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When Threatened By Worms, Bacteria Summon Killer Fungi

When you’re the size of a human, you worry about lions and tigers and bears. But if you’re a bacterium, a tiny nematode worm, just a millimetre long, can be a vicious predator. Nematodes are among the most common animals on the planet, and many of them hunt bacteria in soil and water. The microbes, in turn, have evolved many defences. Some secrete toxins. Others gather in large, invulnerable swarms*.

Now, a team of Chinese scientists have discovered the most outlandish strategy yet: some bacteria transform fungi into worm-killers.

Fungi aren’t known for their speed or mobility, but around 200 species have evolved ways of killing nematodes nonetheless. They use traps, including sticky nets and microscopic lassos made of single coiled cells. Once they ensnare a worm, they grow into it and digest it from the inside out.

These fungi aren’t always killers. One of the most common and best-studied species—Arthrobotrys oligospora—usually feeds on decaying vegetation. It only produces its deadly traps when nematodes are around. Two years ago, one team of scientists showed that it knows when to do this because it can smell its prey, detecting chemicals that the worms can’t help but produce.

But these chemicals aren’t always necessary. Earlier studies have shown that the fungi can also change from death-eaters to death-bringers when they’re exposed to fresh cow dung. Xin Wang, Guo-Hong Li, and Cheng-Gang Zou from Yunnan University reasoned that bacteria in the dung were responsible.

The team isolated a few species of bacteria that could transform the fungi on their own, and identified the chemical that they use—urea. The bacteria mass-produce an enzyme that churns out urea, which then diffuses through the soil. The fungi absorb it and convert it into ammonia, and the ammonia triggers their lifestyle switch. If the team disrupted any part of this pathway, by blocking the various enzymes that make, absorb, or process urea, the fungi no longer set their traps.

The team confirmed the importance of urea by setting up deathmatches in plates of sterilised soil. They seeded the plates with different microbes, unleashed waves of nematodes upon them, and then added the spores of the killer fungi.

Sure enough, the nematodes gorged themselves on the bacteria and their populations bloomed—that is, until the fungi started culling them. If the bacteria couldn’t make urea, the fungi built their traps in a leisurely way and killed the nematodes slowly. But if the team used urea-making microbes, or deliberately added urea to those that couldn’t produce it, the fungi mobilised more quickly and almost completely wiped out the nematodes. By making urea, the bacteria can rally the nematodes’ nemeses to their aid.

These kinds of interaction are common in the natural world. Many plants, for example, defend themselves against very hungry caterpillars by releasing chemicals that summon parasitic wasps, which kill the pests by implanting them with eggs.

We’ve only started to appreciate the scope of these chemical alarms because they are invisible to us, and are often produced by creatures beneath our notice. But they are certainly there. Go for a walk, look at a field, and picture millions upon millions of calls for help, drifting in the wind and cascading through the soil.

Reference: Wang, Li, Zou, Ji, Liu, Zhao, Liang, Xu, An, Zheng, Qin, Tian, Xu, Ma, Yu, Huang, Liu, Niu, Yang, Yuang & Zhang. 2014. Bacteria can mobilize nematode-trapping fungi to kill nematodes. Nature Communications http://dx.doi.org/10.1038/ncomms6776


* PS Both of these traits can coincidentally make bacteria better at infiltrating our bodies and causing disease. Every year, people die because of microbes that were just trying to escape from worms.

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One Lichen Species Is Actually 126, And Probably More

One of the best ways of finding new species is to sequence the genes of existing ones. Often, scientists discover genetically distinct populations that count as species in their own right, hiding in plain sight. So, the African elephant turns out to be two genetically distinct groups of African elephants. A skipper butterfly  is actually ten skipper butterflies. There are two Nile crocodiles, and possibly four killer whales. Time and again, scientists have peered at a creature’s DNA and discovered that one species is actually two, or three, or a dozen.

Or perhaps hundreds.

Until ten years ago, scientists talked about the lichen Dictyonema glabratum as if it were a single species. Its large, conspicuous, and elegant fronds are found throughout the Americas, and many teams have studied its chemistry and ecology. But until Robert Lücking from the Field Museum started looking at its genes, no one realised the most startling truth about D.glabratum: it’s actually 126 different species of lichen, and possibly hundreds more.

It’s “the most spectacular case of unrecognized species richness” in any group of large organisms, says Lücking.

Lichens are fungi that form alliances with either an alga or a bacterium. The fungus captures water and minerals, while its partner makes food by harvesting the sun’s energy. This partnership is clearly a successful one: the beautiful bushes, fronds and pixie cups of lichens are found on every continent, including Antarctica, and there are some 18,000 known species.

D.glabratum was apparently one of them. The late Estonian fungus specialist Erast Parmasto described it in 1978 but Lücking’s team have been slowly chipping away at this single identity since 2004. When they discovered a second distinct lichen in Costa Rica, one species became two. When they compared the genes of a small number of specimens in 2013, two species became 16.

