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.
There are few viruses more capable to grabbing headlines at the moment than H5N1, more commonly known as bird flu. It has certainly been discussed to death in the media over the last several months, after it emerged that two scientists had evolved mutant strains that can spread between ferrets. The first of those papers was published last month (I covered it for Nature News then) and the second comes out today (I’ve covered for Nature News now).
The fact that the papers are out is unlikely to quench the controversy about these mutant viruses. It’s a controversy that threatens to distract from a more important fact: we still know surprisingly little about H5N1. I’ve spent the last few weeks talking to flu researchers and it’s amazing how many basic questions about the virus we still have to answer.
Where is it, and how many people have been infected? How does it kill and, for that matter, why doesn’t it kill more people? Why did one particular lineage spread around the world, when other bird flu viruses have not? Given that the virus apparently evolve the ability to spread between mammals, as the controversial papers show, why hasn’t it already done so? And perhaps most importantly, what will it do in the future?
I’ve written a bigger story for Nature about these issues, corralled into five questions on H5N1. In a brilliant play on words, the story has been titled “Five Questions on H5N1”. Go have a look, if only to smile at the cute little cartoon viruses with their angry teeth and eyes.
Image by Martin Correns
Flesh-eating plants are basically nitrogen thieves. The speed of their growth is limited by this invaluable element, just like all other plants. The difference is that plants that eat animals, like pitcher plants and the Venus fly trap, grow in places like swamps and rocky outcrops, where nitrogen in thin on the ground… or thin in the ground. They have to supplement their supply by stealing nitrogen from the bodies of animals. This is why some plants become killers.
Let me clarify that: this is why some plants become obvious killers. Scott Behie from Brock University has found that a far greater range of plants can inconspicuously assassinate animals by proxy. They partner up with an infectious fungus that kills insects and transfers their precious nitrogen to the plant. Thanks to the fungi, the plants become indirect predators.
Prions are villains worthy of any comic book. They are infectious misshapen proteins that can convert their normal peers into their own twisted images with a touch. As their numbers grow, they gather in large groups and destroy brain tissue. They cause diseases such as mad cow disease, Creutzfeld-Jacob disease (CJD) and scrapie.
And they’re not alone. It seems that many brain diseases are also caused by clusters of misfolded proteins that can seed fresh groups of themselves. The list includes Alzheimer’s, Parkinson’s and Lou Gehrig’s diseases. None of these are infectious – the proteins behind them can’t spread from one individual to another, but there is mounting evidence that they can trigger waves of corrupted shapes within a single brain.
I wrote about the latest such evidence in Alzheimer’s disease for The Scientist. Here’s a taster. Head over there for more.
You’re barely human. For every one of your own cells in your body, there are many microbial ones. They not only outnumber you, but they affect your health and your mind. Bits and pieces of this microbial menagerie have been revealed over time, but a massive study – the Human Microbiome Project – has just unveiled the most thorough picture yet of the microscopic majority that colonises us.
I wrote about this for The Scientist, so head over there to guzzle the details.
The key point, however, is individuality. While some broad groups of microbes that everywhere, the study failed to find any species that are universally present in the same body part across all people. However, those incredibly diverse microbes do very similar things. Curtis Huttenhower, the lead author of this consortium of hundreds, compared the situation to the fact that every city has lawyers, bankers and salesmen, even though different individuals play those roles in different places.
Even though most spiders are harmless to us, many people suffer from a crippling fear of them. Imagine then, what a grasshopper must feel. The threat of venomous fangs isn’t something that the insects can shrug off. It’s a perpetual danger that chemically alters their bodies, triggering changes that ripple through an entire ecosystem.
Now, Dror Hawlena from Yale University has found just how far-reaching these changes can be. In an elegant experiment, he showed that the fear instilled by spiders can extend into the very soil, affecting how quickly leaf litter decays.
Hawlena raised red-legged grasshoppers in outdoor enclosures, half a metre wide. Half the enclosures contained a single nursery-web spider, whose mouthparts had been glued shut, so they couldn’t actually kill any of the hoppers. Their presence, however, was felt.
A desert mouse has found a seed. It bites into it, and gets a pungent mouthful of mustard. Reeling from the chemical party in its mouth, its spits out the seed and unwittingly helps the seed’s producer – a Israeli desert plant called Ochradenus baccatus. By using chemical weapons, it converts rodents into an unwitting vehicles for its seeds.
Ochradenus produces yellow flowers and sweet, succulent, white berries. When a mouse bites into the berries, an enzyme in the seeds called myrosinase mixes with chemicals in the pulp called glucosinolates. Housed in their separate compartments, these substances are harmless. But when they are released by gnawing teeth, and mix together, the enzyme converts glucosinolates into a wide range of toxins. These include isothiocyanates, the substances that give mustard and wasabi their pungent kick. As the mouse breaks the berries, an explosion of mustard goes off in its mouth.
Michal Samuni-Blank from the Technion–Israel Institute of Technology in Israel filmed the spitting mice using motion-activated cameras in the Israeli desert. The mice would carry away clusters of fruit to eat them in sheltered rocky crevices. Once they got a mouthful, they spit out more than two-thirds of the pungent seeds. If Samuni-Blank treated the seeds to deactivate their stash of myrosinase, the mice ate more than 80 per cent of them.