Palaeoanthropologist Rolf Quam of Binghamton University in New York state and his colleagues recovered and analysed a complete set of the three tiny middle-ear bones, or ossicles, from a 1.8-million-year-old specimen of Paranthropus robustus and an incomplete set of ossicles fromAustralopithecus africanus, which lived from about 3.3 million to around 2.1 million years ago. The ossicles are the smallest bones in the human body, and are rarely preserved intact in hominin fossils, Quam says.

In both specimens, the team found that the malleus (the first in the chain of the three middle-ear bones) was human-like — smaller in proportion compared to the ones in our ape relatives. Its size would also imply a smaller eardrum. The similarity between the two species points to a “deep and ancient origin” of this feature, Quam says. “This could be like bipedalism: a defining characteristic of hominins.”

Quam and his colleagues publish their results this week in theProceedings of the National Academy of Sciences¹.

Echo from the past

It is hard to draw conclusions about hearing just from the shape of the middle-ear bones because the process involves so many different ear structures, as well as the brain itself. However, some studies have shown that the relative sizes of the middle-ear bones do affect what primates can hear². Genomic comparisons with gorillas have indicated that changes in the genes that code for these structures might also demarcate humans from apes³.

Callum Ross, an evolutionary morphologist at the University of Chicago in Illinois, says the discovery of these ossicles was “a step in the right direction in the understanding of human hearing”. However he says he is “underwhelmed” by the findings, especially given that his own research⁴ has found that differences in the size and shape of the outer ear have a greater influence on the hearing sensitivities of primates than the dimensions of the middle-ear bones.

Ross also says that changes in the hearing apparatus are unlikely to have had as much impact on human cognition as the other morphological changes our ancestors experienced. “The truly important changes are in bipedalism, the feeding apparatus and, ultimately, brain size,” he says.

But Quam is confident that his team will soon demonstrate the importance of changes in the ossicles. “We are going to try and reconstruct the hearing capacities of these same specimens: then we will be able to say something about their sensory ecology,” he says.

Geraldine Wright at Newcastle University, UK, and colleagues trained bees to associate a scent with a sugary reward. Bees given sugar water laced with caffeine were twice as likely to remember the scent – and stick their tongues out in anticipation – three days later, than bees fed on sugar alone.

To see how the caffeine was affecting the bees’ memories, the team looked at what happened in their brains when they were injected with the stimulant. Sure enough, the caffeine triggered changes in the neurons’ ability to pass messages vital for olfactory learning and memory.

Small amounts of caffeine and other chemicals such as nicotine are present in the nectar of more than 100 plant species. Plants use these often nasty-tasting chemicals to deter predators, but Wright’s work suggests that they also use them to keep pollinators loyal to their flowers. It’s a matter of getting the dose right; leak just the right amount into their nectar to lure in the bees, but not too much so that the bitter taste puts them off.

Looking at how far bees will go to get their caffeine hit – and whether they willingly put themselves in danger – could answer a fascinating question, says Wright: “Can an insect become addicted to a drug?”

More work on bees could also shed light on how coffee affects us. The evidence for caffeine’s memory-enhancing capacity in humans is inconclusive, says Wright. Bees share many of our cerebral molecular building blocks, in particular the receptors for the neurotransmitter adenosine, which caffeine binds to. “We are confident that this is a common property across the animal kingdom,” says Wright.

Journal reference: Science, doi.org/kqq.

“Sure we could do a science podcast – or you guys could just make dick jokes for an hour, as per usual,” I said. “Let me know.”

“Previous investigations into the effect of the gender of a baby on its mother’s lifespan have been mixed, so our new analysis really is just another brick in the wall,” says Samuli Helle of the University of Turku in Finland, the study’s lead author. “I’m not surprised the results have been mixed, because the previous studies have involved different societies, cultural practices and so on.”

A litany of factors could influence a woman’s lifespan, such as affluence and nutrition, as well as the number of children she has. The impact of having a boy compared with a girl is likely to be most pronounced in settings where resources such as food and health care are poor.

