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Bats Jam Each Other’s Sonar

A bat is hunting a moth. As it flies, it makes a series of high-pitched squeaks and listens for echoes rebounding off the insect. It gets closer, and now it makes a much faster series of calls—the feeding buzz—that help it to pinpoint exactly where the moth is. It swoops in for the kill… and fumbles. At the last moment, another set of sounds comes out of nowhere, confusing it and sending it off course.

It has just been jammed by another bat.

Bats live in a world of acoustic warfare. Their sonar, or echolocation, allows them to hunt in total darkness, but it also makes them vulnerable. In 2009, Aaron Corcoran and William Conner from Wake Forest University showed that tiger moths can unleash their own ultrasonic clicks to jam the sonar of approaching bats. The clicks overlap with the echoes of the bats’ own calls, muddying up their ability to gauge their distance from their prey. They know roughly where the moths are, but they can’t coordinate a precise strike. This defence is so effective that even if the moths are tethered to a stump, the bats still miss them on four out of five fly-bys.

Clicking moths aren’t a bat’s only problem. Many of them must contend with the sounds of their neighbours too. The Mexican free-tailed bat roosts in groups of up to 1.5 million individuals, and forms such big swarms that they sometimes show up on radar. This supremely social species uses at least 15 different calls to coordinate with its neighbours and defend its own patch of food. But Corcoran and Conner have discovered a new type of call, with a more antagonistic bent.

It’s called the sinFM. The bats rapidly raise and lower the pitch of their call more than a dozen times over, in bursts or “syllables” that last just a tenth of a second. The bats only ever did this when one of their peers was using its feeding buzz, and was about to snag an insect. And when these hunting bats heard the sinFM, they usually flubbed their strikes, missing their targets between 77 and 85 percent of the time.

It’s possible that the sinFM call could be a bat’s version of shouting, “GET AWAY, THAT’S MINE!” But that seems unlikely. While watching wild bats, Corcoran and Conner noticed that animals that are diverted by a sinFM call will double back to try and grab their prey again, rather than simply flying off. They missed their attacks not because they were deferring to a peer, but because their sonar had let them down.

Corcoran and Conner suspected that the bats use their sinFM calls to actively jam the sonar of their competitors. To test this hypothesis, they set up an experiment. They attached a thin line to a street light, and dangled a moth from it. Whenever a bat approached this bait, they played a recording of a sinFM call from a nearby speaker.

The team recording bat calls in the wild. Credit: Aaron Corcoran.
The team recording bat calls in the wild. Credit: Aaron Corcoran.

Normally, bats capture the dangling moths around 70 percent of the time, and neither a loud tone nor burst of noise put them off. But a sinFM call slashed their success rate to below 20 percent. Even though the moths were hanging in place, the bats couldn’t hit them.

And critically, the sinFM only worked if it overlapped with the bats’ feeding buzz. If the team played it just before an attack, it had no effect. Clearly, this call isn’t an off-putting shout. It really does seem to be a way for bats to jam each other. It isn’t meant to overwhelm a target’s senses like, say, a bright light shone into another person’s eyes. It’s more subtle than that. I imagine it to be more like saddling an opponent with a set of goggles that makes their world fuzzier.

If Corcoran and Conner are right, they’ve discovered the first example of a non-human animal that competes with a rival by disrupting its senses.

Reference: Corcoran & Conner. 2014. Bats jamming bats: Food competition through sonar interference. http://dx.doi.org/10.1126/science.1259512

More on bats and moths:

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The Human Genome Is In Stalemate in the War Against Itself

A moth evolves ears that can hear the sonar of bats, and bats adapt by hushing their calls to whispers. A newt evolves powerful poisons that can kill would-be predators, and a snake evolves immunity to those poisons. A gazelle becomes faster to outrun its hunter, and a cheetah becomes faster still. The natural world is full of these evolutionary arms races—endless battles where one party’s adaptations are met by counter-adaptations from its opponent. Both sides move in and out of check, changing all the time but locked in a perpetual stalemate.

The human genome is engaged in a similar evolutionary arms race… against itself.

The opponents are jumping genes called retrotransposons that can hop around the genome. They increase in number by copying themselves and pasting the duplicates into new locations. This mobile lifestyle is so successful that retrotransposons make up more than 40 percent of the human genome. Some have settled down, and are now static shadows of their once-active selves. Others are still on the move.