Now, the team, including graduate student Manuela Dal-Forno, has finished analysing 356 samples collected throughout Central and South America—more than ten times the number from their earlier study. And with that, 16 species became 126, which the team are classifying under two new groups: Cora and Corella.

The weird thing is that many of these species aren’t hidden ones. Unlike the African elephants or Nile crocodiles, where genetically distinct populations look very similar, these lichens have striking differences. Some are a soothing turquoise blue, others a ghostly white. Some grow on rocks, others on trees and shrubs. Some have distinctive features, like fine hairs or crinkled margins. They’re so different that it really shouldn’t have taken a genetic analysis to tell them apart.

The problem is that you can only see this glorious diversity by studying the lichens in the wild—and most scientists had worked with specimens that were dried and stored in herbariums. Take them out of their natural setting, and important ecological cues vanish. Dry them out, and their stunning palette collapses into a few boring hues. Lücking’s team escaped this trap by snapping a high-resolution photo of every lichen that they took a sample from. “We were absolutely stunned by the result,” he says.

Lücking also suspects that many lichenologists were also hamstrung by a weird circular logic. Lichens can look very different depending on where and how they grow, so a single species can take on many guises. That made it easier to believe that very different specimens were actually the same lichen, or that very big specimens were simply older versions of smaller ones. Only DNA could shatter that unity, and it’s not finished yet.

The team divided North and South America into a grid, and showed that 101 of their 126 species were found in just one square. This suggests that D.glabratum isn’t a continent-spanning lichen, but hundreds of incredibly localised ones. And all of these came from just 20 of the 209 squares, implying that there are probably many more Cora and Corella lichens left to discover in other parts of the Americas.

How many more? The team tried to predict a number by accounting for how many species they know about in different habitats, how widespread each species is, and how thoroughly they sampled each part of the Americas. They ended up with an estimate of 452 of these lichens in total—“an unthinkably dramatic increase from a single species”.

“This work beautifully illustrates how little we know about the numbers of fungi on Earth,” says Anne Pringle from Harvard University, who studies lichens. “I’m struck by the beauty of the lichens illustrated in the paper, and wonder if local peoples knew these species already, even though they aren’t described within the formal scientific literature.”

“We have already identified other groups of macrolichens that likely will show similar patterns of unrecognized species—at least double the number of species, if not more,” says Lücking. “For taxonomy it means there is a huge amount of work left and nothing can be taken for granted.”

Most of these species live in paramos—small habitats in the Andes Mountains, above the forests but below the snow. In these cool worlds, the lichens control the amount of water and nutrients in the soil, setting stable foundations for food webs that include Andean condors, spectacled bears, and a unique range of fast-evolving plants.

“These ecosystems are highly threatened and have disappeared to a large extent,” says Lücking. “Each paramo that disappears takes unique species down with it. Previously, it was believed that all paramos were similar, so their genetic diversity could be conserved by conserving just a few fragments. But now we know that this is not the case.”

“Lichens are ecosystems, housing myriad other organisms within a thallus (or body), including other fungi and bacteria.” adds Pringle.  “If we lose one of these lichens, I wonder what else we might lose?”

Reference: Lücking, Dal-Forno, Sikaroodi, Gillevet, Bungartz, Moncada, Yanez-Ayabaca, Chaves, Coca, Lawrey. 2014. A single macrolichen constitutes hundreds of unrecognized species. PNAS http://dx.doi.org/10.1073/pnas.1403517111

More on lichens: The surprisingly toxic world of lichens

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The Disease, My Friend, Is Blowing In the Wind

In March 2011, a small research aircraft took off from Japan, and flew into winds blowing in from northeast China. It carried a set of special filters, designed to strain small particles from the air. Among these particles, hopefully, would be the culprit behind Kawasaki disease—an illness whose cause has eluded detection for decades and could, quite literally, be blowing in the wind.

Kawasaki disease was first described by Japanese paediatrician Tomisaku Kawasaki in 1967. It largely affects children under the age of 5. Blood vessels throughout a child’s body become inflamed, leading to a weird constellation of symptoms including swollen hands and feet, red lips, strawberry tongue, irritated eyes, and rashes. If the inflammation affects the arteries of the heart, it can lead to fatal aneurysms. Around one percent of children with Kawasaki disease die from heart problems.

But almost 50 years after its discovery, no one knows what causes the disease. It has all the hallmarks of an autoimmune condition, where the immune system turns on the rest of the body, after overreacting to some trigger. But what’s the trigger? A fungus? A bacterium? A virus? Seasoned scientists have thrown state-of-the-art techniques at the problem and failed to find a culprit. They have, however, found important clues.

