Meet the world’s smallest farmer – a “social amoeba” that seeds new land with bacteria, which it then eats. Just as human farmers carry seeds and livestock when they move to new areas, the amoeba can prepare for harsh conditions by bringing a ready food supply with it. It joins ants, termites and humans on the list of creatures that practice agriculture.

The amoeba, Dictyostelium discoideum, is also known as a slime mould, but scientists who work with it sometimes use the more affectionate name of Dicty. Dicty spends most of its time as a single cell, oozing through the undergrowth in search of bacteria to eat. When they run out of prey, the amoebas unite to form a many-celled mobile slug. When the slug finds a good spot, it stretches upwards to form a ball at the end of a stalk. The ball is loaded with spores, which eventually blow free on the wind. When they land, they hatch into new amoebae and the life cycle begins again.

Scientists pieced together Dicty’s life cycle decades ago, but it still carries surprises. Debra Brock from Rice University captured 35 wild amoebas from Virginia and Minnesota and found that a third of them carried bacteria in their slugs and spores. The bacteria hail from a number of different species, and half of these are found on Dicty’s menu. When the spores land in new locations, their bacterial cargo start to multiply, which provides the amoebae with food.

When Brock scattered spores in a sterile dish, she found that the “farmers” fared better. By seeding the dish with their bacterial cargo, they had a ready source of food. If the spores didn’t have any bacteria, the amoebae hatched to find a famine awaiting them. Very few completed their life cycle. Sterile soils may be rare in nature, but Brock found that the farmers kept their advantage when they landed in soil that had the wrong kind of bacteria. Dicty is a fussy eater, so it pays for it to carry around its preferred morsels.

This is a more passive style of farming than ants, termites or humans. Dicty doesn’t actually do anything to grow its bacteria, short of taking it to the right place. By contrast, ants and termites grow fungi by keeping it in just the right conditions, feeding it with leaves, and pruning away weed. Humans do the same for the crops that they farm.

There are, however, many similarities between the amoebae and the ants. Both are social species that spend a lot of time around their close relatives. For the amoeba farmers, this is important. If family (actually, clones) didn’t stick close together, then non-farmers could easily eat the leftover bacteria, or freeload off the ones that are cultivated by the travelling spores. By sticking together, they ensure that their descendants (who share the same genes) reap the benefits of their prudence.

Brock found that the farmers aren’t a special offshoot of Dicty’s family tree; they aren’t more closely related to each other than they are to other amoebae. But they are special. When Brock disinfected all the amoebae with antibiotics, only the former farmers could pick up new bacteria. But if the bacteria are so beneficial, why is it that only a third of the amoebae carry them? Brock got the answer when she scattered spores in a dish that was full of bacteria. With such bountiful meals everywhere, the farmers actually did worse. They were less likely to complete their life cycle than non-farmers.

Brock thinks that these farmers were suffering because of their prior prudence. Dicty only forms spores once it exhausts its supply of bacteria. To bring bacteria along, it needs to stop eating before its food is finished, saving some for later while their peers clean their plates. If they land somewhere without much food, their disadvantage fades into irrelevance because only they can cultivate more meals. If they land in a place with bountiful meals, their weaker condition proves to be their downfall. For the amoebas, agriculture can be a double-edged sword.

In other cases of animal agriculture, the farmer and the crop have come to depend on one another. Some types of fungus only exist because they are farmed by ants, and some damselfishes tend to gardens of unique algae, which don’t have any free-living relatives. By contrast, Dicty has a far more distant connection to its ‘crop’ – most amoebae aren’t farmers, and the bacteria can grow quite happily on their own.

This is probably because the amoebae cultivate a wide variety of bacteria. From a bacterium’s point of view, the risk of being eaten by Dicty is only worth taking if its cousins (carrying the same genes) can hitchhike to new areas. If many species of bacteria go along for the ride, these benefits are diluted. Since Dicty plays host to a wide variety of bacteria, there’s little impetus for any individual species to evolve in tandem with it.

For now, no one knows how long Dicty has been farming for. To find out, Brock will have to look at a diverse range of other amoebas and slime moulds to see if they also carry bacteria in their spores. If they do, then the practice is very old indeed. Dicty belongs to an ancient group of living things that sit next to animals and fungi on the tree of life. Their ancestors were among the first creatures to invade the land. If they have been cultivating bacteria for all that time, they would be the planet’s earliest farmers.

Reference: Brock, Douglas, Queller & Strassmann. 2011. Primitive agriculture in a social amoeba. Nature http://dx.doi.org/10.1038/nature09668

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Virtually all complex cells – better known as eukaryotes – have at least two separate genomes. The main one sits in the central nucleus. There’s also a smaller one in tiny bean-shaped structures called mitochondria, little batteries that provide the cell with energy. Both sets of genes must work together. Neither functions properly without the other.

Mitochondria came from a free-living bacterium that was engulfed by a larger cell a few billion years ago. The two eventually became one. Their fateful partnership revolutionised life on this planet, giving it a surge of power that allowed it to become complex and big (see here for the full story). But the alliance between mitochondria and their host cells is a delicate one.

Both genomes evolve in very different ways. Mitochondrial genes are only passed down from mother to child, whereas the nuclear genome is a fusion of both mum’s and dad’s genes. This means that mitochondria genes evolve much faster than nuclear ones – around 10 to 30 times faster in animals and up to a hundred thousand times faster in some fungi. These dance partners are naturally drawn to different rhythms.