If the copies land in the right place, they could act as clay for building new adaptations. If they land in the wrong place, which is perhaps more likely, they could cause diseases by disrupting important genes. So genomes have ways of keeping these wandering sequences under control. One involves a gene called KAP1. It’s a kind of tranquiliser—it sticks to retrotransposons and stops them from activating.

KAP1 works differently in different species, targeting those retrotransposons that are active in that owner’s genome. Our KAP1 won’t keep a mouse’s jumping genes in line, and vice versa. Some scientists believe that this specificity is caused by another group of genes called KZNFs. They tell KAP1 where to go by searching for, and sticking to, specific retrotransposons. They’re like beat cops that patrol a neighbourhood, look for crime, and radio for back-up. Each KZNF targets a different type of retrotransposon and different species have their own set.

At least, that’s what happens in theory. In reality, it has been hard to confirm this idea,  partly because these cops do such a good job that it’s hard to see jumping genes in action.

Frank Jacobs and David Greenberg from the University of California, Santa Cruz solved this problem by sticking the retrotransposons in mouse cells—a less policed environment. They filled the mouse stem cells with a single human chromosome. Mice are adapted to control their own retrotransposons, so they’re oblivious to ours. The jumping genes on the human chromosome, freed from their usual restraints, started spreading, much like an invasive species running amok on an island with no native predators. Now, the team could pit different human KZNFs against these restless genes to see if any could bring them to heel.

They found two that could—ZNF91 and ZNF93. Each of these represses a major class of retrotransposons—SVAs and L1s, respectively—that are still jumping about in the human genome today.

ZNF91 and ZNF93 are only found in primates, but they have changed a lot even without our narrow lineage. For example, the human version of ZNF91 has deluxe features that are shared by gorillas but not by monkeys. To understand the value of these changes, Ngan Nguyen and Benedict Paten took the modern genes and worked backwards, reconstructing their ancestral versions at different stages of their evolution.

They found that between 8 and 12 million years ago, ZNF91 gained features that dramatically improved its ability to keep retrotransposons in line. That’s the point in primate evolution before humans diverged from gorillas and chimps. ZNF93 went through similarly dramatic changes between 12 and 18 million years ago, before the we (and the other great apes) diverged from orang-utans.

These results suggest that ape KZNFs have rapidly evolved to keep jumping genes in check. Indeed, the KZNFs are one of the fastest growing families of primate genes. We have around 400 of them, and some 170 of these are primate-only innovations. This expanded police force reflects our ongoing genomic arms race.

And the jumping genes are starting to fight back. For example, the team found that ZNF93 represses L1 genes by recognising a short signature sequence that most of them have. But some L1s, especially the most recently evolved ones, have lost this signature entirely. They can jump unnoticed.

The missing sequence would normally makes the jumping genes better at jumping. But this booster rocket ended up as a wheel clamp, since ZNF93 evolved to recognise it. So some of the L1s lost the rocket. They jumped less effectively, but at least they could still jump.

anchorman-well-that-escalated-quicklyThis is a classic evolutionary arms race. The hosts thrusts, the parasite parries, and the duel continues. But unlike more familiar battles between snakes and toads, or hosts and viruses, this is a case where we’re waging war against our own DNA.

There’s a sense of futility about this. Much of our genome seems to be engaged in an ultimately pointless duel whether neither side can give or gain any ground. But these battles aren’t quite as fruitless as they might seem.

The team found that KZNFs partly suppress the genes around a retrotransposon too. When the cops finds their target, they tell all the bystanders to the lie on the ground too. This is important because it seriously affects the activity of many human genes, beyond retrotransposons. It means that KZNFs can eventually be used to control the activity of genes that jumping genes land next to. (“Excuse me, officer, but while you’re manhandling your suspect, would you mind also rescuing my cat?”) This arms race could have given rise to more complicated networks of genes, and perhaps more complicated bodies or behaviours.

Reference: Jacobs, Greenberg, Nguyen, Haeussler, Ewing, Katzman, Paten, Salama & Haussler. 2014. An evolutionary arms race betweenKRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons. Nature http://dx.doi.org/10.1038/nature13760

More on jumping genes

Humans Restrain Jumping DNA That Chimps Allow To Run Free

Under three layers of junk, the secret to a fatal brain disease

How a quarter of the cow genome came from snakes

Flesh-Eating Plant Cleaned Junk From Its Minimalist Genome


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This Mouse Turns Agonising Scorpion Venom Into A Painkiller

Move aside, honey badger. There’s a new contender for the most badass mammal: the southern grasshopper mouse. This little creature from the south-western USA attacks and eats bark scorpions—a group of large arachnids, whose stings are incredibly painful and often fatal. When humans get stung, they say the pain’s like having a cigarette stubbed out on your skin, followed by hours of throbbing. The toxins should easily be powerful enough to kill a small rodent.