The trigger is probably something that you can inhale, since it first affects the airways before causing symptoms elsewhere in the body. It’s probably something seasonal, since Kawasaki cases peak twice a year—once in January and again in June and July. And it might be carried on gusts of wind.

in 2011, a team led by climatologist Xavier Rodó from the Catalan Institute of Climate Sciences compared records of Kawasaki disease against climate patterns, and found that cases in Japan spike whenever strong winds blow from central Asia. If the winds are strong enough to reach Hawaii and California, the disease appears there too.

It was an astonishing result. If true, it would mean that Kawasaki disease is a wind-borne, ocean-spanning illness, caused by something that cross thousands of miles on wisps of air rather than human vehicles. (Jennifer Frazer explores the story of this discovery in her excellent Nature feature.)

Now, Rodó’s team is back with lots of new evidence to support their wind hypothesis. For example, they found that the number of Kawasaki cases in Tokyo and Yokohama— two Japanese cities 28 kilometres apart—were perfectly synchronised during recent epidemics. The disease hit its peak in both cities, on exactly the same days. That’s the pattern you’d expect if something was blowing into Japan and quickly hitting different parts of the nation at once, rather than slowly spreading within it.

Where is this mysterious agent coming from? To find out, Rodó’s team looked at records of KD in Japan between 1970 and 2010. For every time and place with a spike of cases, the team backtracked the path of local winds using software that maps the spread of atmospheric particles. The results consistently pointed to an area of north-east China, on the border with Russia and Mongolia. That’s the source. The area is rife with farmland, and crops like rice, corn and wheat. Maybe Kawasaki disease is caused by something associated with these crops?

The team’s simulations provided another clue about Kawasaki disease: it has a very short incubation time. It typically takes less than a day (and no more than two) for winds from China to start triggering fevers after they reach Japan. That’s too short for even the fastest of viruses to start causing symptoms. “The incubation time makes it absolutely impossible for [the cause] to be an infectious agent unless it’s the fastest one ever found,” says Rodó.

Even then—even if a hypothetical virus reproduced 10 times faster than the speediest ones we know about—it would still take at least a week to spread through the Greater Tokyo area. And that’s not what happens—records show that when Kawasaki disease hits Tokyo, it hits the whole area simultaneously. It’s not caused by something growing in a host, but by something that triggers a fast immune reaction, like an allergen or an inhaled toxin.

An industrial pollutant? The team thinks that’s unlikely: the source region in northeast China has very little industry, and the incidence of Kawasaki disease in Japan doesn’t track with the levels of any atmospheric pollutants.

Pollen? Again, unlikely. The team couldn’t find a link between pollen counts and Kawasaki cases.

The team tried to find the culprit by sending a plane into the skies above Japan, flying against the winds that blow in from China. When they analysed the filters, they found a smorgasbord of fungal spores. And half of these belonged to Candidaa group whose members can cause thrush and other infections.

Their presence is unusual. The team collected samples from the ground and Candida was nowhere to be seen. Other scientists have collected microbes from the skies above the Caribbean, Mediterranean, and other parts of Asia, none of them have ever detected Candida.

There’s not enough evidence to implicate these particular fungi as the cause of Kawasaki disease, but Candida certainly makes for good candidates. Fungal spores are great at riding air currents and their hardy shells allow them to survive tough environmental conditions. Many fungi grow on crop plants, and produce toxins that can cause disease in humans without any need for the spores to actually grow. In mice, molecules on the surface of Candida fungi can trigger immune reactions that inflame the arteries of the heart.

“This only proves that potential human pathogens can be found aloft, can be transported across large distances,” says Rodó. “It might be Candida or it might be something else, but we now need to look along those lines.”

The team now wants to run more sampling flights over Japan, over other parts of the world where Kawasaki disease appears, and over the hypothetical source region in China. They also want to study the people who have the disease, to see if they have antibodies that react to any potential culprits.

Even if the team identifies the cause of Kawasaki disease, there will be more mysteries to solve. For a start, why had no one noticed any cases before 1967, and why is the disease becoming more common? Are farmers in China doing something different? Are changing weather patterns to blame? And does the same region explain Kawasaki cases in India and the Philippines, or are there other source regions.

“It’s the most fascinating scientific problem I’ve been faced with,” says Rodó, who is a climatologist by training. “I would never have imagined that I’d be working on a cardiovascular disease that affects children.”

Related: Kawasaki Disease Wafts to Japan on the Wind

Reference: Rodó, Curcoll, Robinson, Ballester, Burns, Cayan, Lipkin, Williams, Couto-Rodriguez, Nakamura, Uehara, Tanimoto & Morguí. 2014. Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source o Japan. PNAS http://dx.doi.org/pnas.org/cgi/doi/10.1073/pnas.1400380111 (Link not working? Here’s why.)

