two traits of the bacteria inhabiting the nodules—how readily they ramp up nitrogen production in response to more sugar, and how stubborn they are in the war of attrition game.

If both nodules are stubborn but responsive to extra sugar, the plant can negotiate with one nodule by giving the other more sugar and receiving extra nitrogen. This lets the plant hold out longer in the war of attrition. On the other hand, nodules that are not responsive to extra sugar but also not very stubborn yield quickly in the war of attrition even though they don’t help much in negotiations. In either of these two cases, the negotiations find an equilibrium in which the plant receives a benefit about intermediate between what it would recieve if both nodules were infected by the same strain of bacteria.

However, if the plant hosts a stubborn-responsive bacterial strain in one nodule and a yielding-unresponsive strain in the other, it finds itself in a trap: the yielding-unresponsive strain is no help in negotiation against the stubborn-responsive strain, and the help provided by the stubborn-responsive strain isn’t an advantage in negotiating with the yielding-unresponsive strain. Over successive negotiations, the stubborn-responsive strain can ratchet up the sugar it extracts from the plant, and the plant ends up worse off than it would be if the two nodules were identical.

Just like humans haggling in a marketplace, the outcome of the interaction depends strongly on whether the other party plays along as expected.

Akçay and Simms find a way out of this trap by adding another wrinkle to the model. Much like the contract-theory models of mutualism I’ve discussed before, they modify the model to allow cooperative nodules to benefit from being cooperative. This makes a good deal of intuitive sense—if a nodule provides a better deal to the plant, the plant can potentially grow more leaves to produce more sugar, which would allow it to offer a better deal to the bacteria it hosts. Akçay and Simms call this “partner fidelity feedback,” and they find that, if it is sufficiently strong, it can allow the plant to out-negotiate a stubborn strain of bacteria.

Although it has a good deal of intuitive appeal, the model presented by Akçay and Simms does a fair bit of speculating in the absence of data. This is also a problem for the contract-theory model, and really all models of this widespread and important interaction. We know a great deal about the chemical details of plants’ interaction with nitrogen fixing bacteria. However, we don’t have a good sense of whether and how plants can redirect resources among nodules to haggle with the bacteria they host, and we don’t know whether and how bacteria could adjust their behavior to haggle with the plant. Akçay and Simms devote a big section of their online appendix [$a] to discussing just this point.

To figure out what’s going on inside those nodules, we need to determine how different models of interaction between plants and their bacterial mutualists may shape patterns in things that are easier to observe—both in the compatibility between plant genotypes and bacterial strains in greenhouse tests, and in the broader population genetics of both partners.


Akçay, E., & Simms, E. (2011). Negotiation, sanctions, and context dependency in the legume-rhizobium mutualism. The American Naturalist, 178 (1), 1-14 DOI: 10.1086/659997

Heath, K. (2010). Intergenomic epistasis and coevolutionary constraint in plants and rhizobia. Evolution DOI: 10.1111/j.1558-5646.2009.00913.x

Heath, K.D., Stock, A.J., & Stinchcombe, J.R. (2010). Mutualism variation in the nodulation response to nitrate Journal of Evolutionary Biology, 23 (11), 2494-2500 DOI: 10.1111/j.1420-9101.2010.02092.x


Snake-eating opossums have evolved venom-resistant blood

The humble Virginia opossum can shrug off snakebites that would kill larger mammals. Photo by TexasEagle.

ResearchBlogging.orgIf you were going to pick the traits of a single animal to confer on a superhero, you probably wouldn’t pick the Virginia opossum. Possums are ubiquitous, scruffy, ratlike marsupials, their toothy grins giving the not entirely inaccurate impression that they don’t have much going on upstairs. Until recently, the nicest thing I could think to say about them is that they eat a lot of ticks.

Blood-sucking Lyme disease vectors are only a small part of the opossum’s eclectic diet, however. They also eat quite a few poisonous snakes, and this has apparently led them to evolve a trait I could call a superpower without exaggeration: opossum blood is resistant to snake venom.

This curious and useful ability was first documented by J.A. Kilmon in a 1976 paper [$a], in which Kilmon reported field observations and laboratory trials showing that opossums tolerate snakebites without visible ill effect. (If animal experimentation makes you queasy, you might want to go read something else about now. Perhaps a nice post about gerbils?)

A natural bite was observed in the field by a 160 cm eastern diamondback on an adult opossum, Didelphis virginiana. The opossum displayed no apparent distress and this suggested a remarkable tolerance by that animal to envenomation. In order to ascertain if an actual envenomation did take place, Mr. Seashole conducted field experiments by manually causing snakes to inflict actual bites on captured opossums. None of the bites caused visible signs of distress to the opossums.

