Leptopilina boulardi is a wasp that lays its eggs in fly maggots. When the wasp grub hatches, it devours its host form the inside out, eventually bursting out of its dead husk. A maggot can only support a single grub, and if two eggs end up in the same host, the grubs will compete with one another until only one survives. As such, the wasps ensure that they implant each target with just one egg. And if they find a caterpillar that has already been parasitized by another L.boulardi, they usually stay away. Usually, but not always.
L.boulardi is sometimes infected by a virus called LbFV, which stands for L.boulardi filamentous virus. And just as the wasp takes over the body of its maggot target, so the virus commandeers the body of the wasp. It changes her behaviour so that she no longer cares if a maggot is already occupied. She will implant her eggs, even if her target has an existing tenant. After infected wasps are finished, a poor caterpillar might have up to eleven eggs inside it.
The virus’s manipulation is extraordinarily specific. An infected wasp moves much less, and grows slightly slowly, but her odds of survival stay the same. The virus barely harms her health. Nor does it affect her ability to detect the scent of a maggot or a mate. It only seems to affect her attitude to the one-egg-one-maggot rule.
How does it do this? We don’t know. Why does it do it? That much is clearer: by changing the wasp’s behaviour, the virus spreads itself. The virus is heritable, and female wasps transmit it to their own eggs. From there, the virus can jump into any other eggs in the vicinity. So if a wasp implants a maggot that carries someone else’s egg, the virus gets a new lineage of wasps to infect. Julien Varaldi from the University of Lyon first discovered LbFV in 2003, and he has spent the last decade unveiling the quirks of its wasp-management ability. Now, he has found another twist in its relationship with its insect vessels.
The same French countryside is home to a closely related wasp called Leptopilina heterotoma. It targets the same flies as L.boulardi and both species will lay eggs in maggots occupied by the other. If they do, they compete, and L.boulardi typically wins. Varaldi kept maggots in vials with equal numbers of both wasps, and he found that 92 per cent of the insects that eventually burst out of the doomed larvae were L.boulardi. The same thing happened when Varaldi set up more realistic cages containing flies and both wasps. In every case, L.boulardi monopolised the maggots and L.heterotoma died off.
But the LbFV virus turns the tables of this competition. The virus never infects L.heterotoma, and when it infects L.boulardi, it weakens its competitive edge. In the vial experiments, the grubs of both wasp species suddenly did as well as one another. In the cage set-ups, L.heterotoma actually managed to eliminate L.boulardi on three of five trials.
Why? The virus makes L.boulardi waste its eggs. Under normal circumstances, it lays one egg per host, and saturates the supply of available maggots with its spawn. If L.heterotoma lays in these infected caterpillars, its young are bested by L.boulardi’s within their shared host. But thanks to LbFV, L.boulardi puts its eggs into too few baskets, leaving plenty of maggots for L.heterotoma to attack unimpeded.
This discovery helps to explain why there’s room enough in the same French fields for both wasps, even though they compete for the same hosts. Other scientists have suggested that they might keep to different schedules, or stick to restricted areas. Instead, Varaldi’s study suggests that the key to this tenuous co-existence could be a inherited, mind-controlling virus. Using a mathematical model, Melanie Hatcher, Jaimie Dick and Alison Dunn predicted an interaction exactly like this in 2008. They showed that if a parasite has more harmful effects on the ‘stronger’ of two competing species, it’ll allow a ‘weaker’ one to persist, or even dominate an ecosystem. The case of the virus and the two wasps is a perfect example of the trend that they envisioned through equations.
The standard way for [a virus] lambda to get into a cell is to latch onto its outer membrane, attaching to a particular kind of molecule on the surface of E. coli. It can then inject its genes and proteins into the microbe.
Mr. Meyer set up an experiment in which E. coli made almost none of the molecules that the virus grabs onto. Now few of the viruses could get into the bacteria. Any mutations that allowed a virus to use a different surface molecule to get in would make it much more successful than its fellow viruses. “It would have a feast of E. coli,” Dr. Lenski said.