This is a big and underappreciated problem because the nuclear and mitochondrial genomes cannot afford to clash. In a new paper, Nick Lane, a biochemist at University College London, argues that some of the most fundamental aspects of eukaryotic life are driven by the need to keep these two genomes dancing in time. The pressure to maintain this “mitonuclear match” influences why species stay separate, why we typically have two sexes, how many offspring we produce, and how we age.

Dancing out of step

Here’s the problem: both sets of genes help to create proteins that sit in the mitochondria and carry out one of the most important of chemical reactions: respiration. The proteins strip electrons from our food and pass them along from one to another. They eventually deposit the electrons onto oxygen; this produces water and releases energy. These ‘electron transfer chains’ are the stuff of life, and they only work if the proteins involved are built correctly.

The proteins in the chain are made of different subunits. Some are built using instructions from nuclear genes, while others are built using mitochondrial genes. They different parts must fit together with nanometre precision. Even a small change in their shape will produce botched proteins that fumble their electrons. If fewer electrons make it to the end of the chain, the mitochondria produce less energy. The leaking electrons can also react with oxygen directly to produce destructive molecules called free radicals.

So, cells with mismatched nuclear and mitochondrial genes face a double whammy of less energy and leaking free radicals. This has two important consequences for the evolution of eukaryotes: it creates a barrier between different species, and it favours the evolution of two sexes.

Within a species, the nuclear and mitochondrial genomes have adapted alongside one another so that their protein components seamlessly fit together. These dancers don’t swap their partners easily. If different species mate, they destroy this exquisite co-evolution, which might explain why hybrids encounter so many problems. Respiration is difficult for them, their mitochondria can’t produce any energy, they’re bombarded by leaking free radicals, and many of their cells top themselves. With so many problems, it’s no wonder that many hybrids become sterile or weak, or fail to develop properly at all. This is the price of a mitonuclear mismatch.

Why two sexes?

Mismatches can be easily weeded out by natural selection because every individual has the same mitochondrial genome in all of its cells. Those that match up well with the nuclear genome will survive; those that match poorly will die. This weeding process breaks down if individuals have many different types of mitochondria. In this scenario, the bad matches cancel out the good ones in any individual, and everyone ends up being decidedly average. Natural selection has little to work with.

Over time, individuals with a single mitochondrial genome will do better than those with many. The fittest of them will thrive thanks to natural selection, while their peers stagnate. Lane argues that one of the easiest ways of ensuring that an individual has a uniform set of mitochondria is to have two sexes. One (usually female) hands down an identical set of mitochondria to its young, and the other (usually male) doesn’t. That’s a major difference between the two sexes; some (including Lane) would argue it’s the main difference.

There are species that do things differently, but they are exceptions that prove the rule. Some slime moulds have 13 different sexes, but after mating, they destroy all but one set of mitochondria. Some fungi, like baker’s yeast, inherit mitochondria from both parents, but they are quickly separated so that individual cells only contain one type.

Here’s the gist: mitonuclear mismatches are easier to weed out if individuals test-drive one set of mitochondrial genes against one set of nuclear genes. And having two sexes is an easy way to do that.

The death threshold

The threat of mitonuclear mismatch can also explain the different lifestyles of different species. Mismatches cause a leak of free radicals and cells have two ways of dealing with that. If the leak is fairly minor, the cell can make more mitochondria to compensate. If the leak is severe enough, the cell commits suicide through a process called apoptosis. Lane’s idea is that there’s a threshold that determines which route a cell will take – a level of leakage where it chooses to cut its losses rather than fix the problem.

Different species set their ‘apoptotic threshold’ at different levels. For example, birds and bats need a lot of energy to fly, and their nuclear and mitochondrial genomes must match perfectly. The proteins of their mitochondria have to shunt electrons from one to another quickly and efficiently. Even slight mistakes would compromise their energy levels, and that can’t be tolerated.

So, birds and bats have very low leak thresholds. Even a slight trickle of free radicals betrays the fact that their two genomes aren’t meshing properly – time for their cells to die. Dying cells mean dying embryos, and many are eliminated before they fully develop. Only a precious few would make it through this harsh selection process. Lane thinks that this could explain why these species tend to have low fertility rates and few offspring.

By contrast, a rat has less demanding energy needs, and the electron transfer chain in its mitochondria can afford to be leakier and less efficient than that of a bird. The rat can handle a poorer mitonuclear match, so it sacrifices fewer embryos on the altar of perfection. It follows that rats are also more fertile, and produce larger litters.

Ageing apart

Even well-matched nuclear and mitochondrial genomes don’t stay that way forever. As individuals age, leaking radicals will damage and mutate the mitochondrial genome, ruining its match with the nuclear one, and causing even heavier leaks. This happens, even if the initial stream of radicals is small. As time wears on, the dancers inevitably fall out of step with each other. You can see this if you compare young and old tissues: the young cells will all have genetically identical mitochondria, while those in the old cells will be a mix of different mutants.

As more cells pass the tolerance threshold, more of them die. Tissues that use the most energy, like the muscles and brain, have the heaviest leaks and wear away faster. Meanwhile, the surviving cells experience even greater energy demands. They enter a downward spiral with sweeping consequences: they leak free radicals like sieves; their DNA becomes more fragile; their genes become switched on in different ways; they release chemicals that trigger inflammation. In short, they create the perfect set-up for cancer, heart disease, diabetes, Alzheimer’s and many of the other diseases of old age.