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Zombies Snipers At The Doorstep

Somewhere in the Brazilian rainforest, a lone carpenter ant marches out of its nest towards its doom.

The ant is infected with a fungus called Ophiocordyceps unilateralis, which has both infiltrated and commandeered its body. While it devours the ant alive, it also sends its zombified host scurrying up a plant stem. The ant walks along the underside of a leaf and vigorously locks its jaws around a vein. This is a death-grip; those jaws will never open again. In a week or so, a long stalk erupts from the ant’s head growing outwards and downwards into a bulbous capsule, which releases a rain of spores. If other ants walk underneath, they become infected.

The fungus controls its zombie host with incredible precision. The ant always climbs to around 25 centimetres above the soil—a zone with just the right temperature and humidity for the fungus to grow.

But why does the ant leave its nest in the first place?

Outside, the fungus needs to drive its host to a spot that offers the best chance of raining spores down upon passing workers. But inside the nest, there are thousands of such workers nearby. With this dense smorgasbord of new hosts to infect, why does the fungus send its current host into the great outdoors?

Perhaps these forays are the ants’ doing. Colony-living insects like ants have a kind of social immune system—they behave in ways that prevent infections from spreading through their nests. They clean each other and remove the corpses of their nestmates. Sick ants, which have been infected by killer fungi, are often shunned by their fellow workers, and sometimes leave the nest to die alone. Biologists often view these as acts of self-sacrifice, as if the ant was a six-legged Captain Oates.

But Raquel Loreto and David Hughes from Pennsylvania State University see things differently. The duo first realised what was going on when they collected carpenter ant nests, and seeded them with ants that had been freshly killed by Ophiocordyceps. The ants detected and removed around half of these remaining cadavers—a clear example of their vaunted “social immunity” at work.  But they needn’t have bothered. It turns out that the fungus simply cannot grow inside the nests of its hosts. Even if the cadavers were placed in nests that had no ants, the fungus still wouldn’t sprout.

“The best place for the sick individuals is at home!” says Hughes, who had been studying the zombifying fungi for many years. “In a naive framework, leaving the nest appears to be altruistic but it’s actually part of the fungus’ manipulation.”

So, what happens outside the nest? To find out, Loreto trekked into the same stretch of Brazilian rainforest for 20 months to study 17 specific carpenter ant nests. She ventured into the jungle at night with infrared torches to map the foraging trails that the workers walk along.

She also marked out a 200-cubic-metre zone around four of the nests nest —an area that she calls the “doorstep” of the colony. It’s the zone that all workers must pass through on their way in and out of the nest. Once a month, Loreto walked through these doorsteps and checked the underside of every single leaf within them for the zombified corpses of infected ants.

“This is important because it’s one of the few field studies of ant-parasite interactions,” says Sylvia Cremer from the Institute of Science and Technology Austria. Most people who study social immunity have exposed ants to parasites within the artificial confines of a laboratory. “It’s always good to bring some realism to these discussions,” says Hughes.

At the end of her Herculean effort, Loreto had found zombified corpses around every one of the 17 nests she studied. And she kept on finding new corpses every month around the four nests she studied in detail. The results were clear: despite the ant’s vaunted social immunity, the fungus infects close to 100 percent of the nests in the area, and does so throughout the year. It’s a permanent and omnipresent threat.

The team thinks that the fungus is so successful precisely because it sends its hosts outside the nest. Inside, the ants’ social immune system can protect them. Outside, it doesn’t work. “Over 20 months, Raquel never saw the colony disinfecting its borders,” says Hughes.

The ants also rely on the same trails, so the fungus is virtually guaranteed to find new hosts if it positions its current one in the right spot. Hughes compares it to a sniper’s alley. “The foragers come out at night and pass under the cadavers of their siblings that are now shooting spores at them,” he says.

But why wouldn’t the carpenter ants evolve a countermeasure? Over time, surely you’d expect them to start removing infected corpses from the leaves around their nests, as other species of ants do elsewhere in the world. Hughes suggests that they might not need to. Young carpenter ants stay exclusively within their nests. They only venture out to forage when they get older, so the fungus can only ever infect ants that are near the end of their lives anyway.

This strategy seems to suit both parties. The ants ensure that only their weakest members face death by zombifying fungus, and the fungus get a continually renewed supply of susceptible hosts to infect. It’s as close to a win-win as you get in evolution.

Reference: Loreto, Elliot, Freitas, Pereira & Hughes. 2014. 3D mapping of disease in ant societies reveals a strategy of a specialized parasite. BiorXiv. http://dx.doi.org/10.1101/003574

For more on surprising and counter-intuitive world of mind-controlling parasites, have a look at my TED talk:

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Worm-Eating Fungi Eavesdrop on the Chemicals of Their Prey

Fungi are fantastic at breaking down living tissues. They discolour pieces of bread and fruit, cause outbreaks of thrush and athlete’s foot, and wipe out harvests of rice and species of frog. All of these examples rely on fungal spores landing somewhere they can grow. But not all fungi are so passive. More than 200 species have evolved into predators that ensnare and devour their own meat.