The scientists found that in just 15 days, there were viruses using a new molecule — a channel in E. coli known as OmpF. Lambda viruses had never been reported to use OmpF before.
Mr. Meyer was surprised not just by how fast the change happened, but that it happened at all. “I thought it would be a wild goose chase,” he said.
To see if this result was just a fluke, Mr. Meyer ran his experiment again, this time with 96 separate lines. The viruses in 24 of the lines evolved to use OmpF.
The researchers sequenced the genomes of the evolved viruses and were surprised to find that this transformation always required four mutations. In all the lines that could grab OmpF, those four mutations were identical, or nearly so. No single mutation could allow the viruses to start latching onto OmpF. Even three out of four mutations brought no change. Only after they developed all four mutations could the viruses make the switch. …
Some critics have argued that full-blown evolution would not be able to mimic the highly artificial Dutch experiment. The chances that a single virus would acquire so many mutations at once are certainly small. In the case of lambda viruses, Mr. Meyer estimates the chance of all four mutations arising at once is roughly one in a thousand trillion trillion. [emphasis added]
Yet the lambda viruses repeatedly acquired all four mutations in a matter of weeks. “There’s this thinking that it all has to come together at once,” Dr. Lenski said. “But that’s just not how evolution works.”
[Hagfish] are disgusting feeders. They burrow deep into corpses and eat their way out, and can even absorb nutrients through their skin. And if they’re threatened or provoked, they produce slime – lots of slime, oozing from the hundreds of pores that line their bodies. ...
The hagfish in the videos are attacked by sharks, conger eels, wreckfishes and more. In less than half a second, the predator’s mouth and gills are filled with slime. It leaves, gagging and convulsing, slime hanging in long wisps from its head. Even voracious seal sharks turn tail. ...
Hagfish are well known for their ability to tie themselves in knots, which can travel down the length of their bodies. This could help to clear their own bodies of slime (they can choke on their own mucus) or free themselves from the grip of a predator.
Nuclear and mitochondrial genes must produce proteins that work together. This has some significant implications.
Life on us
- Rob Dunn
- Carl Zimmer
From Zoologger in NewScientist.
Ciliates [use] their hair-like cilia to motor around rapidly in water. Most get their food by eating other organisms, rather than by synthesising the nutrients themselves. This marks them as quite animal-like.
Some Mesodinium species are different, though. They engulf other microorganisms, generally algae called cryptomonads. The two then form a partnership: the algae produce sugars by photosynthesis, while the Mesodinium protects them and carries them around.
Such hybrid organisms are animals and plants at the same time. One such species, M. rubrum, only eats red algae and is often found in the algal blooms that form the famous red tides. …
M. chamaeleon takes in algal cells, just like M. rubrum, but it doesn't keep them permanently. Nor does it digest them immediately, as a hungry animal-like organism might. Instead, the cells remain intact for several weeks before being broken down, during which time they keep producing sugar by photosynthesis. M. chamaeleon also changes colour depending on whether it is hosting red or green algae or both.
"It is quite unusual," says Moestrup. Other Mesodinium species either retain their captured cells for ages or digest them immediately.
The ability to take in other cells and put them to work is called endosymbiosis, and is one of the most important inventions in the history of life. Some 2 billion years ago, a single cell swallowed a bacterium and used it as an energy source. The descendants of the enslaved bacterium eventually became the mitochondria that now power all complex cells, including ours. Without endosymbiosis, there wouldn't be any multicellular life.
While the first endosymbiosis may have been a lucky chance, the process now seems to be common, at least among the more complex single-celled organisms. Some are so good at taking in cells that over the years they have switched symbionts. "It happens quite regularly," Moestrup says.
Plants have evolved to eat animals at least six times, and over 600 species of them now do so. They catch their prey with slippery water-filled pitchers, fast-snapping traps, sticky leaves and sucking bladders.