But the grasshopper mouse doesn’t care.

It viciously attacks and eats bark scorpions. When it gets stung—and it gets stung a lot—it barely seems to notice. Ashlee Rowe from Michigan State University (and formerly the University of Texas at Austin) has discovered how it copes.

The mouse is armed with a protein that stops its nerves from firing whenever it recognises the toxins in a bark scorpion’s venom. This doesn’t just stop the venom from triggering intense pain; it means that the scorpion’s venom actually prevents pain! The southern grasshopper mouse turns a scorpion’s sting from a painful killer into a painkiller.

“It’s like an evolutionary martial art,” says Rowe. “The mouse is using the scorpion’s strength against it.”

The bark scorpion’s venom works by attaching to a protein called Nav1.7, which is found on the surface of pain-sensing nerve cells. The protein acts like a doorway and the venom forces it open, allowing sodium ions to flood into the nerve and causing it to fire. Nav1.7 is very similar across different mammals, which is why a bark scorpion’s venom is equally effective at causing pain in humans as in rodents.

At first, Rowe guessed that the grasshopper mouse must have mutations in Nav1.7 that change its shape, so that the venom can’t recognise it any more. That’s the usual way in which animals evolve resistance to otherwise deadly toxins.

But she was wrong—the grasshopper mouse’s version of Nav1.7 opens in the presence of scorpion venom as readily as that of any other rodent. Instead, its secret lies in a second protein called Nav1.8. This one sits in the same neurons in Nav1.7, and it’s responsible for maintaining the pain signals that its counterpart initiates. Rather than tweaking Nav1.7 to ignore scorpion venom, the mouse has tweaked Nav1.8 to recognise it.

By reconstructing Nav1.8 in the lab, Rowe’s team found that scorpion venom has no effect on the house mouse version, but readily sticks to the grasshopper mouse’s one… and blocks it. This immediately kills any pain signals that are initiated by Nav1.7.

“That’s what is so cool about this paper,” says Michael Nitabach from Yale University, who studies similar proteins. “The evasion mechanism is based on the accumulation of mutations in a second, distinct sodium channel in the pain-sensing neurons of the mouse.”

And by blocking Nav1.8, the venom also dulls the signals caused by other painful stimuli too. When the team injected small doses of irritants into the paws of mice, they saw that the grasshopper mouse was more bothered by an injection of saline than one of scorpion venom! And when they injected formaldehyde into a grasshopper mouse’s paw, the rodents were less bothered after a dose of scorpion venom.

Southern grasshopper mouse takes out a scorpion. Credit: Matthew and Ashlee Rowe
Southern grasshopper mouse takes out a scorpion. Credit: Matthew and Ashlee Rowe

The team then sequenced the gene that encodes Nav1.8 in both mouse species, and discovered that the differences between them boil down to just two amino acids, out of hundreds. In the house mouse, the 859th amino acid in Nav1.8 is a glutamic acid, while the 862nd one is a glutamine. In the grasshopper mouse, they’re reversed. That’s it. That swap is enough to make Nav1.8 respond to a scorpion’s venom, and to make a rodent impervious to its sting.

There’s an interesting parallel to this evolutionary story in a bizarre African rodent called the naked mole rat. They’re not threatened by bark scorpions, but they do face chokingly high levels of carbon dioxide in their underground colonies. This acidic gas increases the levels of protons in their blood, which triggers acid sensors in their neurons. That would normally cause pain, but the naked mole rat’s version of Nav1.7 also recognises protons, and shuts down in their presence. And that makes the animal insensitive to acids.

Both Nav1.7 and Nav1.8 are very similar across a lot of different species, but small changes can clearly have profound effects. They allow the naked mole rat to live underground, and they allow the grasshopper mouse to feast upon well-defended prey.

But what about the scorpions? Surely they would eventually evolve a way around the mouse’s impunity. Rowe suspects that this might be happening. “I’ve begun to look at population differences in the scorpions,” she says. “There are some populations that are a little more toxic than others, and they tend to the be the ones that co-exist with the grasshopper mouse. I haven’t looked at pain levels yet, but there might be some sort of arms race.”