Helle and his co-author, Virpi Lummaafound, investigated parish records for individuals in eight parishes who lived during the seventeenth to mid-twentieth centuries. They found that if a woman in these communities was 37 years old at the time of having her last child, her life expectancy would vary depending on the sex of her children. She would live for another 33.1 years if she had no sons, another 32.7 years if she had three and another 32.4 years if she had six.

The study, which appears in Biology Letters, builds on previous research published by the same team in the journal Science more than ten years ago, which found that for every son she had, a woman’s life would be shortened by an average of 34 weeks. By contrast, daughters actually lengthened their mother’s lifespan very slightly (though not statistically significantly). In both studies, the life-shortening effects were experienced only by mothers, not fathers.

Biological factors

But the reason behind this small difference is the big puzzle. “The relative importance of biological versus cultural factors remains an open question,” says Helle, who speculates that it could be that girls are more likely to help their parents in household duties. “We need more data, such as how many sons versus daughters helped in everyday tasks, what age they actually started to work outside the home and so on.”

Erik Lindqvist of the Research Institute of Industrial Economics in Stockholm, who has looked at lifespan and births in Sweden, is not convinced. “We have never been able to replicate their results,” he says.

But Grazyna Jasienska, who studies longevity and reproductive health at Jagiellonian University Medical College in Cracow, Poland, believes that the effects of sons on a woman’s lifespan are certainly real — and are probably due to biological factors, such as breastfeeding.

Other studies have found that boys can take more of a toll on their mother biologically because they tend to be slightly heavier at birth than girls. And a few studies have found that women expend more energy in producing breast milk for boys — although the results of such studies have been mixed.

“I think the costs of having boys over girls are more social than biological,” she says. “But we still ultimately don’t know.”

Tiny and delicate it may be, but the red spotted newt (Notophthalmus viridescens) has tissue-engineering skills that far surpass the most advanced biotechnology labs. The newt can regenerate lost tissue, including heart muscle, components of its central nervous system and even the lens of its eye.

Doctors hope that this skill relies on a basic genetic program that is common — albeit often in latent form — to all animals, including mammals, so that they can harness it in regenerative medicine. Mice, for instance, are able to generate new heart cells after myocardial injury.

The newt study, by Thomas Braun at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany, and his colleagues, suggest that it might not be so simple.

Attempts to analyse the genetics of newts in the same way as for humans, mice and flies have so far been hampered by the enormous size of the newt genome, which is ten times larger than our own. Braun and his colleagues therefore looked at the RNA produced when genes are expressed — known as the transcriptome — and used three analytical techniques to compile their data.

The team compiled the first catalogue of all the RNA transcripts expressed in N. viridescens, looking at both primary and regenerated tissue in the heart, limbs and eyes of both embryos and larvae.

The researchers found more than 120,000 RNA transcripts, of which they estimate 15,000 code for proteins. Of those, 826 were unique to the newt. What is more, several of those sequences were expressed at different levels in regenerated tissue than in primary tissue. Their results are published in Genome Biology.

Modern or ancestral?

The findings add to existing evidence that the ability evolved recently, says Jeremy Brockes of University College London, whose research provided the first evidence that regenerating tissue in salamanders express proteins that are not found in other vertebrates.

“I no longer believe that there is an ancestral program that is waiting to be reawakened,” Brockes says. “However, I absolutely do believe it’s possible to coax mammal tissues into regenerating to a greater degree with the lessons we learn from newts.”

But saying that the trait is either ancestral or recent is probably too “black and white”, says Elly Tanaka of the Center for Regenerative Therapies in Dresden, Germany. The truth, she says, could be somewhere in the middle. “It may in fact be that regeneration is ancestral, but that newts have species-specific adaptations that allow it to have such spectacular regenerative capacities compared with other vertebrates.”

Moreover, Tanaka adds, scientists would do well to look for more grey zones in the potential for harnessing the regenerative capacities of newts (and of other animals, such as fish). Rather than focusing on spectacular, but perhaps unlikely, scenarios in which amputees could regrow entire limbs, researchers should instead focus on more plausible options, such as improving the healing of scars and burns or increasing the speed of organ regeneration.

The molecule, TIC10, activates the gene for a protein called TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand), which has long been a target for cancer researchers looking for drugs that would avoid the debilitating effects of conventional therapies.