Glowing bacteriaFrom Not Exactly Rocket Science.
The glowing waters are the work of bioluminescent bacteria – microbes that can produce their own light. ...
Creating light takes energy, and it’s not something that’s done needlessly. So why do the bacteria shine? One of the most common answers … is that the bacteria are screaming “Eat me!” at passing fish. A fish’s guts are full of nutrients, and it can carry bacteria across large distances. The bacteria, by turning themselves into glowing bait, get a lift and a meal. …
The shrimp and other zooplankton aren’t out to eat the bacteria themselves. Instead, they’re after what the microbes are sitting on. The bacteria cluster around bits of food floating around the ocean. They only glow when they gather in enough numbers, so their light is indicative of a big enough morsel. …
For the bacteria … the benefits are clear: they get to bathe in the slosh of nutrients within a fish’s guts, and they get to travel a thousand times further than they could manage on their own.
Zombie antsFrom Parasite of the day.
For the fungus (which had infected an ant) to successfully reproduce, the ant must die - but it must die in a particular position to maximise the viability and dispersal of the fungal spores, specifically in the humid understory, hanging from the underside of a leaf, about 25 cm (about 10 inches) above the ground. But once the fungus maneuver the ant into position, how does it get the host to comply and stay there? The researchers made fine histological cross-section of the infected ant's head and found that once the fungus has made the ant locks its mandible in place, it busily gets to work dissolving the muscles which control those mandibles, ensuring that the ant will be locked in a death grip forevermore. A few days after the ant dies while gripping onto, the fungal stalk emerges from the head of the ant, ready to spray its spores down to the soil below to create more drunken "zombie ants".
Midsize cane toads lure younger cane toads, which the bigger toads then swallow whole. A mother caecilian, top right, stays by her young and literally feeds them herself. Tamarin monkeys don't eat their offspring, except when they do. The female redback spider makes a meal of her mates.
Flowers and bees
From Smithsonian Magazine.
[The bees] evolved first, …, at least 12 million years before the orchids. “The bees evolved much earlier and independently, which the orchids appear to have been catching up,” says the study’s lead author, Santiago Ramirez, a post-doc at the University of California at Berkeley. And as the bees evolve new preferences for these chemical compounds, the orchids follow, evolving new compounds to lure back their bee pollinators.Illustrates making use of a service that already exists.
[A] sexually transmitted virus … infects corn earworm moths, transforming females into infertile but sexually irresistible zombies, which then spread infection to unsuspecting smitten males.
The females attract males through a pheromone, Burand said, and in experiments infected females were found to be sending out five times as much as uninfected ones. The experiments also showed that males chose infected females twice as often as their healthy counterparts.
In the normal mating scenario, the male leaves behind not only his sperm but a protein that causes the female to stop wafting out her scent, so she mates only once per night.
When she's infected, Burand said, the male chastity-inducing protein stops working, and instead of mating with one male per night, a female will mate with about 12. But since the virus renders her infertile, the only organism to benefit from her newfound promiscuity is the virus.
It is dawn in a European forest, and gypsy moth caterpillars are looking for somewhere to hide. With early birds starting to rise, the caterpillars will spend the day in bark crevices or buried in soil. But one of them is behaving very strangely. While its peers head downwards, this one climbs upwards, to the very top of the highest leaves. It has come to die.
At the top of its plant, the caterpillar liquefies. Its body almost seems to melt. As it does, it releases millions of viruses, dripping them onto plants below and releasing them into the air. These viruses are the agents that compelled the caterpillar to climb, and eventually killed it. They are baculoviruses, and they cause a condition known aptly as Wipfelkrankheit – the German for “tree top disease”.
By ensuring that their hosts die in a high spot, the viruses benefit in two ways. First, that’s where uninfected caterpillars pupate and turn into adults. Female gypsy moths don’t fly. When they emerge, they walk over the same bark and leaves that their infected peers, now dead and molten, have laced with viruses. They risk infection with every footfall, and they might even contaminate their own eggs. The high position also allows the viruses to spread on gusts of wind. They can travel over long distances before descending upon fresh hosts in bursts of infectious rain.