Reference: Rowe, Xiao, Rowe, Cummins & Zakon. 2013. Voltage-Gated Sodium Channel in Grasshopper Mice Defends Against Bark Scorpion Toxin. Science http://dx.doi.org/10.1126/science.1236451

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Parasitic Bird Fights Evolutionary Arms Race… With Itself

Top row: cuckoo eggs. Bottom row: eggs from cuckoo victims. Credit: Mary Caswell Stoddard, Harvard University
Top row: cuckoo eggs. Bottom row: eggs from cuckoo victims. Credit: Mary Caswell Stoddard, Harvard University

In the image above, all the eggs in the top row are laid by cuckoos and those in the bottom row belong to their victims. These uncanny similarities help cuckoos to fob off their parental duties by laying their eggs in the nests of other species. If the hosts can’t tell the difference between their eggs and the foreign ones, they’ll end up raising the cuckoo chick as their own. And they pay a hefty price for their gullibility, since cuckoo chicks often kill or outcompete their foster siblings.

The relationship between cuckoos and their hosts is a classic example of an evolutionary arms race. Cuckoos, should evolve eggs that more closely match those of their hosts, while the hosts should evolve keener senses to discriminate between their own eggs and a cuckoo’s.

But in Africa, this classic story takes an unusual twist.

Greater honeyguide chick. Credit: Claire Spottiswoode
Greater honeyguide chick. Credit: Claire Spottiswoode

The greater honeyguide isn’t a cuckoo but uses the same tactics—it parasitises the nests of little bee-eaters by laying eggs of the same size and shape. But this mimicry doesn’t help it to fool the bee-eaters, which seem to accept any old egg no matter how different it looks. Instead, Claire Spottiswoode from the University of Cambridge has found that the parasitic honeyguides are fighting an evolutionary arms race against… each other.

Bee-eaters build their nests underground, usually within abandoned aardvark burrows. When honeyguides invade, they’ll puncture the bee-eater’s eggs before laying their own. This kills some of the eggs outright and weakens others. If any chicks survive to hatching, they’re finished off by the honeyguide chick, which stabs its foster siblings to death with a vicious hooked bill.

Greater honeyguide chick killing little bee-eater chicks. Credit: Claire Spottiswoode
Greater honeyguide chick killing little bee-eater chicks. Credit: Claire Spottiswoode

Spottiswoode filmed this brutal behaviour in 2011, and she showed that honeyguides are a huge problem. Two-thirds of the nests are parasitised, and a third of these contain eggs from more than one honeyguide. That’s important—it means that honeyguides aren’t just trying to dupe the bee-eaters, but are also competing with each other.

The honeyguide eggs are reasonably similar to those of the bee-eaters in both size and shape. But when Spottiswoode added very dissimilar eggs to the clutches, including those from doves, woodpeckers or kingfishers, the bee-eaters almost never noticed. The honeyguide eggs can’t have evolved to fool the bee-eaters, since the bee-eaters apparently have the discriminatory prowess of a brick.

Host = little bee-eater eggs. Control = little bee-eater egg from a different nest. Honeyguide = honeyguide egg. Experimental = egg from a completely different bird.
Host = little bee-eater eggs. Control = little bee-eater egg from a different nest. Honeyguide = honeyguide egg. Experimental = egg from a completely different bird.

But the honeyguides are more savvy. Whenever they visited a nest where Spottiswoode had added an extra egg, they inflicted at least twice as many punctures upon it as they did to the others. They could tell if an egg looked different to the usual bee-eater shape, and concentrated their efforts on destroying it.

Spottiswoode thinks that the honeyguides have evolved bee-eater-esque eggs to fool each other, because they go easier on such eggs than on those that feel very different. After all, honeyguides can’t puncture everything. If they go overboard, they might cause so much damage that the hosts abandon their nests altogether. So, their best play is to puncture the bee-eater eggs a little bit, enough to give their murderous chick an advantage when it hatches but not so much that the bee-eaters desert.

If a honeyguide egg was obviously different to a bee-eater’s one, it would be thoroughly destroyed by other honeyguides that arrived at the same nest. If its mimicry is good, it gets a chance at surviving.