Kilmon brought possums back to the lab, anesthetized them, hooked them up to heart monitors, and “inflicted” bites on them from diamondback and timber rattlesnakes, water moccasins, and at least one cobra. (Kilmon reports he used 15 snakes in total, but doesn’t break that number down by species.) “None of the five opossums,” he wrote, “developed observable local reactions other than trauma attributable to fang penetration and none developed observable systemic effect, exhibiting negligible alteration of heart rate and respiration.”

A timber rattlesnake—no big deal to an opossum. Photo by Tom Sprinker.

Finally Kilmon injected an anesthetized opossum with enough water moccasin venom to kill five fifteen-kilogram dogs, and observed no reaction beyond a brief drop in blood pressure and small spike in pulse rate—when the possum awoke, it was “apparently healthy.” Upon sacrificing and dissecting the animal, Kilmon found no evidence of organ damage.

Kilmon concludes his brief scientific report with a weird aside about the evolutionary history of opossums, which, had he been writing in 2011, would have made me think his research consisted mainly of skimming the Wikipedia entry for Didelphis virginiana. In the course of reporting the opossum’s taxonomic affiliations and known diet, Kilmon notes offhandedly,

This polyprotodont marsupial is a primitive but also very successful mammal. The opossums of varying species are the only marsupials surviving in the placental world, the predominant marsupial and monotreme mammals of Australia having probably survived due to their isolation. The opossum has remained unchanged for millions of years and probably reached his peak of evolutionary specialization several millions of years ago.

I don’t think he could’ve gotten away with that last sentence in an evolutionary biology journal. It’s true that the common ancestor of opossums and placental mammals (i.e., us) diverged quite a long time ago, that opossum-like critters are known from the fossil record going back that far, and that many opossum traits are thought to be shared with early mammals. But that doesn’t mean opossums “remained unchanged for millions of years.” The lineage leading to modern opossums has been evolving exactly as long as the lineage leading to modern humans—and if the opossum’s lifestyle hasn’t led it to such evolutionary heights as the wheel, war, New York and so forth, then it also hasn’t left the opossum unchanged.

As it happens, a pretty good illustration of this point is the paper that led me to Kilmon’s morbid little study in the first place. Mammalogists Sharon Jansa and Robert Voss have just published a study of one blood protein that may underlie opossums’ resistance to venom. The venom of pit vipers like rattlesnakes and water moccasins targets the blood clotting system—one of the unpleasant effects of a snake bite is internal hemorrhage. So Jansa and Voss examined the evolution of a venom-targeted clotting protein called von Willebrand Factor, or vWF, comparing it across the entire family of opossums, the didelphidae.

Photo by Maggie Osterberg.

Since the evolutionary origin of the family, the vWF of opossum species that prey on snakes has accumulated more changes than vWF in non-snake-eating species. That’s circumstantial evidence for the effect of natural selection continuously acting on vWF over millions of years. Jansa and Voss picked out several specific changes that are unique to snake-eating opossums, and found that they’re associated with a region of vWF that is known to bind with one of the toxins in pit viper venom.

The authors suggest that opossums may have been engaged in a evolutionary “arms race” against snake venom toxins since they first developed a taste for rattlesnake. In other words, not only is the opossum not unchanged since the early history of mammals, one of the traits that has changed continuously since then may be the very feature that piqued Kilmon’s interest.


Jansa, S., & Voss, R. (2011). Adaptive evolution of the venom-targeted vWF protein in opossums that eat pitvipers. PLoS ONE, 6 (6) DOI: 10.1371/journal.pone.0020997

Kilmon, J., Sr. (1976). High tolerance to snake venom by the Virginia opossum, Didelphis virginiana. Toxicon, 14 (4), 337-40 DOI: 10.1016/0041-0101(76)90032-5


The intelligent homosexual’s guide to natural selection and evolution, with a key to many complicating factors

San Francisco Pride, 2008. Photo by ingridtaylar.

This is a cross-posting of my latest contribution to the Scientific American guest blog. Since the original went up at SciAm, P.Z. Myers has pointed out a few more complicating factors. If you read one paper to follow up on what I’ve written here, I’d suggest Nathan Bailey and Marlene Zuk’s excellent 2009 review [PDF], which is posted in PDF format by none other than The Stranger.