Almost all of the major traits of ageing can be predicted by a growing rift between two genomes, and a widening leak of free radicals. The leak worsens with time, so tissues die, especially gas-guzzling ones. Those that survive are more likely to become diseased. And the fast the leak, the faster all of this happens. This explains why species that tolerate less free radical leaks tend to enjoy longer lives. Consider pigeons and rats: both species are similar in both size and metabolic rates, but pigeons have far lower rates of leaking electrons in their mitochondria. They also live ten times longer.

A simple idea

For now, this is all a grand hypothesis, albeit one that is grounded on a lot of existing evidence. Lane now wants to explore ways of testing his idea. The most obvious first step would be to see if there actually is a lea threshold that varies between cells. It should be straightforward to measure the extent of free radical leaks in cells, and the level that makes them kill themselves.

He also wants to look at species with high energy needs like birds, to see whether a large proportion of their embryos are being lost. He’s also interested in how this applies to humans. “It would be interesting to get data from fertility clinics to see if there are any groups or populations that struggle to conceive,” he says, “and if any of this can be put down to incompatibilities between mitochondria and nuclear backgrounds. Around 40% of pregnancies end in miscarriage and we don’t know why.”

There is compelling majesty to Lane’s idea. At its heart, it is deceptively simple: we have two genomes that need to work together, and you can tell how well they’re doing this by the strength of the free radical leak. From that simple concept, you can logically derive how fitness, fertility and lifespan are linked in different species. You can also predict the process of ageing and the onset of age-related diseases within individuals.

“A lot of this has to be true on logical grounds,” says Lane. “We know that there is co-adaptation between these two genomes and many predictions emerge seamlessly from some simple reflections on that process. The big question is whether it’s important in the greater scheme of things.”

Reference: Lane, N. (2011). Mitonuclear match: Optimizing fitness and fertility over generations drives ageing within generations BioEssays DOI: 10.1002/bies.201100051

Lane, N. (2011). The Costs of Breathing Science, 334 (6053), 184-185 DOI: 10.1126/science.1214012

Image: by Ticipico

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It couldn’t be easier to make sweeping edits on a computer document. If I were so inclined, I could find every instance of the word “genome” in this article and replace it with the word “cake”. Now, a team of scientists from Harvard Medical School and MIT have found a way to do similar trick with DNA. Geneticists have long been able to edit individual genes, but this group has developed a way of rewriting DNA en masse, turning the entire genome of a bacterium into an “editable and evolvable template”.

Their success was possible because the same genetic code underlies all life. The code is written in the four letters (nucleotides) that chain together to form DNA: A, C, G and T. Every set of three letters (or ‘codon’) corresponds to a different amino acid, the building blocks of proteins. For example, GCA codes for alanine; TGT means cysteine. The chain of letters is translated into a chain of amino acids until you get to a ‘stop codon’. These special triplets act as full stops that indicate when a protein is finished.

This code is virtually the same in every gene on the planet. In every human, tree and bacterium, the same codons correspond to the same amino acids, with only minor variations. The code also includes a lot of redundancy. Four DNA letters can be arranged into 64 possible triplets, which are assigned to only 20 amino acids and one stop codon. So for example, GCT, GCA, GCC and GCG all code for alanine. And these surplus codons provide enough wiggle room for geneticists to play around with.

Farren Isaacs, Peter Carr and Harris Wang have started to replace every instance of TAG with TAA in the genome of the common gut bacterium Escherichia coli. Both are stop codons, so there’s no noticeable difference to the bacterium – it’s like replacing every word in a document with a synonym. But to the team, the genome-wide swap will eventually free up one of the 64 triplets in the genetic code. And that opens up many possible applications.

“We are actively pursuing three of them,” says Isaacs. First, they could assign the empty triplet to unnatural amino acids that sit outside the standard twenty. “This [could] expand the diversity of possible enzymes and create new classes of drugs, industrial enzymes and biomaterials.”

Second, the team could use the tweaked genetic codes to make living things resistant to viruses. Viruses make copies of themselves by hijacking the protein-making factories of their hosts. They depend on the fact that their proteins are encoded by the same triplets as those of their hosts. If their hosts stray from this universal genetic code, their factories will mangle the virus’s instructions, creating distorted and useless proteins. That would be useful for industry as well as medicine. The biotechnology company Genzyme had to shut down a manufacturing plant for several months after it was hit by a contaminating virus. Millions of dollars were lost.

Third, and for similar reasons, the altered codes could be used to contain genetically modified organisms, preventing them from breeding with wild populations. It’s the geneticist’s version of the Tower of Babel story – modified creatures would be imprisoned by their own genetic tweaks, unable to productively exchange genes with natural counterparts.

All three applications are some distance away in the future, but Isaacs, Carr and Wang have taken an important step towards them. Their genome-wide edits relied on two complementary technologies, invented by their team – MAGE, which substitutes TAA for TAG in separate pieces of bacterial DNA, and CAGE, which knits the pieces together into a whole genome.

MAGE, the older of the two techniques, made its debut two years ago. It stands for “multiplex automated genome engineering”, a fancy way of saying that it can easily change a genome many times over. It was originally used to create millions of small variants of bacterial genomes, producing a multitude of strains that can be tested for new abilities. As Jo Marchant puts it in her excellent feature, it’s an “evolution machine”. In its debut, within a matter of days, it had evolved a strain of E.coli that would produce large amounts of lycopene, a pigment that makes tomatoes red.