This story reminds me of some recent discoveries in bacteria. In 2010, I wrote about how the harmless gut bacterium Escherichia coli can sometimes make us ill because disease-causing strains are better at fending off hungry amoebas. The bacteria evolve in response to the threat of predators and by complete coincidence, they also become deadlier to us. Along similar lines, the normally harmless nose bacterium Streptococcus pneumonia can become infectious when it competes with another species called Hameophilius influenzae. It defends itself against this rival by producing a thicker coat, which also happens to shield it from our immune system.

We have this knee-jerk tendency to view parasites in terms of their hosts (since we ourselves are host to legions). But as the honeyguide, E.coli and S.pneumonia show, parasites also have to compete with each other. This competition can drive their evolution just as readily as the need to outfox a host.

Reference: Spottiswoode. 2013. A brood parasite selects for its own egg traits. Biology Letters http://dx.doi.org/10.1098/rsbl.2013.0573

More on cuckoos and other brood parasites:

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Water striders evolved to literally grab female eyes

The worst sex you have ever had pales in comparison to what female water striders have to put up with. Put it this way: you have never been held down by your eyes.

As the female skates over the surface of ponds and lakes, males will try to force themselves upon her. She resists by struggling vigorously. But in some species, males can avoid being thrown off with antennae that have evolved into antler-shaped restraints. They bend in on themselves and are loaded with an array of prongs and spikes that perfectly fit to the shape of a female’s head.

Locke Rowe from the University of Toronto has been studying water striders for almost 20 years. In many species, males have evolved structures that give them an edge in their indelicate liaisons with females. “But the traits I studied before were rather simple – a spine here or there,” says Rowe. The subject of his latest study, a species called Rheumatobates rileyi – is… well, the opposite of simple.


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Giant squids’ huge eyes see the light of charging whales

The giant squid sees the world with eyes the size of soccer balls. They’re at least 25 centimetres (10 inches) across, making them the largest eyes on the planet.

For comparison, the largest fish eye is the 9-centimetre orb of the swordfish. It would fit inside the giant squid’s pupil! Even the blue whale – the largest animal that has ever existed – has measly 11-centimetre-wide eyes.

So why the huge leap in size? Why does the giant squid have a champion eye that’s at least twice the size of the runner-up?

Dan-Eric Nilsson and Eric Warrant from Lund University, Sweden, think that the squid must have evolved its eye to cope with some unique challenge that other animals don’t face – to spot one of the world’s biggest predators, the sperm whale.


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Flies drink alcohol to medicate themselves against wasp infections

Some people drink alcohol to drown their sorrows. So does the fruit fly Drosophila melanogaster, but its sorrows aren’t teary rejections or lost jobs. It drinks to kill wasps that have hatched inside its body, and would otherwise eat it alive. It uses alcohol as a cure for body-snatchers.

D.melanogaster lives in a boozy world. It eats yeasts that grow on rotting fruit, which can contain up to 6 per cent alcohol. Being constantly drunk isn’t a good idea for a wild animal, and the flies have evolved a certain degree of resistance to alcohol. But Neil Milan from Emory University has found that alcohol isn’t just something that the insect tolerates. It’s also fly medicine.


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House mice picked up poison resistance gene by having sex with related species

Since 1948, people have been poisoning unwanted rats and mice with warfarin, a chemical that causes lethal internal bleeding. It’s still used, but to a lesser extent, for rodents have become increasingly resistant to warfarin ever since the 1960s. This is a common theme – humans create a fatal chemical – a pesticide or an antibiotic – and our targets evolve resistance. But this story has a twist. Ying Song from Rice University, Houston, has found that some house mice picked up the gene for warfarin resistance from a different species.

Warfarin works by acting against vitamin K. This vitamin activates a number of genes that create clots in blood, but it itself has to be activated by a protein called VKORC1. Warfarin stops VKORC1 from doing its job, thereby suppressing vitamin K. The clotting process fails, and bleeds continue to bleed.

Rodents can evolve to shrug off warfarin by tweaking their vkorc1 gene, which encodes the protein of the same name. In European house mice, scientists have found at least 10 different genetic changes (mutations) in vkorc1 that change how susceptible they are to warfarin. But only six of these changes were the house mouse’s own innovations. The other four came from a close relative – the Algerian mouse, which is found throughout northern Africa, Spain, Portugal, and southern France.