ResearchBlogging.orgJune is Pride Month in the United States, and in communities across the country, lesbian, gay, bisexual, and transgendered Americans are celebrating with carnivals, parades, and marches. Pride is a rebuke to the shame and marginalization many LGBT people face growing up, and a celebration of the freedoms we’ve won since the days when our sexual orientations were considered psychological diseases and grounds for harrassment and arrest. It’s also a chance to acknowledge how far we still have to go, and to organize our efforts for a better future.

And, of course, it’s a great big party.

I’m looking forward to celebrating Pride for the first time in my new hometown of Minneapolis this weekend–but as an evolutionary biologist, I suspect I have a perspective on the life and history of sexual minorities that many of my fellow partiers don’t. In spite of the progress that LGBT folks have made, and seem likely to continue to make, towards legal equality, there’s a popular perception that we can never really achieve biological equality. This is because same-sex sexual activity is inherently not reproductive sex. To put it baldly, as the idea is usually expressed, natural selection should be against men who want to have sex with other men–because we aren’t interested in the kind of sex that makes babies. An oft-cited estimate from 1981 is that gay men have about 80 percent fewer children than straight men.

Focusing on the selective benefit or detriment associated with particular human traits and behaviors gets my scientific dander up, because it’s so easy for the discussion to slip from what is “selectively beneficial” to what is “right.” A superficial understanding of what natural selection favors or doesn’t favor is a horrible standard for making moral judgements. A man could leave behind a lot of children by being a thief, a rapist, and a murderer–but only a sociopath would consider that such behavior was justified by high reproductive fitness.

And yet, as an evolutionary biologist, I have to admit that my sexual orientation is a puzzle.

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Freeloading caterpillars get in the way of plant-ant mutualism

Cecropia obtusifolia provides food for ants that come and protect it—unless caterpillars get there first. Photo by wallygroom.

ResearchBlogging.orgImagine you need a team of security guards. To find them, you decide not to place an ad in the local paper or on Craigslist. Instead, you build an apartment complex next to your home, complete with a full-service cafeteria providing free hot meals 24 hours a day. You leave the front doors unlocked, then hope that anyone who shows up to live in the apartments will also keep an eye on your home.

If you took that strategy to protect your assets, you’d have to be crazy. But that’s pretty much what ant-protected plants do all the time. They grow hollow structures called domatia, secrete nectar from special structures, and even produce tasty and nutritious “food bodies.” Then they wait for ants to move into the domatia, eat the nectar and the food bodies, and hopefully chase away anything that might want to do the plant harm. The crazy thing is, it works.

Well, it mostly works.

One gap in the ant-protection mutualism is the period when an ant-protected plant hasn’t grown big enough to support a whole colony of ants. In this early stage, ants won’t colonize the plant, but other insects might be quite happy to take the rewards that are already being offered. That’s exactly what larvae of the butterfly Pseudocabima guianalis do—they make themselves at home on unprotected ant-plants.

The ant-plant Pseudocabima caterpillars target is Cecropia obtusifolia, a shrubby Central American tree that relies on ants in the genus Azteca for protection. Azteca ants make vicious and well-coordinated bodyguards. Here’s video Ed Yong posted last year, showing a bunch of the ants flushing a hapless moth into an ambush.

However, Cecropia saplings can’t produce enough food to support a colony of ants until the plants grow to more than a meter tall. What’s too little for thousands of ants is a feast for a Pseudocabima caterpillar, however. Each caterpillar builds a silk shelter around a region of the plant that grows food bodies, and settles in to eat. As it grow larger, the caterpillar moves into a domatium near its original shelter, covering the entrance hole with silk. Finally the caterpillar pupates inside the domatium, emerging as an adult to lay eggs on another unprotected Cecropia plant.

Eventually the Cecropia saplings grow large enough to attract ants, who run off the caterpillars. However, as the paper I linked to above describes, the caterpillars seem to be able to resist an ant colony’s establishment on the plant—the silk shelters prevent ants from getting to the best sources of food. Cecropia saplings occupied by caterpillars didn’t seem to suffer more herbivore damage than ant-protected plants, but they did grow more slowly over the course of several years’ observations. Caterpillar-infested Cecropia plants were also more vulnerable to infection by a fungus, which the ants removed quite effectively.

Interestingly, though, caterpillar-infested plants also produced less food than those guarded by ants. This is a point of circumstantial evidence for a new model of mutualism I wrote about earlier this year, in which cheating is reduced or prevented when a host like Cecropia better mutualists help create better rewards. An ant-protected plant can divert more resources to feeding its tenants, so their work rewards itself. However, Pseudocabima caterpillars are glad to take the lower level of rewards that Cecropia plants offer up to all comers.

In other words, if you’re going to give out free lunches, you can’t really expect everyone who eats to pay you back.