Their victims are nematodes—small worms that are some of the most common animals on the planet. It’s said that four in every five animals is a nematode, which means there’s plenty of food for carnivorous fungi that can trap them.

Such meat-eaters evolved at least 100 million years ago, and they have since developed a wide variety of traps. Some fungi use sticky nets. Others use microscopic lassos made of single coiled cells, which can constrict round a blundering nematode. The fungi then penetrate the immobilised worms with root-like projections called hyphae, which break down their bodies from the inside out.

But these killers aren’t always so murderous. One of the most common and best-studied species—Arthrobotrys oligospora—usually feeds on decaying matter. It only manufactures traps (this one uses sticky nets) when nematodes are around. Only when there’s food does it become a predator. And that means it has some way of sensing its prey.


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The Fungus Behind the Frog Apocalypse Hides in Crayfish

A Bd-infected frog, by Forrest Brem.

Imagine that a new disease started wiping out mammals in their hundreds. Whether human or cow, bat or anteater, every species of mammal seems to succumb to this unfamiliar blight. No one understands how one infection could kill so many distantly related animals, but that doesn’t stop the bodies from piling up. Within decades, entire species go extinct. This doomsday scenario is only a partial fiction. It’s actually happening – the only difference is that it’s happening to amphibians and not mammals.

Since at least the 1990s, a fungus called Batrachochytrium dendrobatidis, or ‘Bd’ for short, has been slaughtering its way through the world’s frogs. It has severely slashed the populations of some 200 species, and dozens of these may already be completely wiped out. (Here’s a roll call of the dead.)

The disease it causes—chytridiomycosis—is like no other, in both the number of species it infects—some 600 amphibians so far and counting—and its ability to drive them to extinction. “Disease ecologists have been pulling their hair out trying to understand how a pathogen that dives its host to extinction could persist in the wild to infect the next host that comes by,” says Vance Vredenburg from San Francisco State University.

One possibility is that the fungus isn’t just the amphibian specialist that most people see it as. Maybe it uses other animals as reservoirs, where it can hide between amphibian infections. That would allow it to drive its usual hosts extinct, without itself fading into oblivion.

What could this mysterious reservoir animal be? There have been plenty of false leads, but no solid evidence that Bd infects anything other than amphibians. That is, until now. Through a combination of lab and field experiments, Taegan McMahon from the University of South Florida has found that the fungus can infect freshwater crayfish, which can then pass their infections on to amphibians.

“When I first heard about this, I was very sceptical,” says Vrendenberg. “I’ve been working on this since 2000, and I even get people telling me they’ve been infected by the chytrid fungus. But now I’ve read through the paper, they have really covered their bases.”

Louisiana crayfish, Procambarus clarkii, an alternative host for Bd, by Mike Murphy

Vredenberg’s scepticism is understandable. One group supposedly found the fungus growing on Australian shrimp, but later retracted their claims. Others have found Bd on algae, ducks, and nematode worms, and shown that it can grow on feathers, bird feet, and reptile skin. But since the fungus kills amphibians by massively overwhelming them, the presence of a few spores says very little. None of these studies showed that the fungus actually infects these alternative animals, or spreads from them to amphibians.

McMahon was far more thorough. She surveyed four species of crayfish in Louisiana and Colorado streams and found Bd zoosporangia—cases full of mobile spores—in 10 to 20 percent of them. These cases weren’t just sitting on the crayfish’s shells, but were deeply embedded inside their guts. They grew just as they do in frog skin, and McMahon confirmed through lab experiments that the fungus can infect the crayfish. Their guts become riotous masses of zoosporangia, and around a third of them die as a result.

In one of these surveys, done in September, McMahon found that one in every six crayfish was infected with the fungus, even though none of the local frogs were. This fits with previous studies showing that Bd kills amphibians in the spring, but is absent during the autumn. Maybe it hides in crayfish during this off-peak season, and jumps into frogs later. Certainly, the infected crayfish can harbour the fungus for months.

But McMahon hadn’t yet shown that the fungus could jump from crayfish to frogs. To close the loop, her team did a more thorough survey of 97 Colorado wetlands, swabbing the skins of more than 9,000 amphibians. They found that those from wetlands with Orconectes crayfish were twice as likely to be infected with Bd, and that the presence of crayfish predicted the levels of infection better than anything else.

And then, the smoking gun: McMahon placed uninfected tadpoles in the same tanks as infected crayfish, and found that 70 percent of them picked up the fungus.