The two species separated from each other between 1.5 and 3 million years ago. They rarely meet, but when they do, they can breed with one another. The two species have identifiably different versions of vkorc1. But Song found that virtually all Spanish house mice carry a copy of vkorc1 that partially or totally matches the Algerian mouse version. Even in Germany, where the two species don’t mingle, a third of house mice carried copies of vkorc1 that descended from Algerian peers.


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Fighting evolution with evolution – using viruses to target drug-resistant bacteria

We are losing the war against infectious bacteria. They are becoming increasingly resistant to our antibiotics, and we have few new drugs in the pipeline. Worse still, bacteria can transfer genes between each other with great ease, so if one of them evolves to resist an antibiotic, its neighbours can pick up the same ability. But Matti Jalasvuori from the University of Jyvaskyla doesn’t see this microscopic arms-dealing as a problem.  He sees it as a target.

Usually, antibiotic-resistance genes are found on rings of DNA called plasmids, which sit outside a bacterium’s main genome. Bacteria can donate these plasmids to one another, via their version of sex. The plasmids are portable adaptations – by trading them, bacteria can rapidly respond to new threats. But they aren’t without their downsides. Plasmids can sometimes attract viruses.

Bacteriophages (or “phages” for short) are viruses that infect and kill bacteria, and some of them specialise on those that carry plasmids. These bacteria may be able to resist antibiotics, but against the phages, their resistance is futile.


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Staying out of the arms race, or when evolution goes “meh”

“He who knows when he can fight and when he cannot will be victorious.” – Sun Tzu, The Art of War

Some battles aren’t worth fighting. The rewards of victory are too small or the costs of combat are too high. Good generals know this, and so does evolution. The natural world is full of intense arms races between predators and prey, hosts and parasites. If one side evolves a small advantage, the other counters it with an adaptation of their own, and both species are locked in an ever-escalating stalemate. But sometimes, these arms races never take off. The  costs of engagement just aren’t worth it.

Oliver Kruger from the University of Bath has found one such example in South Africa, where a small local bird called the Cape bulbul is plagued by the Jacobin cuckoo. Like many other cuckoos, the Jacobin is a “brood parasite”, an animal that relies on others to rear its young. It lays its eggs in a bulbul nest, palming off its own young to unwitting surrogate parents.

Cuckoos and their hosts are usually excellent examples of evolutionary arms races. Over time, the cuckoo eggs evolve to look like the eggs of their hosts. In turn, the hosts evolve a sharper eye to tell the difference between the fakes and their own young. But that’s not the case for the Jacobin. Its egg is twice the size of a bulbul one, and its white shell stands out among the speckled brown colours of the others in the nest. It should be very easy for a bulbul to recognise and deal with the interloper. But instead, it doesn’t harm the egg and its feeds the hatchling as if it were its own. Why?


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Evolutionary arms race turns ants into babysitters for Alcon blue butterflies


This is an old article, reposted from the original WordPress incarnation of Not Exactly Rocket Science. I’m travelling around at the moment so the next few weeks will have some classic pieces and a few new ones I prepared earlier.

In the meadows of Europe, colonies of industrious team-workers are being manipulated by a master slacker. The layabout in question is the Alcon blue butterfly (Maculinea alcon) a large and beautiful summer visitor. Its victims are two species of red ants, Myrmica rubra and Myrmica ruginodis.

The Alcon blue is a ‘brood parasite’ – the insect world’s equivalent of the cuckoo. David Nash and European colleagues found that its caterpillars are coated in chemicals that smell very similar to those used by the two species it uses as hosts. To ants, these chemicals are badges of identity and the caterpillars smell so familiar that the ants adopt them and raise them as their own. The more exacting the caterpillar’s chemicals, the higher its chances of being adopted.

The alien larvae are bad news for the colony, for the ants fawn over them at the expense of their own young, which risk starvation. If a small nest takes in even a few caterpillars, it has more than a 50% chance of having no brood of its own. That puts pressure on the ants to fight back and Nash realised that the two species provide a marvellous case study for studying evolutionary arms races.


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Ninja bat whispers to sneak up on moths

Batman's logo became much more detailed over the yearsBatman’s logo became a lot more detailed over the years…

The night sky is the setting for an arms race that has been going on for millions of years: a conflict between bats and moths. Many bats can find their prey by giving off high-pitched squeaks and listening out for the echoes that return. This ability – echolocation – allows them to hunt night-flying insects like moths, which they skilfully pluck out of the air. But moths have developed countermeasures; some have evolved ears that allow them to hear the calls of a hunting bat and take evasive action. And bats, in turn, have adapted to overcome this defence.