What makes C. hypocistis unusual is that while most fruit-bearing plants rely upon vertebrate animals to disperse their seeds, C. hypocistis mainly uses a beetle. Researchers found that the seeds collected from beetle frass (fancy name for insect poop) are just as viable as seeds which are collected directly from the fruit. While rodents and rabbits also frequently consume C. hypocistis fruits, because they have a tendency to eat immature fruits and deposit their dung (with any viable seeds) at ground level, they are not as effective as the beetles. Not only do the beetles consume only fully-ripened fruits, they also have a tendency to bury themselves into the sand during midday, which can bring the seeds closer to the roots of the host plant.
Among the back-boned vertebrates, there are only four groups that can sense infrared radiation. Vampire bats are one, and the other three are all snakes – boas, pythons, and pit vipers like rattlesnakes.
Last year, Gracheva and Cordero-Morales showed that the serpents’ sixth-sense depends on a gene called TRPA1, the same one that tells us about the pungent smells of mustard or wasabi. Boas, pythons and vipers have independently repurposed this irritant detector into a thermometer.
Vampire bats evolved their ability in a similar way, but they have tweaked a different protein called TRPV1 that was already sensitive to heat. Like TRPA1, TRPV1 also alerts animals to harmful substances. It reacts to capsaicin, the chemical that makes chillies hot and allyl isothiocyanate, the pungent compound that gives mustard and wasabi their kick. In humans, it also responds to any temperature over 43 degrees Celsius. The vampire has simply tuned it to respond to lower temperatures, such as those of mammal blood.
More Wasp tricksFrom "Parasitic Wasp Employs Zombie Ladybug to Guard Cocoon."
Dinocampus coccinellae hatches inside the belly of a host [ladybug] following some makeshift, catastrophic surgery by its parent … Normally, the host organism mercifully dies at this point, but DC’s ladybug is not so lucky. Not only does it live, but a little behavior modification forces it to hang around and “guard” its parasite-baby as it grows into adulthood beneath its protective bulk. Scientists believe that secretions left by the larva when it bursts out might play a role in reprograming the host.
But then the ladybug dies right? Surely once the wasp reaches adulthood, our long-suffering host can at last rest in peace. No such luck. This is the insect world, after all. The researchers found that 25 percent of the manipulated ladybugs recovered normal behavior following their ordeal.
Sensing magnetic fields
The connections between light, cryptochrome and a magnetic sense were laid out by Klaus Schulten and Thorsten Ritz in 2000, in a bravura paper that united biology and quantum physics. They suggested that when cryptochrome is struck by blue light, it transfers one of its electrons across to a partner molecule called FAD. Electrons normally waltz around in pairs, but thanks to the light, cryptochrome and FAD now have lone electrons. They are known as a “radical pair”.
Electrons also have a property called “spin”. In a radical pair, the spins of the two solo electrons are linked – they can either spin together or in opposite directions. These two states have different chemical properties, the radical pair can flip between them, and the angle of the Earth’s magnetic field can influence these flips. In doing so, it can affect the outcome or the speed of chemical reactions involving the radical pair. This is one of the ways in which the Earth’s magnetic field can affect living cells. It explains why the magnetic sense of animals like birds is tied to vision – after all, cryptochrome is found in the eye, and it’s converted into a radical pair by light.
Subsurface lifeFrom Not Exactly Rocket Science
There are more microbes in the subsurface (bacteria, and the extreme archaea) than there are up top, and collectively, they might even outweigh all surface life. Put every tree, elephant and human on a giant scale, and they’d be balanced by the microscopic masses that lurk underground.
To H.mephisto and the other nematodes, the subterranean world is an all-you-can-eat larder. They feed on bacteria and other microbes that grow in rich mats on the rocky surface. There are up to a trillion such cells for every one nematode, a feast that could keep H.mephisto going for around 30,000 years. There’s no risk of starving underground.