It’s an unparalleled suite of experiments. And it offers the first conclusive proof that Bd can infect hosts other than amphibians, in a way that eventually loops back to its favoured victims. “It was extremely important to me to make sure we did a very thorough job because I was worried others might be a little sceptical,” says McMahon. “[We wanted to present] the most concrete story possible.”

Bd zoosporangia on a frog’s leg, by the CDC

Now what?

Why is the fungus so wide-ranging in its tastes? Because of keratin, the substance found in your nails, skin and hair. Bd consumes keratin and related proteins in amphibian skins, and the same proteins line the guts of many invertebrates, like crayfish. “Given the appropriate conditions, like the right moisture and acidity, it’s possible that Bd could infect other organisms that contain the appropriate food source,” says McMahon.

The study threw up one more surprise: Bd doesn’t need to infect crayfish in order to kill them. The first clue was that the fungus seems to damage a crayfish’s gills, even though it infects its guts. When McMahon placed crayfish in water that had once contained Bd, but had been filtered to remove every spore, the animals still became sick. Clearly, the fungus releases some sort of chemical that can kill in its absence. Maybe it’s one of Bd’s several protein-destroying enzymes? Maybe it’s something else? Either way, it’s not clear if these chemicals could also kill amphibians at a distance.

Identifying a reservoir species seems like a blow for the many scientists who are trying to save amphibians from the fungus. If this frog-killer can hide out in other hosts, it will be more difficult to eradicate. But McMahon is optimistic. “It’s possible that managing alternative hosts offers a new and potentially more effective approach to managing Bd,” she suggests. Since crayfish are traded nationally and internationally for food and bait, and are often accidentally released, they could be helping to spread the fungus from place to place. If that’s true, then managing the spread of crayfish might help reduce the spread of Bd.

To Vredenburg, understanding these issues is crucial not just for saving amphibians, but for safeguarding our own health. It would be foolish for us to ignore a pandemic of this scale, even if it does not affect us directly. “There’s nothing like it in recorded history,” he says. “It makes the bubonic plague, which killed around 30 percent of the European population, look like nothing. We’re talking about 100 percent of not just one species, but probably hundreds.”

“Yes, this is occurring in amphibians, but they’ve been around for hundreds of millions of years, and are more historically successful than we are,” he adds. “We desperately need to understand how this could happen in a vertebrate group. We need to understand the biology that could lead to this global pandemic even though it’s not in humans or the species we rely on.”

Reference: McMahon, Brannelly, Chatfield, Johnson, Joseph, McKenzie, Richards-Zawackib, Veneskya & Rohr. 2012. Chytrid fungus Batrachochytrium dendrobatidis has nonamphibian hosts and releases chemicals that cause pathology in the absence of infection. PNAS http://dx.doi.org/10.1073/pnas.1200592110

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You can thank wasps for your bread, beer and wine

If wasps didn’t exist, picnics would be a lot more fun. But the next time you find yourself trying to dodge a flying, jam-seeking harpoon, think about this: without wasps, many of your ingredients might not exist at all. Irene Stefanini and Leonardo Dapporto from the University of Florence have found that the guts of wasps provide a safe winter refuge for yeast – specifically Saccharomyces cerevisiae, the fungus we use to make wine, beer and bread. And without those, picnics would be a lot less fun.

S.cerevisiase has been our companion for at least 9,000 years, not just as a tool of baking and brewing, but as a doyen of modern genetics. It has helped us to make tremendous scientific progress and drink ourselves into stupors, possibly at the same time. But despite its significance, we know very little about where the yeast came from, or how it lives in the wild.

The wild strains do grow on grapes and berries, but only found on ripe fruits rather than pristine ones. And they’re usually only found in warm summery conditions. So, where do they go in the intervening months, and how do they move around? They certainly can’t go airborne, so something must be carrying them.

Stefanini and Dapporto thought that wasps were good candidates. They’re active through the summer, when they often eat grapes. Fertilised females hibernate through the winter and start fresh colonies in the spring, feeding their new larvae with regurgitated food. In the digestive tracts of wasps, yeasts could get a ride from grape to grape, from one wasp generation to the next, and from autumn to spring.


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How the fungus that can punch through Kevlar becomes a cereal killer

There’s a microscopic fungus that can starve nations and punch through Kevlar. It kills on such as scale that its effects can be seen from space. It’s called Magnaporthe oryzae and it causes a disease known as rice blast. The fungus doesn’t infect humans, but it does kill rice. It kills a lot of rice, destroying up to 30 per cent of the world’s total crop every year – enough to feed 60 million people. Slowly, scientists have worked out how this cereal killer claims its victims.

A rice plant’s woes begin when one of the fungal spores lands on its leaves. As soon as it is surrounded by water, the spore sprouts a dome-shaped structure called the appressorium. This is infection HQ – it’s what the fungus uses to break into the plant. Once inside, it reproduces, eventually causing lesions that kill the leaf.