“TRAIL is a part of our immune system: all of us with functional immune systems use this molecule to keep tumours from forming or spreading, so boosting this will not be as toxic as chemotherapy,” says Wafik El-Deiry, an oncologist at Pennsylvania State University in Hershey and lead author of the study, which is published today inScience Translational Medicine.

Experiments showed that TIC10 had potent effects against a variety of tumours, including breast, lymphatic, colon and lung cancer. It was especially effective at triggering cell suicide in glioblastoma, a kind of brain tumour that is notoriously difficult to treat. Mice with glioblastomas that were treated with TIC10 in combination with bevacizumab — a drug used against diseases including brain tumours, and sold under the name Avastin — survived three times as long as untreated mice. Even mice treated with TIC-10 alone still had better survival rates (6% longer) than those treated with bevacizumab alone.

Quick and collaborative

El-Deiry says that TIC10 is so effective because it is much smaller than proteins that have previously been tested as TRAIL-based drugs. The molecule is so compact that it can cross the blood–brain barrier, which separates the main circulatory system from the brain. This barrier normally acts to prevent hazardous agents such as microbes from infecting the brain, but can also thwart anti-cancer drugs by keeping them out. “We didn’t actually anticipate that this molecule would be able to treat brain tumours — that was a pleasant surprise,” says El-Deiry.

Furthermore, it seems that TIC10 activates the TRAIL gene not only in cancerous cells, but also in healthy ones. This gives it enormous potential to create a ‘bystander effect’, in which apoptosis — or cell death — is induced in cancer cells immediately next to healthy ones. Healthy cells are also stimulated to increase the amount of TRAIL receptors on their cell surface. These receptors can then bind to the adjacent cancerous cells, triggering their demise. “It’s almost like TRAIL-plus — it does so much more,” says El-Deiry.

Tough TRAIL

This is by no means the only mechanism thought to trigger cell death in cancer. In particular, cancer researchers have been developing a number of drugs, including TRAIL-based therapeutics, that work by activating the cellular messenger tumour protein 53 (p53). But p53-based methods are not always effective, says El-Deiry. “Most tumours have dysfunctional p53, so in order to develop new therapeutics for cancer, one needs them to be effective in tumours with mutated p53,” he explains. His team’s approach bypasses p53 entirely.

Although the study was limited to mice, the team is confident that a similar approach would work in humans. Other researchers are sceptical, in part because TRAIL-based strategies have not lived up to past hype.

The potential for TRAIL to usher in a new age in cancer therapy was first identified in the mid-1990s³. However, although early clinical trials for TRAIL-based therapies showed little toxicity, they were not very successful at treating cancer, says Andrew Thorburn, an oncologist at the University of Colorado Denver, who co-authored a review on the subject last year⁴. “All the large clinical trials found no significant survival benefit to adding TRAIL-based therapeutics to standard treatments,” he ads. Many large biomedical research groups have shelved their TRAIL-based drugs.

Diseased trees in nurseries — and those that have been newly planted — will be identified and destroyed. Mature trees will be left standing, as they take longer to die and are valuable to wildlife, and can help in the search for naturally resistant trees. The import ban on ash trees that was implemented at the end of October will remain in place.

These measures, however, will not eradicate the disease from the United Kingdom. “There is absolutely no magic wand we can wave to make this disappear,” UK environment secretary Owen Paterson said at a press briefing in London this morning. Ash is the third most common tree in the United Kingdom, and with as many as 90 million ash trees at risk, the disease threatens to irreversibly change the shape of the British countryside.

This all comes on the heels of the largest tree survey ever undertaken in the United Kingdom, in which 500 staff and volunteers combed through 2,500 square kilometres of British countryside looking for sites of infection, which as of today number 129. It is possible that the disease reached the United Kingdom via infected ash timber or imported plants, but Ian Boyd, chief scientific adviser for the Department for Environment, Food and Rural Affairs (Defra) says that it is more likely that the spores arrived naturally. Because the sites of infection are scattered across the country, the spores were probably blown on the wind from continental Europe, where the fungus has ravaged ash trees from Poland to France for more than a decade.