There’s clearly more going on below our feet that anyone had previously thought. “The nematodes eat the deep subsurface bacteria and the bacteria will certainly feast on dead nematodes,” says Borgonie. Nematodes aren’t the only threats that the subsurface bacteria face. In deep Swedish groundwater, Pedersen has found hordes of viruses that infect bacteria, often in numbers greater than those of their prey. The bacteria aren’t the only inhabitants of this underground world – they’re just part of its food web.
We live on a microbial planet. There are one million microbial cells per cubic centimeter of water in our oceans, lakes and rivers; deep within the Earth's crust and throughout our atmosphere. We have more than 100 trillion microbes on and in each of us. The Earth's diversity of life would have seemed like science fiction to our ancestors. We have microbes that can withstand millions of Rads of ionizing radiation; such strong acid or base that it would dissolve our skin; microbes that grow in ice and microbes that grow and thrive at temperatures exceeding 100 degrees C. We have life that lives on carbon dioxide, on methane, on sulfur, or on sugar. We have sent trillions of bacteria into space over the last few billion years and we have exchanged material with Mars on a constant basis, so it would be very surprising if we do not find evidence of microbial life in our solar system, particularly on Mars.
VirusesThis is from (Zimmer, Carl (2011). A Planet of Viruses (Kindle Locations 346-356). University of Chicago Press. Kindle Edition.)
Many … viruses, such as rhinoviruses and influenza viruses, reproduce violently. They make new viruses as fast as possible, until the host cell brims with viral offspring. Ultimately, the cell rips open and dies. HPV uses a radically different strategy. Instead of killing its host cell, it causes the cell to make more copies of itself. The more host cells there are, the more viruses there are.
Speeding up a cell’s division is no small feat, especially for a virus with just eight genes. The normal process of cell division is maddeningly complex. A cell “decides” to divide in response to signals both from the outside and the inside, mobilizing an army of molecules to reorganize its contents. Its internal skeleton of filaments reassembles itself, pulling apart the cell’s contents to two ends. At the same time, the cell makes a new copy of its DNA—3.5 billion “letters” all told, organized into 46 clumps called chromosomes. The cell must drag those chromosomes to either end of the cell and build a wall through its center. During this buzz of activity, supervising molecules monitor the progress. If they sense that the division is going awry—if the cell acquires a defect that might make it cancerous, for example—the monitor molecules trigger the cell to commit suicide. HPV can manipulate this complex dance by producing just a few proteins that intervene at crucial points in the cell cycle, accelerating it without killing the cell.
Jennifer Frazer (4/2011) on Bombardier Beetles, Bee Purple, and the Sirens of the Night
With algae inside them, the [salamander larvae] become solar-powered animals, capable of directly harnessing the energy of the sun in the style of plants. …
When the salamanders are still larvae, and well before they become adults, most of their algae disappear. The adults, after all, have opaque bodies and spend most of their lives underground—conditions that are less than ideal for a light-dependent alga. Kearney thinks that the dying algae could provide one final boon to their hosts, providing them with an extra burst of nutrients.
From NewScientist Zoologer.
When migratory moths and butterflies emerge from their chrysalises in autumn in northern Europe, they immediately start flying south. When the next generation emerges on the Mediterranean coast the following spring, they start flying north. How do these creatures know where their breeding grounds are, when none of them lives to make the return trip?
It seems they don't. After the adults emerge, they simply travel in a hard-wired direction until they become sexually mature. How far an insect migrates depends on the length of this genetically determined phase. Migrants don't decide where to land based on the weather or the vegetation: they land when they reach the insect equivalent of puberty.
Many will land in unsuitable locations and fail to breed, but that's not a huge problem as long as a few of them end up somewhere sensible. A mating pair of insects produces thousands of eggs. The offspring that migrate to inhospitable climes will die, but the chances are that hundreds of their siblings will land somewhere more appropriate. Insects only need about 1 per cent of their offspring to survive to sustain the species.