The appressorium produces glycerol as it grows, which lowers the relative amount of water inside the dome, and draws water in from outside. This builds up enormous pressure, around 40 times more than that within a car tyre. That pressure is directed into a narrow ‘penetration peg’ that travels through a pore at the bottom of the dome, and pierces the helpless plant.


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The surprisingly toxic world of lichens

Peltigera membranacea – one of the species analysed in this study

One of the most successful alliances in the natural world often goes unnoticed. It involves either an alga or a bacterium that harvests energy from the sun to make its own nutrients. It shares this bounty with a fungus, which reciprocates by providing it with shelter. Together, the associates form a dual organism known as a lichen.

This alliance is so successful that lichens have colonised every continent, including Antarctica. They’re often ignored, but look closely, and you’ll find a hidden world of jellies, bushes, worms and pixie cups. Look even closer, and you’ll find a world of poison.

Ulla Kaasalainen from the University of Helsinki has discovered that one in eight species of lichens wield microcystins, a group of poisons that cause liver damage in humans and other animals. These chemicals are manufactured by blue-green bacteria known as cyanobacteria. These microbes are best known for creating large ‘blooms’ in lakes and rivers, which discolour the water with greenish swirls, and poison it with harmful toxins like microcystins. These toxins can accumulate in the food chain, affecting humans via shellfish and fish.


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A realm of world of fallen leaves held aloft by fungal nets

A leaf falls from the rainforest canopy, but it never hits the ground. Instead, it becomes trapped by nets of sticky fungi. While other lost leaves litter the forest floor, this one has joined the jungle’s mezzanine level – a layer of litter suspended in mid-air and hanging by a thread.

The fungi belong to a single genus called Marasmius, which extend networks of root-like filaments through the air. They act like a web that catches falling matter from the branches above. They have gone unappreciated, but Jake Snaddon from the University of Oxford has found just how important they can be.

By snaring leaves, the fungi provide room and board to insects, spiders and other canopy creepy-crawlies that might otherwise be confined to the ground. When Snaddon removed the fungi, the numbers of these animals plummeted by 70 percent.


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Raise your pints to the Patagonian fungus that helped us to brew lager

Every time you drink a pint of lager, you owe a debt to a small fungus that lives in the beech forests of Patagonia. This previously undescribed species – Saccharomyces eubayanus – merged with a close relative to create a hybrid, whose fermenting abilities produce all of today’s lagers. Without it, our pints would have a much darker complexion.

Ask someone to think of a domesticated species and they’ll probably think of something like a dog, cat, cow or horse. But domesticated fungi are just as close to our hearts or, at least, our livers.  The yeast, Saccharomyces cerevisiase, has been used to bake bread and ferment wine or ales for centuries. But it’s only partially involved in lagers.

Lager is fermented at a lower temperature than either ale or wine, and the fungus for the job is a cold-tolerant species called S.pastorianus. It has never been found in the wild, and its genes tell us why. It has four of each chromosome, and appears to be a fusion of two different yeast species. One of these is S.cerevisiae but the identity of the second partner has been a long-running mystery. Until now, the best guess was yet another species of cold-tolerant yeast called S.bayanus. But like S.pastorianus, S.bayanus has never been found in the wild.


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The world’s biggest market (and it’s underground)

It is very easy to find the world’s most extensive marketplace – just find your nearest forest, field or garden, and look underground.

The planet’s land plants are engaged in an ancient alliance with the so-called “AM fungi” that grow into their roots. One plant might be colonised by many fungi, and a single fungus could connect up to many plants. The fungi harvest nutrients like phosphorus and nitrogen from the soil and channel them to their hosts.  In return, the plants provide the fungi with the sugars and carbohydrates they need to grow.

This symbiotic partnership covers the planet in green. It’s common to 80 percent of land plants, and is credited with driving the evolution of this group some 470 million years ago. Now, Toby Kiers from Vrije University in Amsterdam has found that plants and fungi have maintained their grand alliance by setting up a strong market economy.


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Need to feed could have driven single cells to evolve into colonies

Most life on this planet goes about their business as single cells. Only rarely do these singletons unite in cooperative societies, creating bigger and more complex living things, from trees to humans. This transition from single-celled to ‘multicellular’ life is one of the most important transitions in the evolution of life on Earth and it has happened many times over.

There are two main routes to a multicellular life. Single cells can merge together, and some modern species recap how this might have happened. Individual slime moulds join to form mobile slugs, while myxobacteria can merge into predatory swarms. Alternatively, cells can multiply but remain attached, staying united in their division. The choanoflagellates, possibly the closest living relatives of animals, can do this, creating simple colonies from single cells.

So we have a reasonable, if basic, understanding of how multicellular creatures first evolved. But we’re still largely in the dark about why. What benefit did cells gain from sticking together, rather than swimming solo? John Koschwanez from Harvard University thinks he has one answer: by sticking together, clumps of cells became better at foraging for nutrients. The multicellular life was a well-fed one.