MAGE is a versatile editor. Not only can it create many diverse changes in a group of cells, it can also create many specific changes in a single cell. That’s what Isaacs, Carr and Wang have now done. TAG appears in 314 places throughout the E.coli genome as a stop codon. For each one, the team created a small stretch of DNA that had TAA instead of TAG, surrounded by exactly the same letters. They fed these edited fragments into bacteria, which used them to build new copies of their own DNA. The result: daughter bacteria with edited genomes.

In this way, Isaacs, Carr and Wang created 32 strains of E.coli that, between them, had every possible substitution of TAG to TAA. This might seem overly complicated, but replacing every TAG with TAA in a single step would be inefficient, slow, and error-prone. A single mistake could be lethal for the microbes. By taking things slowly, and spreading the substitutions among 32 strains, the team could better troubleshoot any tricky snags.

To combine the 32 strains into one, Isaacs, Carr and Wang developed CAGE (or “conjugative assembly genome engineering”). The technique relies on the bacterial equivalent of sex – a process called conjugation where two cells sidle up, form a physical link between one another, and swap DNA.

The team matched their 32 strains up in pairs, in a league that looked like a knock-out sports tournament. One strain of each pair would deliver its edited genes into its partner, and the incoming genes were designed to merge with those of the recipient in specific ways. Thirty-two strains with 10 edits each became sixteen strains with 20 edits each. Sixteen turned into eight and eight into four.

At the time of publication, the team had reached this “semi-final” stage. They had four strains of E.coli, each with a quarter of its genome stripped of TAG codons. The strains seem to be growing normally, proving that, individually at least, the TAG codons aren’t necessary for the bacterium’s survival. Whether E.coli can survive without any TAG codons at all is still unclear, but the team suspects this will be the case. If so, they’ll set about reprogramming the unused TAG codon to represent an unusual amino acid beyond the normal set of 20.

Why publish a paper at the semi-finals? “It is indeed an odd stopping point,” admits Carr. “[We’ve] been working on this project for 7 years and we decided to publish at this point largely because we have so much to talk about: the successful innovation of the CAGE technology and it’s integration with MAGE for genome engineering at large and small DNA scales. If you dig into the supplemental data of this paper, there’s another 1-2 more papers worth of stuff in there.

Isaacs points out that only one other research group is “working on genome engineering at this scale”: the J. Craig Venter Institute (JCVI). Last year, they made headlines by creating a bacterial genome, 1.1 million DNA letters (base pairs) long, and implanting it into the shell of a different bacterium.

Isaacs says, “[They] took 10 articles to get to a slightly-modified one million base pairs. We hope to get to a highly-modified, industrially useful 4.7 million base pair genome in three papers.” That includes the one that introduced MAGE to the world in 2009, and the current one that couples it with CAGE. The third one, due in the next year or so, will complete the trilogy – it will feature the final strain, . “All the pieces are in place,” says Carr. “We have a high degree of confidence we will reach our goal.”

What does the JCVI make of this? In a statement released to the press, Dan Gibson and Craig Venter point out that the MAGE/CAGE method still requires an existing genome to work from. Replacing an entire codon is a remarkable achievement, but it’s still a tweaking game. The end result will still be a genome that’s at least 90% similar to the original one. Gibson and Venter say, “Ultimately, we at JCVI would like to design cells from scratch.” The only way to do this is to synthesise an entirely fresh genome, rather than modify an existing one.

They add, “We continue to believe there will be and must be many different techniques developed to engineer and construct genomes so that the field can mature, allowing new and important products to be made. We believe the Isaacs et al paper is a positive addition to the field.”

Reference: Isaacs, Carr, Wang, Lajoie, Sterling, Kraal, Tolonen, Gianoulis, Goodman, Reppas, Emig, Bang, Hwang, Jewett, Jacobson & Church. 2011. Precise Manipulation of Chromosomes in Vivo Enables Genome-Wide Codon Replacement. http://dx.doi.org/10.1126/science.1205822

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In September 1941, Hu Chengzhi placed several skulls into two wooden crates. Around him, China was at war with Japan, so he was sending the skulls to the US for safekeeping. They never arrived. Hu was among the last people to see one of the most important palaeontological finds in history. These lost skulls belonged to Homo erectus pekinensis, known as Peking Man.

You can read all of them free online, which include the Maxberg Archaeopteryx, Nixon’s moon rocks, the recipe for Damascus steel and moon trees.

Dengue fever affects thousands of Queenslanders every year. It is caused by an alliance of two parasites – the dengue virus, and the Aedes aegypti mosquito that spreads it. In an ambitious plan to break this partnership, Scott O’Neill from the University of Queensland turned to yet another parasite – a bacterium called Wolbachia. It infects a wide variety of insects and other arthropods, making it possibly the most successful parasite of all. And it has a habit of spreading with great speed.

Wolbachia is transmitted in the eggs of infected females, so it has evolved many strategies for reaching new hosts by screwing over dead-end males. Sometimes it kills them. Sometimes it turns them into females. It also uses a subtler trick called “cytoplasmic incompatibility“, where uninfected females cannot mate successfully with infected males. This means that infected females, who can mate with whomever they like, enjoy a big advantage over uninfected females, who are more restricted. They lay more eggs, which carry more Wolbachia. Once the bacterium gets a foothold in a population, it tends to spread very quickly.

O’Neill started trying to exploit this ability around 20 years ago. It was a long struggle. Wolbachia infects several species of mosquitoes, but none of the ones that cause human diseases. O’Neill had to find or engineer versions of the bacterium that could live inside these species.

