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.
We’ve all had that annoying feeling when we fail to find a word that’s just at the tip of our tongues. Usually, these moments are passing nuisances, but they are a more severe impediment for a British family known as JR. Eight of them suffer from an unusual problem with “semantic cognition” – the ability to bind words to their meanings during thought or communication.
They can’t remember words, names, or topics of conversation – all of us get this, but the JR family experiences a more extreme version. They make errors in everyday conversations when they use words with related meanings in the wrong places. Their comprehension falters to the extent that reading books or following films is hard work.
These difficulties have caused them much social anxiety, and hampered their ability to cope with school and work. But for scientists, they are undeniably exciting because they seem to stem from a single errant gene. If that’s the case, the gene apparently affects the intertwining of concepts and language, but not any other mental abilities – the affected family members are otherwise intelligent and articulate. The JR family could lead us to new insights about language, thought and memory, just as similar families have done in the past.
The tunes embedded above weren’t written by a composer, but fashioned through natural selection. They are the offspring of DarwinTunes, a program which creates bursts of noise that gradually evolve based on the preferences of thousands of human listeners. After hundreds of generations, tracks that are boring and grating soon morph into tunes that are really quite rhythmic and pleasant (even if they won’t be topping charts any time soon).
DarwinTunes is the brainchild of Robert MacCallum and Armand Leroi from Imperial College London. “We suspected that musical styles evolve through Darwinian natural selection,” says MacCallum. “They are copied and modified from artist to artist and generation to generation, with popular styles more likely to be copied as they get more exposure. “ The duo created DarwinTunes to see if music could actually evolve in this way.
The DarwinTunes tracks are all 8-second-long loops, each encoded by a ‘digital genome’ – a program that determines which notes are used, where they’re placed, the instruments, the tempo, and so on. The genomes of two parent loops can shuffle together in random ways to produce daughter loops, which also develop small random mutations. This mimics the way in which living things mate and mutate. It also mimics the way in which composers merge musical styles together, while inventing new motifs.
The experiment began with 100 randomly generated loops. On the DarwinTunes website, listeners could listen to these and rate them on a five-point scale, from “I can’t stand it” to “I love it”. Every time 20 loops were rated, the top 10 pair off, mate with each other to produce two daughters, and die. At any time, there are only 100 loops in the total population.
To date the loops have been evolving for 3,060 generations, and over 50,000 of them have been born. By taking loops from DarwinTunes’ entire history and asking volunteers to rate them, MacCallum and Leroi showed that they became more appealing with time. For example, they were more likely to contain chords found in Western music and they contained more complex rhythms. “We hoped for slightly more “advanced” music, but were very happy with the results,” says MacCallum.
This upward rise in appeal only lasted for 500 or 600 generations. After that, the loops hit a plateau and apparently stopped evolving. MacCallum and Leroi think that this is because the loops become so complex that their intertwining melodies and rhythms don’t merge very well. The act of mating, rather than combining the best of both parents, ends up splitting up elements that work well together.
Alternatively, it may be that as the loops become well adapted to the tastes of their listeners, it becomes harder to change them without messing something up – they become trapped in an adaptive peak, unable to reach a new peak without first crossing into a valley. Both of these processes have their counterparts in the world of real genetics. MacCallum and Leroi argue that this might explain why many old musical styles tend to be very conservative, changing little over thousands of years.
DarwinTunes is the latest in a line of digital evolution programs, where computer code copies itself, mutates, evolves and adapts. For example, in The Blind Watchmaker, Richard Dawkins describes a programme of the same name that can evolve complex shapes from initially simple collections of lines. These programs never fully reflect the reality of evolution, but they allow scientists to ask basic questions about evolution in a controlled way. They can set up controlled experiments, repeat them, replay evolution from specific points, and analyse how specifically their artificial creations have changed. It’s incredibly hard (but not impossible) to do that with actual living things.
But Michael Scott Cuthbert, who works on computer-aided musical analysis at MIT, is sceptical that the approach tells us anything about the evolution of music. “They have shown that people can sense a glimmer of the things they like about music even when most of it consists of sounds they hate,” he says. “But it doesn’t give any information about why music sounded differently in the past, why people like different things today, or how music might evolve in the future.”
“Suppose you randomly threw car parts into piles and asked people to rate those they’d most like to buy,” he says. “Then you took parts from the highest-rated heaps, and rearranged them into new heaps. People might hate all of them at first, but they’d probably rate the ones with four tires or a trunk in the back or a steering wheel in the drivers’ seat higher than the rest. Do that long enough and I wouldn’t be surprised that you’d eventually get something that looked like a 2011 Honda Civic. But that doesn’t mean that that’s how a car is made.”
MacCallum and Leroi acknowledge that real music changes in a more complex way than DarwinTunes currently captures. Composers write music with their own intentions, while listeners choose music based not just on what it sounds like, but on whether other people like it too. DarwinTunes could be changed to include these dynamics – volunteers could combine the loops themselves, and listeners could see earlier ratings.
“The big question for me is can we bring the quality up a level where you don’t have to be curious about the science to take part?” says MacCallum. “We can do that if we had millions of users, and segregated them based on musical genre preferences. It’s a chicken and egg problem though!”
Reference: MacCallum, Mauch, Burt & Leroi. 2012. Evolution of music by public choice. PNAS http://dx.doi.org/10.1073/pnas.1203182109
Image by Pedro Sanchez
More on music:
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.