There is evidence that climate change is already altering insect migration patterns. Steadily increasing numbers of migratory moth and butterfly species are being recorded arriving in a cliff-top garden at the Portland Bird Observatory in Dorset, on England's south coast. From data collected between 1982 and 2005, it appears that for every 1 °C increase in temperature, an extra 15 species will arrive (Journal of Entomology, vol 104, p 139).
Anthrax as controlled by phages (viruses)
From Scientific America.My Comment.
This is a beautiful example of a complex system that we are beginning to understand. It would be very useful as an illustration of how complex systems function.
Assassin bugs stalk and lure their hapless preyFrom New Scientist.
Moths hitch rides on wind currents
Every year, an enormous migration takes place in Western Europe. Millions of moths fly for days, riding wind currents southward in the fall and north in the spring.
Scientists thought these insects were simply blown to their destinations, but now they've discovered something remarkable: The moths actually select the fastest wind currents, and even change course to shorten their trip.
See Moths hitch rides.
When Built-In Antifreeze Beats a Winter CoatFrom Sean Carroll in the NY Times.
To tolerate freezing, it is crucial that insects minimize the damage that freezing (and thawing) would normally cause.
Insects have evolved a variety of cryoprotective substances. As winter approaches, many freeze-tolerant insects produce high concentrations of glycerol and other kinds of alcohol molecules. These substances don’t prevent freezing, but they slow ice formation and allow the fluids surrounding cells to freeze in a more controlled manner while the contents of the cells remain unfrozen.
For maximum protection, some Arctic insects use a combination of such cryoprotectants and antifreezes to control ice formation, to protect cells and to prevent refreezing as they thaw.
Whatever Doesn’t Kill Some Animals Can Make Them Deadly
Sea slugs can produce chlorophyllFrom MSNBC.
The green sea slug, which is part animal and part plant, produces its own chlorophyll and so can carry out photosynthesis, turning sunlight into energy.See Sea slug.
From A Gazillion Tiny Avatars by Olivia Judson in the New York Times.
Fortunately for us, most viruses don’t attack humans; they attack bacteria and other microbes, which they kill on a colossal scale. In the oceans alone, viruses are reckoned to kill about 100 million metric-tons’-worth of microbes every minute. One hundred million metric tons! Given that a typical bacterium only weighs a tiny, tiny fraction of a gram (and there are a million grams in a ton), that is one huge number of dead microbes. (For anyone who doesn’t use the metric system, one metric ton is a little bigger than the American short ton; there are just over 28 grams in an ounce.) Viruses are thus important, if tiny, avatars of the grim reaper.
Which has several interesting consequences.
One is that viruses play a fundamental role in regulating the food chain. This is because death-by-virus is different from death-by-predator. When a predator kills a microbe, it consumes it: the microbe’s cell is incorporated into the predator’s body. In contrast, when a virus kills a microbe, the microbe’s cell bursts open, or “lyses,” releasing new viruses and a lot of cellular debris back into the environment. This debris can then be consumed by other microbes. In other words, by lysing their victims, viruses are constantly making food available to other life forms.
A second consequence of all this viral activity is the role viruses play in evolution. An ability to resist viral attack has sculpted the genomes of all known organisms, from bacteria to humans. (Why, then, do viruses remain dangerous? The answer to this is complex, but part of the reason is that they are often able to stay one step ahead of their hosts, because viruses tend to evolve very fast. So if the host evolves a new way to detect and disable an intruder, sooner or later the virus will evolve a new way to evade the trap. This is one reason viral diseases are so hard for us to treat.)But here’s what I find most interesting of all. Viruses don’t just cause other organisms to evolve. They are also important sources of new genes. The reason is that as viruses move in and out of host cells, they sometimes take a few host genes with them, or leave some of their own behind. Thus, although viruses are among the most destructive forces of nature, they are also among the most potent forces of creation. …
See also, Moreira, David and Purificación López-García (2009) "Ten reasons to exclude viruses from the tree of life," Nature Reviews Microbiology, April 2009 | VOlUME 7. Also see some responses and the author's response to the responses.