At first, he thought he could get Wolbachia to carry an antibody against dengue virus, and spread it through a mosquito population. That didn’t work. More recently, he had more luck with a strain that halves the lifetimes of infected females. Only older mosquitoes can transmit dengue fever because it takes several weeks for the virus to reproduce in the insects’ guts. If you knock off the older ones early, you could slash their chances of spreading disease.

Now, O’Neill’s team, together with Ary Hoffmann at the University of Melbourne, have infected A.aegypti mosquitoes with a strain of Wolbachia called wMel, which has spread through the world’s fruit flies in the last 80 years. It spreads even more quickly among caged populations than the life-shortening strains and it doesn’t harm the insect in any significant way. Best of all, its very presence seems to interfere with the mosquito’s ability to transmit dengue, as if the bacterium and virus were fighting an internal battle inside the insect.

Perhaps Wolbachia primes the mosquito’s immune system to fight off other invaders, such as dengue virus. Perhaps the bacterium uses up molecules like fatty acids that the virus needs to copy itself. Either way, here, at last, was a strain of Wolbachia that could turn Australia’s mosquitoes into dead-ends for dengue. All that was left was to test it.

Wolbachia doesn’t spread from mosquito to mosquito. They have to mate and pass the bacteria through the generations, so O’Neill had to start by releasing infected mosquitoes into local communities. “That was a fairly big ask!” he says. For three years, his team explained their plans to the residents of Yorkeys Knob and Gordonvale in Cairns, while carrying out a thorough risk analysis. “The community was incredibly supportive,” says O’Neill. “Dengue is such a big problem and people really want to see a solution to it.”

Between January and February of this year, O’Neill’s team released almost 300,000 mosquitoes at fences throughout the two suburbs. Every two weeks, they placed traps throughout the neighbourhoods and counted the proportion of eggs that carried Wolbachia.

The results were astonishing. By May, the proportion of Wolbachia-infected mosquitoes had risen from nothing to 80 percent in Gordonvale and over 90 percent in Yorkeys Knob. In just five months, the bacteria had swept through virtually the entire A.aegypti population. O’Neill also found that Wolbachia had started to spread beyond the two suburbs into surrounding neighbourhoods. “We were extremely happy,” he says. “It went better than we could have hoped for.”

This is the first time when scientists have transformed a population of wild insects to reduce their ability to pass on human diseases. “There is no precedent for this,” says Jason Rasgon, who studies mosquito-borne diseases at Johns Hopkins School of Public Health, who describes the study as “important and groundbreaking”. Jan Engelstadter from ETH Zurich, who studies host-parasite evolution, is also impressed. He says, “There is a lot of very hard work behind this. The idea to use Wolbachia in this way has been around for a long time, but finally it seems that this may really work.”

The same approach might even work for other diseases. Wolbachia also seems to prevent the growth of other mosquito-borne parasites, including West Nile virus and Plasmodium, which causes malaria. However, it’s proving more difficult to get the bacterium to stably infect the species of mosquito that carry these diseases.

Meanwhile, Engelstadter sounds a note of caution. “The virus cannot be expected to sit around passively,” he says. Dengue virus mutates very quickly and it might rapidly evolve to circumvent Wolbachia’s protection. There might already be precedent for this. The fruit fly where wMel comes from also carries sigma-virus, a type that Wolbachia does nothing to protect against. “One could speculate that this might be a case where the virus has overcome a protection that Wolbachia may once have conferred,” says Engelstadter.

Engelstadter is also concerned that the strategy might change how good dengue virus is at causing disease – its virulence. It could become more or less virulent, but it is impossible to predict. “When one imposes such a strong reduction in fitness on the virus life cycle, there might be also strong and unexpected responses,” he says.

O’Neill acknowledges these problems. “No matter what your intervention is, you should expect resistance to occur,” he says. “It’s difficult to predict how quickly it’ll occur or what its nature will be. We’ll have to wait and see.” But Rasgon adds, “Evolutionary issues are not unique to this. They are common to every mosquito control strategy, including ones that are currently used today.” Dengue control involves spraying a lot of insecticides and mosquitoes have already started to evolve resistance to them. The Wolbachia strategy would be less toxic and much cheaper. “It’s a fraction of the cost,” says O’Neill. “Once you implement it, it stays in place whereas for insecticides, you need to keep spraying.”

For his next trick, O’Neill is headed to Vietnam, where he plans on testing his mosquitoes in an even larger trial, to see if they actually lead to fewer dengue cases. It is easier to do this in a country where the disease is endemic, rather than Queensland, where outbreaks are unpredictable. “We wanted to do it in Australia to show that we were prepared to do it in our own backyard. Having shown we can implement it, we want directly measure the impact on disease.”

Reference: Walker, Johnson, Moreira, Iturbe-Ormaetxe, Frentiu, McMeniman, Leong, Dong, Axford, Kriesner, Lloyd, Ritchie, O’Neill & Hoffmann. 2011. The wMel Wolbachia strain blocks dengue and invades caged Aedes aegypti populations. Nature http://dx.doi.org/10.1038/nature10355

Hoffmann, Montgomery, Popovici, Iturbe-Ormaetxe, Johnson, Muzzi, Greenfield, Durkan, Leong, Dong, Cook, Axford, Callahan, Kenny, Omode, McGraw, Ryan, Ritchie, Turelli & O’Neill. 2011. Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission. Nature http://dx.doi.org/10.1038/nature10356

Image: by Muhammad Mahdi Karim

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If you walk by a European river on a summer’s day, you might get to hear the animal kingdom’s champion vocalist. His song sounds like a train of chirps, and from a metre away, it’s as loud as whirring power tools. The din is all the more incredible because it is produced by an insect just two millimetres in length – the lesser water boatman, Micronecta scholtzi

Micronecta means “small swimmer” and it is aptly named. It’s among the smallest of the several hundred species of water boatmen that row across the bottom of ponds and streams with paddle-shaped legs. The males are the ones that sing, and they often do so in large choruses to attract the silent females. These songs are famously loud. Even though the insect lives underwater, you can hear its call from the riverbank, several metres away.