Holger Goerlitz from the University of Bristol has found that the barbastelle bat is a stealth killer that specialises in eating moths with ears. Its echolocation calls are 10 to 100 times quieter than those of other moth-hunting bats and these whispers allow it to sneak up on its prey. It’s the latest move in an ongoing evolutionary dogfight and for now, the barbastelle has the upper wing.


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Rotifers find answer to parasites by blowing on the wind

When our lives are in danger, some humans go on the run, seeking refuge in other countries far away from the threats of home. Animals too migrate to escape danger but one group – the pond-living bdelloid rotifers – have taken this game of hide-and-seek to an extreme.

If they are threatened by parasitic fungi, they completely remove any trace of water in their bodies, drying themselves out to a degree that their parasites can’t stand. In this desiccated state, they ride the wind to safety, seeking fresh pastures where they can establish new populations free of any parasites.

This incredible strategy may be partially responsible for another equally remarkable one – the complete abandonment of sex. For over 80 million years, the bdelloids (pronounced with a silent ‘b’) have lived an asexual existence. Daughters are identical clones of their mothers, budded off from her body. No males have ever been discovered. For this reason, Olivia Judson once described bdelloid rotifers as an “evolutionary scandal”. Their sexless lifestyles simply shouldn’t work in the long run.

Ditching sex allows an animal to efficiently pass all of its genes to the next generation without having to seek out a mate. This should give asexual animals a big advantage but not so. Sex provides fuel for evolution. Every time two individuals meet in flagrante, their chromosomes are joined, shuffled and re-dealt to the next generation. In this way, sex begets diversity, remixing genes into exciting new combinations.

This diversity is a vital weapon in the never-ending war against parasites. Parasites, with their large populations and short generations, are quick to evolve new ways of exploiting their hosts. They could have their run of a genetically uniform population and soon bring it to its knees. A sexually active species is a harder target. With genes that shuffle every generation, new anti-parasite adaptations are always just one bout of mating away. And so it goes, again and again, with hosts constantly having to outrun their parasites and sex acting as the getaway vehicle.

So asexual reproduction, for all its immediate gains, should be a poor long-term strategy compared to the dynamic nature of sex. Bdelloids have clearly addressed this problem and thanks to the last few years of research, we know how. They have evolved ways of achieving every single one of the many benefits of sex, without actually doing the deed. Escape parasites? They’ve got that covered. Shuffle their genes? They do that too. Generate genetic diversity? Check. 


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Tobacco plants foil very hungry caterpillars by switching pollinators to hummingbirds

The partnerships between flowering plants and the animals that pollinate them are some of the most familiar in the natural world. The active nature of animals typically casts the plants as the passive partners in this alliance, but in reality, they’re just as involved. That becomes particularly apparent when the animals renege on their partnership.

Nicotinia attenuata, a type of wild US tobacco, is usually pollinated by hawkmoths. To lure them in, it opens its flowers at night and releases alluring chemicals. But pollinating hawkmoths often lay their eggs on the plants they visit and the voracious caterpillars start eating the plants. Fortunately for the plant, it has a back-up plan. It stops producing its moth-attracting chemicals and starts opening its flowers during the day instead. This simple change of timing opens its nectar stores to a very different pollinator that has no interest in eating it – the black-chinned hummingbird. 

Danny Kessler from the Max Planck Institute first noticed the tobacco plant’s partner-swapping antics by watching a population of flowers that was overrun by hawkmoth caterpillars. Nearly every plant was infested. To Kessler’s surprise, around one in six flowers started opening between 6 and 10am, rather than their normal business hours of 6 and 10pm. To see if the two trends were related, Kessley deliberately infested plants from another population with young hawkmoth larvae. 

Eight days later, and 35% of the flowers had started opening in the morning, compared to just 11% of uninfested plants. The flowers use a cocktail of various chemicals to lures in night-flying moths, but the main ingredient is benzyl acetone (BA). A large plume gets releases when the flower opens at night. It’s so essential that genetically modified plants, which can’t produce BA, never manage to attract any moths. Nonetheless, the flowers that opened in the morning never produced any BA.

By artificially boosting the nectar yield of specific flowers, Kessler showed that hawkmoths are more likely to lay eggs on plants that reward them with the most nectar. So by putting off the adult hawkmoths from visiting the flowers, the plants gained a reprieve from future onslaughts by their larvae.