Sea urchin "see" with their entire bodies
See Sea urchin for the complete story.
Brussels Sprouts Like to Live, Too
From NY Times.
The more that scientists learn about the complexity of plants — their keen sensitivity to the environment, the speed with which they react to changes in the environment, and the extraordinary number of tricks that plants will rally to fight off attackers and solicit help from afar — the more impressed researchers become, and the less easily we can dismiss plants as so much fiberfill backdrop, passive sunlight collectors on which deer, antelope and vegans can conveniently graze. It’s time for a green revolution, a reseeding of our stubborn animal minds.
When plant biologists speak of their subjects, they use active verbs and vivid images. Plants “forage” for resources like light and soil nutrients and “anticipate” rough spots and opportunities. By analyzing the ratio of red light and far red light falling on their leaves, for example, they can sense the presence of other chlorophyllated competitors nearby and try to grow the other way. Their roots ride the underground “rhizosphere” and engage in cross-cultural and microbial trade.
“Plants are not static or silly,” said Monika Hilker of the Institute of Biology at the Free University of Berlin. “They respond to tactile cues, they recognize different wavelengths of light, they listen to chemical signals, they can even talk” through chemical signals. Touch, sight, hearing, speech. “These are sensory modalities and abilities we normally think of as only being in animals,” Dr. Hilker said.
See Intelligent plants for the complete article.
Assembling Gradient Sensors
- Bacteria cluster thousands of transmembrane chemoreceptors at opposite ends of the cell, allowing them to detect and follow food molecule gradients. Might the formation and maintenance of such clusters occur via stochastic assembly? To test this idea, Greenfield et al. used photoactivated localization microscopy (PALM) to count single fluorophore-tagged receptors with an optical resolution of 15 nm. They analyzed 1 million receptors and observed that many were present as singletons or small clusters in lateral regions of the cell (shown at left). A mathematical model in which the receptors are inserted randomly into the membrane, but can then be captured and incorporated into existing clusters, accounted for the observed distribution and predicted that the density of new clusters would be highest at a point farthest from a large cluster. Hence, through stochastic assembly, a cell with a large cluster at one pole will form a new large cluster at the opposite pole. Receptor clusters of appropriate size and stability thereby assemble without any specific cellular machinery to position the receptors.
Upward growing root systems
- Land plants have evolved a variety of specialized adaptations to gather nutrients from unlikely substrates, such as Amazonian trees whose roots grow upward on the bark of neighboring trees. The latest discovery—the snow roots of an alpine plant—comes from 2800 m in the Caucasus Mountains. Onipchenko et al. found that the herbaceous plant Corydalis conorhiza (a member of the poppy family) produces extensive networks of roots that grow upward and laterally into the snowpack that carpets the high slopes until the July thaw. Isotope experiments showed that these roots, which are anatomically distinct from the normal roots that grow downward into the soil, take up nitrogen directly from the snow-pack, thus exploiting a resource that would otherwise disappear down the mountainside during the brief summer.
Adding oregno to corn
- Many plants emit signals to augment their defenses against attack by insects; some of these signals are known to work by attracting predators of the attackers. Maize roots under threat from larvae of the western corn rootworm normally emit the terpene caryophyllene, which serves to mobilize nematodes that then kill these larvae. However, most cultivated maize has lost the capacity to produce this terpene.
- Degenhardt et al. have engineered transgenic maize plants that carry a caryophyllene synthase gene from oregano. This manipulation restored the production of this compound, with the consequence that nematodes reduced the number of rootworms by more than half, resulting in much less root damage. This finding confirms that nematodes can be recruited effectively by caryophyllene and provides the basis for a pest biocontrol strategy to improve cultivated plants.