Now, Jérôme Sueur from the Natural History Museum in Paris has measured Micronecta’s song using underwater microphones. He found that it the small swimmer is a record-breaker. On average, it reaches 79 decibels, about the level of a ringing phone or a cocktail party. But at its peak, it reaches 105 decibels – more like a car horn, a power tool or a passing subway train.

There are animals that make far louder calls. The record goes to the sperm whale, which can create clicks of around 236 decibels underwater (equivalent to 170 decibels on land). Other animals, including elephants, hippos and dolphins can produce louder calls than Micronecta.

But pound for pound, there is no competition. All of these animals are very big, and it stands to reason that large objects can produce louder sounds – think about the difference between a concert amp and a set of headphones. The sperm whale, for example, grows up to 16 metres in length and weighs up to 14 tonnes. Micronecta, on the other hand, produces its phenomenal song with a body that’s no bigger than one of these letters. Sueur compared the ratio of call intensity to body size for 227 different animals, from whales to insects, and found that the water boatmen out-sang them all.

How does such a tiny insect make such a loud noise? It’s not clear. It seems to do so by rubbing its ribbed penis against ridges on its belly, playing its genitals like a miniature fiddler. But the “bow” here is just 50 micrometres long, and there are no obvious body parts to amplify the noise.

But maybe the amplifier isn’t a body part at all. Like other water boatmen, Micronecta traps a layer of air around its body using microscopic hairs. This layer helps it to breathe, but Sueur speculates that it could also act as an echo-chamber, reflecting the sound of the penis-fiddling again and again. The details, however, are a mystery. As Sueur writes, “To observe the micro-mechanics of such a small system remains a significant challenge.”

Sueur also has an idea about why the water boatman’s song is so loud. He compares the song to the complex melodies of birds or the long antlers of deer – it’s a sexual signal that indicates a strong, powerful mate. If females prefer loud males over quiet ones, the male’s song would become exaggerated over time.

There are some obvious ways of testing this. If Sueur is right, females should prefer louder males, which should be easy to test with speakers and some recordings. Sueur also thinks that M.scholtzi probably has no predators that hunt by sound – otherwise, such hunters would limit the evolution of an extreme song by snatching up the loudest males. We know nothing about what eats M.scholtzi and Sueur plans on finding out.

Reference: Sueur, Mackie and Windmill. 2011. So Small, So Loud: Extremely High Sound Pressure Level from a Pygmy Aquatic Insect (Corixidae, Micronectinae). PLoS ONE http://dx.doi.org/10.1371/journal.pone.0021089

More on animal calls:

• City birds struggle to make themselves heard
• Orang-utans use leaves to lie about their size
• Cats manipulate their owners with a cry embedded in a purr
• Female antbirds jam their partners’ songs when other females approach
• Mosquitoes harmonise their buzzing in love duets
• Eland antelopes click their knees to prove their dominance
• Singing fish reveal shared origins of vertebrate vocals
• Sound the alarm – crested pigeons give off warning whistles simply by taking off
• Boom-boom-krak-oo – Campbell’s monkeys combine just six ‘words’ into rich vocabular

A great post from Athene Donald on impostor syndrome. Don’t miss the commenter who illustrates the Dunning-Kruger effect

#IamScience, the movie – Kevin Zelnio’s awesome initiative set to music. I Am Science continues to produce some amazing posts. Here’s one by LalSox, a teacher: “I accept their dissonance and scepticism, and I repay them with evidence and data, and another by psychologist Melanie Tannenbaum on her route in to science.

Photo essay of an incredible spider that mimics the ants it hunts, by Alex Wild.

“Thank you for loving me. I’m done.” – leading ALS researcher Richard Olney dies of ALS

The 20 Most Beautiful Bookshops in the world

Meet Me Halfway: Jennifer Ouellette on what happens in our brains when we connect with someone

Editor identifies some of the major problems in 21st century journalism… in 1923.

This is what a scientist looks like – a Tumblr

“Jonathan is a highly enterprising researcher, and he normally eats every animal he studies.” Great Natalie Angier piece on mammals that coat themselves with poison.

Extinct life is like a box of chocolates. Al Dove on the thrill of potentially discovering something very new.

Must-read post by Melanie Tannenbaum on benevolent sexism and why “compliments” can still hurt. Bonus: data!

The perks and pitfalls of scientific databases

Purple Doesn’t Exist: Cedar Reiner on male privilege in science. A great post.

Forget the internet. Here are some things that can ACTUALLY destroy your brain, from Bradley Voytek.

The sky is on fire! The Atlantic’s complete visual guide to the Aurora Borealis

News/science/writing

Killer Whale Menu Finally Revealed. Based on interviews with Inuit hunters, which surely is an intriguing but skewed data set

Why isn’t caffeine as addictive as cocaine?