Roux, O., Céréghino, R., Solano, P.J., & Dejean, A. (2011). Caterpillars and fungal pathogens: Two co-occurring parasites of an ant-plant mutualism. PLoS ONE, 6 : 10.1371/journal.pone.0020538


Passive aggression: Parasitic wasp larvae interfere with each other via their host’s host plant

A large white butterfly caterpillar weaves a cocoon around the wasp larvae infesting its body. Photo by EntomoAgricola.

ResearchBlogging.orgI’m embarrassed to admit that I’ve only just gotten around to picking up Carl Zimmer’s book Parasite Rex. It’s turned out to be a wonderful compendium of all the peculiar ways parasites evade, confound, and resist the defenses of their hosts. Some of the wildest cases Zimmer examines, though, are parasites that manipulate their hosts’ behavior.

One grotesque and well-studied example is the wasp Cotesia glomerata. Female C. glomerata wasps inject their eggs into butterfly caterpillars, and when the eggs hatch, the wasp larvae eat the caterpillar from the inside, saving critical organs so the poor thing stays alive the whole time. Then, when the wasp larvae are ready to burrow out of the caterpillar and form pupae to complete their devlopment, they induce the half-dead caterpillar to spin a web around them and stand guard against predators. (In technical language, this life history makes the wasp a parasitoid, rather than a parasite.) Christie Wilcox has written up a fuller description of the whole grisly process, if you want more detail.

That sounds like a pretty incredible set of manipulations for one clutch of wormy-looking wasp larvae, but they’re not all that Cotesia glomerata can do. New evidence published in Ecology Letters suggests that C. glomerata can somehow make the plants that its host caterpillar feeds on less hospitable [$a] to the larvae of another caterpillar-infesting wasp. In other words, the wasp larvae may manipulate not just their host, but their host’s host.

First off, here’s video of Cotesia glomerata in action. Don’t watch this on your lunch break.

Now, the wasp’s plant manipulations. Lots of plants have what are called induced defenses against herbivores like the butterfly larvae that host C. glomerata larvae. Induced defenses are usually protective toxins that plants produce in response to herbivore damage [PDF]. Erik Poelman and his collaborators reasoned that, since C. glomerata can manipulate it’s host’s behavior, the parasites might change how plants respond to herbivory by infested caterpillars.

To test this, the team first had to induce plant responses. They grew Brassica oleracea—Brussels sprouts—plants in the greenhouse, then infested them with either un-parasitized caterpillars of the cabbage white butterfly Pieris rapae, cabbage white caterpillars infected with Cotesia glomerata, or cabbage white caterpillars infected with larvae of the related wasp C. rubecula. Once the caterpillars had nibbled on the plants enough to induce defensive responses, Poelman et al. removed the caterpillars in preparation for the experiment proper.

The team then introduced parasitoid-free caterpillars and caterpillars infested with one or the other parasitoid species onto host plants that had been through one of the three induction treatments, or that had never been exposed to herbivores. They then tracked the development of the caterpillars, and whether or not the wasp larvae inside them survived.

A healthy cabbage white butterfly caterpillar feeds on a piece of broccoli stem. Photo by Sam Fraser-Smith.

Larvae of C. rubecula fared more-or-less equally well no matter what kind of plant their host caterpillar fed on. But C. glomerata larvae had substantially higher mortality when their hosts fed on plants induced by caterpillars infested with the competitor species. While about 50 percent of C. glomerata larvae died if their hosts fed on plants induced by uninfested caterpillars or caterpillars infested with C. glomerata, almost 75 percent of C. glomerata larvae died when their hosts fed on plants that had previously been occupied by caterpillars infested with C. rubecula.

This impact isn’t because the host caterpillars fared poorly—in fact, caterpillars developed a little faster on plants induced by rubecula-infested caterpillars. So somehow, Cotesia rubecula seems to have influenced its hosts in a way that makes their host plants less hospitable to C. glomerata.

Poelman et al. are scrupulous to point out that this effect might not be anywhere nearly as strong in nature—host plants and host caterpillars might be plentiful enough that Cotesia glomerata can simply avoid the competitor species. On top of that, any natural selection that C. rubecula could be exerting on C. glomerata via induced responses in their shared hosts’ host plants is occurring at multiple removes. The effect Poelman et al. documented is probably not an adaptation for competition with C. glomerata so much as a side effect of C. rubecula‘s effect on its host.

So although this result shows that one parasitoid wasp can reach out and influence another through three other organisms—its own host, that host’s host plant, and the other wasp’s host—it’s not clear how strong that impact has been over the evolutionary history of these two Cotesia species. That said, this is a pretty nifty proof-of-concept.