The larvae themselves prompt the switch. As they munch away, their saliva releases complex mixtures of fats and amino acids into the wounds they create. This cocktail trigger a genetic alarm in the plant’s cells, which culminates in a burst of jasmonic acid. This all-important plant chemical coordinates a variety of defences, from producing poisons to summoning predators and parasitic wasps. In this case, it’s responsible for shifting the flowers’ blooming schedule.

Kessler demonstrated the role of the caterpillars’ saliva and jasmonic acid through a clever series of experiments. Even if no larvae are around, just adding their saliva to artificial wounds causes some plants to switch to the morning opening hours. If the plants are genetically modified so that they can’t produce jasmonic acid, the entire process grinds to a halt, rescued only by the artificial addition of jasmonic acid.

Having solved the problem of the very hungry caterpillars, the plants still need pollinators. Again, the revised opening schedule provides the solution. Through painstaking field observations, Kessler showed that hummingbirds were strongly attracted to the morning blossoms, almost always visiting these flowers first. The birds have apparently learned to associate the shape of the opened flowers with the prospect of a rich, early-morning beakful of nectar. The plant gets a new partner, while avoiding the unwanted shenanigans of its old one.

Hummingbirds, of course, never eat other parts of the plant but if they’re such compliant partners, why doesn’t the tobacco plant always open its flowers in the morning? We don’t know, but Kessler suggests that the birds, for all their strengths, may not be quite as reliable as the moths. Hummingbirds are more likely to drink from multiple flowers on the same plant, which would lead to a lot of self-fertilisation. They’re more restricted by geographical factors, such as the presence of nearby nest sites. And, unlike hawkmoths, they can’t be summoned across long distances through the simple use of smell.

Picture by Stan Shebs

Reference: Kessler et al. 2010. Changing Pollinators as a Means of Escaping Herbivores. Current Biology http://dx.doi.org/10.1016/j.cub.2009.11.071

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Museum butterfly collections chronicle evolutionary war against male-killers

The drawers of the world’s museums are full of pinned, preserved and catalogued insects. These collections are more than just graveyards – they are a record of evolutionary battles waged between animals and their parasites. Today, these long-dead specimens act as “silent witnesses of evolutionary change”, willing to tell their story to any biologist who knows the right question to ask.

This time round, the biologist was Emily Hornett, currently at UCL, and her question was “How have the ratios of male butterflies to female ones changed over time?” You would think that the sex ratios of insects to mirror the one-to-one proportions expected of humans but not if parasites get involved.

The bacterium Wolbachia is arguably the world’s most successful parasite, infecting around 20% of all insects, themselves an extraordinarily successful group. It can infect eggs but not sperm, which means that females can pass the bacteria on to their offspring, but males cannot. As a result, Wolbachia has it in for males – they are evolutionary dead-ends, and the bacterium has many strategies for getting rid of them. It can kill them outright, it can turn them into females and it can prevent them from mating with uninfected females.  As a result, populations infected with Wolbachia can be virtually male-free.

To study the effect of Wolbachia on butterfly populations, Hornett (great name for an entomologist)turned to collections of the blue moon butterfly (Hypolimnas bolina). This beautiful species was heavily collected by entomologists between 1870 and 1930 and their efforts have stocked the museums of the world with specimens. While these were long dead, Hornett found that many of them contained viable DNA and she used them to develop a genetic test for Wolbachia infections.

She validated her Wolbachia test by using butterflies collected by the entomologist H.W.Simmons in Fiji over 70 years ago. Simmons carefully recorded the numbers of males and females in his butterflies and noted some very unusual all-female brood. Sure enough, Hornett confirmed that only mothers who tested positive for Wolbachia produced these skewed clutches, while those that were infection-free gave birth to the standard bisexual broods.

Satisfied that her test was accurate, Hornett cast her net further. She looked at specimens collected from five populations of blue moon butterflies collected from the Phillippines, Borneo, Tahiti, Fiji and Samoa between 73 and 123 years ago. The butterflies are well studied to this day, so Hornett could compare the proportion of Wolbachia infections then and now. In butterfly time, this represents a gap of 500 to 1000 generations separating the specimens from their modern descendants.

The results show that the butterfly and the bacterium have been engaging in a heated evolutionary battle throughout the Pacific. The male-killer’s dominance has fluctuated greatly, rising in some areas and falling in others, while the butterfly has repeatedly evolved to resist its sex-skewing antics.