Mammals get small 100x faster than they get big

Cultures of the past, brought low by changing climates

Incredible. An actual news organisation (well, sort of… the Times of India) ran the nonsensical Andrulis/gyre paper.

Paper denying HIV–AIDS link sparks resignation

Three words: Self. Guided. Bullets. Two more words: Oh. F**K.

The age of the great plant hunter continues

An arXiv for all of science? F1000 launches new immediate publication journal

Wall Street Journal rejects climate essay from 255 National Academy of Science scientists; accepts anti-climate essay from 16 others

Rant: I really hate it when people in science communication embrace sloppy evidence for some imagined problems with science. For example, this new report makes a big thing of the fact that 83% of UK 10-year-olds say a science career is ‘not for me’. Great! If the 17% who are interested in a science career actually try for one, there’s going to be a lot of unemployed people. I mean, look at Fig 1! That is BRILLIANT. And yet we get a boring science-in-trouble narrative.

How do female insects keep sperm fresh for 30 years?

How unfeasibly intricate ocean microbes called radiolarians brought Ernst Haeckel back to science

Klaatu barada nikto! A history of books bound in human flesh

Improbable evolution: how life beats the odds.

Does the human speech centre need to be shifted in textbooks? Sophie Scott wonders if it was ever lost

Leslie Brunetta talks candidly about getting a different type of breast cancer in each breast

1989: cystic fibrosis gene sequenced. 2012: 1st drug targeted at gene approved

The Story Collider reminds us that science is a story, not a set of “facts.”

No, seriously, I’m dead. Cotard’s delusion is endlessly fascinating.

Ancient DNA as anthrovoyeurism

Vincent Racaniello, a leading virologist & peerless communicator, is putting his Columbia Univ virology course online

Why gorillas “grin” when they play

Massive congrats to Alex Witze & Jane Qiu for winning the EGU Science Journalism Fellowship, which I helped to judge.

Cancer drugs can destabilise mouse genomes for generations. Lead researcher “cautions against extrapolating results… to humans.” Note the responsible reporting: the fact that this is in mice is mentioned in the hed, sub-hed, and first three paragraphs.

Sir David Attenborough responds to Lord Lawson’s inaccurate and misleading claims about ‘Frozen Planet’

True Confessions of a Dolphin-Loving Marine Biologist

Sea cucumber poo could save reefs from acidification

Bill Gates, Margaret Chan & 9 pharma CEOs met to eliminate neglected tropical diseases by 2020. A live-blog of the event.

Waging war by killing scientists in Iran.

The three deadliest words in the world: “It’s a girl.”

An interesting perspective on the foetal-cells-in-soda fearmongering by Matthew Herper

Heh/wow/huh

Gorgeous: desert rivers that look like trees

Parkour + trampolining = Wall trampolining = AWESOME

Behold: Etymology Man

Watch Lugnut the bear giving birth

No, CNN, London isn’t there.

I love this. A newspaper recycling bin that itself (sort of) gives you the news

Flying People in New York City

All the things Tyrannosaurus couldn’t do with those small

Decline in marine life possibly due to all the shit in the sea, say experts

The world’s largest island in a lake on an island in a lake on an island, which displaced the previous contender!

Journalism/internet/society

Is it good for journalism when sources go direct? Of course it is.

Klout Myth Busters: Thoughts From the Experts. Surely top myth is that it is in any way useful?

Great letter from ex-slave to his former owner in 1865, after being asked to return to work

Sari. Stove. Fire. Heartbreaking post in which Madhusudan Katti mourns his mother

Why Google thinks you are (a) male and (b) old

Nick Davies on why “Data Pool 3” could be a “nightmare” for News International

Your memory sucks – Great advice about documenting your reporting from Paige Williams.

Don’t gather string for stories – start a fire, says Brendan Maher. Plus more good advice on moving from news to features

In response to Jonathan Franzen, Carl Zimmer argues that e-books are a boon to literacy, not a threat to democracy

Great first diagram. Rest also good. 25 Things About Story Structure

Four ways to track & recover your belongings if they get stolen while travelling

Slovenian library creates surprise book packs based on genre

Be Better at Twitter – the definitive, data-driven guide

What PIOs/scientists/journos should expect from each other – good post from Matthew Shipman; so much more helpful than the “you’re doin it wrong” approach.

Tumours are bundles of cells that grow and divide uncontrollably, and their genes are deployed in unusual ways. By analysing the genes from different tumour samples, scientists have tried to pin down the chaotic events that lead to cancer. They seem to be making headway. Dozens of papers have reported “gene expression signatures” that predict the risk of dying or surviving from cancer, and new ones come out every month.

These signatures purportedly hint at how healthy cells transform into tumours in the first place. If, for example, the genes in question are involved in wound healing, this tells you that the healing process is somehow involved in a tumour’s progression. These collections of genes reveal deeper truths about the disease they’re associated with.

This idea sounds reasonable, but David Venet from the Université Libre de Bruxelles has thrown a big spanner into the works. He has shown that completely random sets of genes can predict the odds of surviving breast cancer better than published signatures.

Venet found three signatures that are completely unconnected to cancer. Instead, these collections of genes were associated with laughing at jokes after lunch, with the experience of social defeat in mice, and with the positioning of skin cells. All of them were associated with breast cancer outcomes.

Head over to Naturally Selected for the rest, including how long it took to get this study published.

Image by Hakan Dahlstrom

Our lives are full of instances where have to hold ourselves back. We stop ourselves from eating that tempting slice of cake to avoid putting on weight. We bite our tongues to avoid insulting our friends. We slam on the brakes to avoid killing a pedestrian.  To quote Yoda: “Control! Control! You must learn control.”