Agrawal, A., Conner, J., Johnson, M., & Wallsgrove, R. (2002). Ecological genetics of an induced plant defense against herbivores: Additive genetic variance and costs of phenotypic plasticity. Evolution, 56 (11), 2206-2213 DOI: 10.1111/j.0014-3820.2002.tb00145.x

Poelman, E., Gols, R., Snoeren, T., Muru, D., Smid, H., & Dicke, M. (2011). Indirect plant-mediated interactions among parasitoid larvae. Ecology Letters DOI: 10.1111/j.1461-0248.2011.01629.x


Pesticides and parasites add up to an evolutionary Catch-22

When Daphnia evolve resistance to pesticides, they become more vulnerable to bacterial parasites. Photo by Chantal Wagner.

ResearchBlogging.orgIf you haven’t read Joseph Heller’s classic Catch-22, cancel your plans for next weekend and spend the time with a copy from the nearest library. It’s a hilarious, bracingly bleak satire of military bureaucracy, as epitomized in the titular clause governing when bomber pilots can be grounded for reason of insanity:

There was only one catch and that was Catch-22, which specified that a concern for one’s safety in the face of dangers that were real and immediate was the process of a rational mind. Orr was crazy and could be grounded. All he had to do was ask; and as soon as he did, he would no longer be crazy and would have to fly more missions.

Heller conceived Catch-22 as a product of malicious middle management, but a similar situation crops up in the natural world when living things are under natural selection from conditions that favor contradictory traits. Biologists most commonly call these tradeoffs.

Over the course of evolution, tradeoffs set up “choices” that natural selection must make—a population can adapt to one alternative set of conditions, or another, or settle on a middle ground. A trivial example is that elephants have long ago “chosen” not to fly (Dumbo notwithstanding) in the course of evolving large, un-aerodynamic bodies suitable for massive-scale herbivory. A more relevant example is a new finding that the evolution of pesticide resistance creates vulnerability to parasites [$a].

The US Environmental Protection Agency estimated [PDF] that in 2006 and 2007 (the latest years for which reports are online) we used upwards of five billion pounds of pesticides to kill unwanted plants, insects, fungi, and other organisms worldwide. Once they’re sprayed, we don’t have much control over where pesticides end up—rain runoff takes them into lakes, ponds, and the ocean. In those bodies of water, critters at the base of the food chain are the first to feel the effects—critters like the tiny, translucent crustacean Daphnia magna.

Of course, those critters may be able to evolve resistance to the pesticides contaminating their environment—but that resistance may come at a cost.

Pesticide application, via the most picturesque method available. Photo by Scott Butner.

Anja Coors and Luc De Meester had already found a hint of this cost [$a] in an experiment using a single clonal line of Daphnia, in which Daphnia exposed to both sublethal concentrations of the widely-used insecticide carbaryl and a parasitic bacterium fared much worse than Daphnia exposed to only carbaryl or bacteria.

In the new study, Coors, De Meester, and three collaborators expand on that initial observation by determining whether Daphnia become more vulnerable to parasites as they evolve resistance to carbaryl, and whether this costly evolution could occur in natural populations. The coauthors took samples of Daphnia from natural populations in four separate lakes and exposed them to carbaryl over several generations—then sampled the resultant evolved populations and tested their vulnerability to the bacterium. Compared to Daphnia left unexposed to carbaryl, the evolved populations were more resistant to the pesticide—and were also more badly hurt by bacterial infection.

It’s hard to say how general this particular result is to the many, many other species that, like Daphnia, must cope with pesticides and other pollutants humans have introduced into the environment. Evolution to resist one pesticide leads to lowered resistance to infection in one aquatic crustacean; in other species, facing different chemicals, maybe such costs are different or lesser or nonexistent. But living things are not infinitely pliable as they evolve in response to the many and rapid changes we’re making in the world. To slow the extinction crisis going on around us, we need to avoid trapping other living things in Catch-22.


Coors, A., & De Meester, L. (2008). Synergistic, antagonistic and additive effects of multiple stressors: predation threat, parasitism and pesticide exposure in Daphnia magna.Journal of Applied Ecology, 45 (6), 1820-8 DOI: 10.1111/j.1365-2664.2008.01566.x

Jansen, M., Stoks, R., Coors, A., van Doorslaer, W., & de Meester, L. (2011). Collateral damage: Rapid exposure-induced evolution of pesticide resistance leads to increased susceptibility to parasites. Evolution DOI: 10.1111/j.1558-5646.2011.01331.x