On the upside, ash trees reproduce and grow quickly, with a high capacity for self seeding, so reforestation may not be too arduous. The main task now is to identify resistant strains of ash — a challenge that European scientists are already trying to tackle — so that they can be bred, cultivated and used to repopulate ash trees across the continent.

“If a small number of trees have survived the very intense epidemic in Demark, then there is hope for us here,” says Boyd. “By next season, we could have resistant ash growing as saplings in this country.”

Zig-zag science

Part of the reason it has taken so long to tackle the disease was confusion in Europe over what exactly was causing the dieback, says Joan Webber, a pathologist at Forest Research in Surrey, UK. Was it a new species of fungus, or a variant of an old, endemic species of fungus?

Mycologists first attributed ash dieback to Hymenoscyphus albidus, a species endemic to Europe that they thought had developed into a new, more virulent strain. But in 2011 a group of mycologists determined that the disease was caused by a different species altogether, which they namedHymenoscyphus pseudoalbidus¹ (H. pseudoalbidus is the sexually reproducing form of C. fraxinea).

“We had this zig-zagging in the science — is it new or is it old? — which led to the European Union being unable to regulate this as a quarantine organism,” says Webber. “Mycologists argued back and forth, and meanwhile the pathogen moved west across Europe.”

The latest research indicates that H. pseudoalbidus is native to Japan, says Stephen Woodward, a plant pathologist at the University of Aberdeen, UK, who was part of the group that advised the UK government on the action plan. When the spores reached European ashes in Poland, the trees had little ability to cope with the pathogen, and Woodward says that there is little that can be done now. “Estimates of 90% fatality are over-optimistic. It will be far more than that,” he says.

Global problem

Even if biologists can halt the spread of C. fraxinea in the United Kingdom, the worldwide spread of plant pathogens shows little sign of abating in a globalized economy.

“We are going to have to re-prioritize the Department for Environment, Food and Rural Affairs. We need to treat plant diseases as seriously as we do animal diseases,” Paterson said this morning. “We need a radical rethink in how we deal with plant diseases, and the word is ‘radical’.”

Cell cultures from two species of blind mole rat, Spalax judaei and Spalax golani, behave in ways that render them impervious to the growth of tumours, according to work by Vera Gorbunova at the University of Rochester in New York and her colleagues. And the creatures seem to have evolved a different way of doing this from that observed in their better known and similarly cancer-resistant cousin, the naked mole rat (Heterocephalus glaber).

Some 23% of humans die of cancer, but blind mole rats — which can live for 21 years, an impressive age among rodents — seem to be immune to the disease.

“These animals are subject to terrific stresses underground: darkness, scarcity of food, immense numbers of pathogens and low oxygen levels. So they have evolved a range of mechanisms to cope with these difficulties,” explains co-author Eviatar Nevo at the University of Haifa in Israel, who has published papers on the creatures since 1961. “I truly believe work with these animals will bring a dramatic revolution in medicine.”

Claustrophobic cells

Three years ago, Gorbunova was involved in another study that described the unusual way in which the cells of the naked mole rat behave in the lab. The authors say that this hints at how the rats resist cancer. When cells from most animals are grown in a culture dish, they divide until they form a single layer of cells covering the base of the dish. At this point, healthy cells stop dividing, whereas cancerous ones continue. But the cells of naked mole rats behave as if they are ‘claustrophobic’, ceasing to divide much sooner than cells from other species.

“We thought the blind-mole-rat cells would use the same mechanism as those of naked mole rats,” says Gorbunova, “so the fact that they do not was a big surprise”. Rather than ceasing to divide, the cells of blind mole rats reach a point at which they die en masse in a bout of cell suicide that Gorbunova and her co-authors call “concerted cell death”.

This seems to be triggered by the collective release of a signalling molecule called interferon-beta, although what causes this is unclear. “The cells have some way of sensing when they are overproliferating, but we still don’t know precisely how they sense that,” Gorbunova says. “This is what we need to find out next, because it could provide some clue as to how we could activate the same process in human cells.”

Inadequate methods?

However, this is not necessarily the mechanism that allows blind mole rats to resist cancer, points out Jerry Shay, who studies mechanisms of cellular ageing and death at the University of Texas Southwestern Medical Center in Dallas. “It is possible the researchers simply have not worked out adequate methods to maintain these cells long-term in culture,” he says. “It’s possible that the culture conditions are causing increased stress on the cells, resulting in cell death.”