People with drug problems clearly have a problem with this. Their ability to resist their own impulses falters at the promise of the next hit. Now, scientists are starting to understand the changes in the brain that underlie these problems.

Karen Ersche from the University of Cambridge found that drug users have abnormalities in parts of the brain that are important for inhibiting unwanted actions. These same anomalies even exist in the brains of their siblings, who don’t have any drug problems themselves. They could act as a marker for people who are vulnerable to addiction. “Our findings provide further evidence for drug addiction being a brain-based disorder,” says Ersche.

This is far from the first study to examine the brains of drug users. But it’s never been clear whether changes in such brains were caused by drugs, or made people vulnerable to addiction in the first place. Both are possible. Stimulant drugs typically act on parts of the brain involved in motivation, and interfere with those that inhibit our impulses. But these effects could be worse if these neural circuits are already weak.

To separate these possibilities, Ersche studied 50 volunteers who had a long history of drug abuse. She compared them to their siblings, who had no drug problems, and to 50 unrelated volunteers who were also drugs-free. All of the recruits sat through a stop-signal test – a commonly used way of measuring self-control. Volunteers have to respond as quickly as possible to a stream of on-screen symbols – say, by pressing a key. If they hear a tone, which pops up unpredictably, they have to restrain themselves. (Try it yourself here).

The drug users struggled with the test compared to the unrelated volunteers, and needed more time to withhold their responses. Critically, their siblings fared just as badly, even though they weren’t using drugs. This strongly suggests that poor self-control isn’t the result of the drugs themselves, but of a shared (and probably inherited) vulnerability. “If you have brain with existing problems, the drugs have an easier play. It’s easier for them to take over,” says Ersche.

Ersche found the same pattern when she looked at her volunteers’ brains. First, she focused on their white matter tracts – the fibres that transmit signals from one area to another. These are the brain’s communications network, and their density indicates how good different areas are at shuttling information between them.

These connections were weaker among both the drug users and their relatives, compared to the healthy unrelated volunteers. The fibres were particularly sparse around the right inferior frontal cortex (IFC), an area involved in controlling our inhibitions. These abnormalities were linked to the volunteers’s scores on the stop-signal test – the weaker the connections, the slower their reaction times. With its communication lines weakened, the IFC was less able to exert its suppressive influence.

The siblings also shared anomalies in the size of some brain areas. Their putamens and medial temporal lobes were bigger, and their posterior insulas were smaller. All of these areas have been implicated in learning and memory. “This may be an indicator of an enhanced propensity to form habits,” says Ersche.

From these results, a cohesive picture emerges. Some parts of the brain are larger, increasing the attractiveness of potential rewards, and the odds of habitual, addictive behaviour. The IFC, which would normally suppress such desires, has less of a say because the fibres connecting it to other parts of the brain are weaker. It’s like having a mob of reckless friends who are egging each other on over fast broadband connections, while their sensible parents send them words of caution on a dial-up modem.

This is uncannily similar to what happens in  the teenage brain, where areas associated with reward mature before the prefrontal areas that exercise restraint. Other scientists have suggested that this gap in timing explains why teens are so prone to risky and impulsive behaviours. They’re not making thoughtless decisions – they simply weigh risks and rewards in a different way to adults. Perhaps people who are vulnerable to addiction never grow out of this asymmetry between desire and inhibition. “It does look like a developmental problem,” says Ersche, “but we really need to compare these brains to those of adolescents to know for sure.”

“This is a very important and well-designed study,” says Susan Tapert from the University of California, San Diego. She adds, “It will be important to understand how the non-drug dependent volunteers were able to avoid drug problems given same brain features as their siblings.”

This is a key point. Drug dependence runs in families, and it is clearly influenced by a person’s genes. But genes do not determine behaviour; they merely influence it. The non-addicted siblings in Ersche’s study illustrate the point beautifully. “They share so much,” says Ersche. “They have the same vulnerabilities as their drug-dependent brothers and sisters. They had a lot of domestic violence and troubled childhoods but they didn’t get into drugs. Their average age was 33. They may have had many opportunities to develop dependence, but they didn’t.”

Perhaps the other one had environmental influences that set them down a different path. Perhaps they also had inherited some “resilience factors” that their siblings did not.  In an earlier study with some of the same siblings, Ersche found that all of them are more impulsive, but only the drug users were “sensation-seekers”. These are subtly different traits. “Impulsive people act on the spur of the moment,” Ersche explains, “but sensation-seekers crave excitement and adventure. In contrast to the drug-dependent individuals, their siblings do not seem to crave for excitement and sensations, which might have protected them from taking drugs in the first place.

In the meantime, Ersche’s study suggests that the white fibre tracts around the IFC could be used as a marker for vulnerability to addiction. That’s useful for two reasons. We could use it to identify people who are most at risk of abusing drugs, before they actually encounter any problems. We could also see if people can strengthen the connections in this critical area. Many scientists have developed programmes for improving self-control at an early age. Monitoring the IFC’s white matter could provide an objective way of measuring whether those programmes are working. As Tapert says, “We might be able to modify these risky brain characteristics, to see if the misuse of drugs can be reduced.”

Reference: Ersche, Jones, Williams, Turton, Robbins & Bullmore. 2011. Abnormal Brain Structure Implicated in Stimulant Drug Addiction. Science http://dx.doi.org/10.1126/science.1214463