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Fungus loaded with scorpion toxin to fight malaria

Meet our newest potential weapon against malaria – a fungus loaded with a chemical found in scorpion venom. Metarhizium anisopliae is a parasitic fungus that infects a wide variety of insects, including the mosquitoes that spread malaria. Their spores germinate upon contact and the fungus invades the insect’s body, slowly killing it. Now, Weiguo Fang from the University of Maryland has modified the fungus to target the malaria parasites lurking inside the mosquitoes.

Fang loaded the fungus with two chemicals that attack the malaria parasite Plasmodium falciparum. The first is a protein called SM1 that prevents the parasites from attaching to the mosquito’s salivary glands. By blocking Plasmodium‘s path, SM1 stops the parasite from travelling down the mosquito’s mouthparts into the people it bites. The second chemical is scorpine – a toxic protein wielded by the emperor scorpion, which kills both bacteria and Plasmodium. This double whammy of biological weapons slashed the number of parasites in mosquito saliva by 98%.


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Pocket science – swordfish and flatfish are close kin, and ancient death-grip scars


Flatfish are the closest living relatives to swordfish and marlins

At first glance, a swordfish and a flounder couldn’t seem more different. One is a fast, streamlined hunter with a pointy nose, and the other is an oddly shaped bottom-dweller with one distorted eye on the opposite side of its face. Their bodies are worlds apart, but their genes tell a different story.

Alex Little from Queen’s University, Canada, has found that billfishes, like swordfish and marlin, are some of the closest living relatives to the flatfishes, like plaice, sole, flounder and halibut. This result was completely unexpected; Little was originally trying to clarify the relationship between billfishes and their supposed closest relatives – the tunas. That connection seems to make more sense. Both tunas and billfishes are among a handful of fish that are partially warm-blooded. They can heat specific body parts, such as eyes and swimming muscles, to continuously swim after their prey at extremely fast speeds with keen eyesight.

But it turns out that these similarities are superficial. Little sequenced DNA from three species of billfishes and three tunas, focusing on three parts of their main genome and nine parts of their mitochondrial one (a small accessory genome that all animal cells have). By comparing these sequences to those of other fish, Little found that the billfishes’ closest kin are the flatfish and jacks. Indeed, if you look past the most distinctive features like the long bills and bizarre eyes, the skeletons of these groups share features that tunas lack. Indeed, billfish and tuna proved to be only distant relatives. Their ability to heat themselves must have evolved independently and indeed, their bodies product and retain heat in quite different ways.

Little’s work is testament to the power of natural selection. Even closely related species, like marlins are flounders, can end up looking vastly different if they adapt to diverse lifestyles. And distantly related species like tuna and swordfish can end up looking incredibly similar because they’ve adapted to similar challenges – pursuing fast-swimming prey. This shouldn’t come as a surprise – a few months ago, a French team found that prehistoric predatory sea reptiles were probably also warm-blooded.

Reference: Molecular Phylogenetics and Evolution: http://dx.doi.org/10.1016/j.ympev.2010.04.022; images by Luc Viatour and NAOA


Ancient death-grip scars caused by fungus-controlled ants

Forty-eight million years ago, some ants marched up to a leaf and gripped it tight in their jaws. It would be the last thing they would ever do. Their bodies had already been corrupted by a fungus that, over the next few days, fatally erupted from their heads. The fungus produced a long stalk tipped with spores, which eventually blew away, presumably to infect more ants. In time, all that was left of this grisly scene were the scars left by the ants’ death-grip. Today, David Hughes from Harvard University has found such scars in a fossilised leaf from Germany.

Today, hundreds of species of Cordyceps fungi infect a wide variety of insects, including ants. Like many parasites, they can manipulate the way their hosts behave. One species, Cordyceps unilateralis, changes the brains of its ant hosts so that they find and bite into leaves, some 25cm above the forest floor. The temperature and humidity in this zone are just right for the fungus to develop its spore capsules. In its dying act, the ant leaves a distinctive bite mark that’s always on one of the leaf’s veins on its underside. And that’s exactly what Hughes saw in his fossil leaf.

Hughes originally thought that the marks were made by an insect cutting the veins of the leaf to drain away any potential poisons, something that modern insects also do. But these marks look very different – those on the fossil leaf bear a much closer resemblance to those of Cordyceps-infected ants. This is the first fossil trace of a parasite manipulating its host, but it’s not the oldest evidence for such a relationship. In 2008, another American group found a 105-million-year-old piece of amber containing a scale insect, with two Cordyceps stalks sticking out of its head. The war between insects and their Cordyceps nemeses is an ancient one indeed.

Reference: Biology Letters http://dx.doi.org/10.1098/rsbl.2010.0521