Indeed, no biologist has yet worked out how to keep the cells of blind mole rats alive long-term in culture. “If we apply the same technique that works for 20 other species of rodent, for some reason that’s not good enough for blind-mole-rat cells — they always die,” says Gorbunova.

But, counter-intuitively, this mass cell death might be the very thing that makes the animals so long-lived: it could be a natural mechanism their bodies use to clear precancerous cells, stopping tumours in their tracks.

The species — Acomys kempi and Acomys percivali — have skin that is brittle and easily torn, which helps them to escape predators by jettisoning patches of their skin when caught or bitten. Researchers report today in Nature that whereas normal laboratory mice (Mus musculus) grow scar tissue when their skin is removed, African spiny mice can regrow complete suites of hair follicles, skin, sweat glands, fur and even cartilage.

Tissue regeneration has not been seen in mammals before, but it is common in crustaceans, insects, reptiles and amphibians. Some lizards can regrow only their tails, whereas some salamanders can regenerate entire limbs, complete with bones and muscle.

The researchers say that their next step will be to work out the molecular mechanisms and genetic circuits that direct the regeneration process. It’s unlikely that these mice have evolved an entirely new method of regrowing tissue, says Ashley Seifert, a developmental biologist at the University of Florida in Gainesville, who led the study. Rather, the genes that direct regeneration in salamanders are probably switched off in mammals, but have been switched back on in African spiny mice.

Seifert thinks that the ability to regenerate damaged tissue could even be switched on in humans. “By looking at the common genetic blueprints that exist across vertebrates, we hope to find the ones that we could activate in humans,” he says. “We just need to figure out how to dial the process in mammals back to do something the entire system already knows how to do.”

Jeremy Brockes, who studies limb regeneration in newts at University College London, agrees that it should be possible to use this work to improve wound healing in people. “The genomic resources are so powerful now that one could easily identify some aspect of regeneration in mice that could be helpful for human health,” he says.

The idea of regenerating entire limbs in humans may seem far-fetched, but regenerative medicine has made great advances in the past decade, with lab-grown bladders, stem-cell-seeded wind pipes and other regenerated human organs in part made possible through research on the genetic circuits humans share with flies, salamanders and mice.

Seifert says that this study is also a good example of how combining different fields of biology can lead to interesting results. “My initial conversations with a developmental biologist led me to chat with a mammalogist, eventually bringing me to field work in Africa with an ecologist, followed up by lab work with engineers, completed by molecular work,” he says. “Cross-talk among scientists can lead to really cool things.”

In a soggy field in Cambridgeshire, an unsuspecting crowd was summoned from the tent where they were sheltering from the incessant rain to observe an exotic species of wildlife.

“Over there you can see the green quark – that’s an up quark,” explained the silver-clad tour guide to the onlookers as they watched the twirling figure in a green boiler suit. Dancing nearby were two more, in blue and red. “Quarks have three genders: red, green and blue. They’re only really happy when the three are together in a loving bond.”

With smiles, hugs, and cheers from the crowd, the three embraced and linked arms. “Ladies and gentlemen, we have observed the formation of a proton.” Suddenly from behind a wooden sign sprang a golden-spandexed shape, running hysterically around the newly formed proton.

“Oh my god: it’s an electron!”

The Particle Zoo Safari, hosted by Guerilla Science at the Secret Garden Party arts and music festival last weekend, observed the formation of another proton and hydrogen atom, the sparring of two combative electrons, polyamorous covalent bond formation, sunlight manufacture through fusion (and a ping pong ball), and the creation of deuterium – complete with dubstep to mirror the atomic weight of the heavy form of hydrogen.

With polystyrene magnets our audience-cum-collider recreated the Large Hadron Collider (LHC) to produce the star of the show: the Higgs boson, sumo-suited and angry, the weightiest particle of all. “I’m hungry,” it grumpily announced, before we threw a net over it and dragged it into the tent. Too much had been spent on the particle’s discovery to let it escape now.

“The idea of the safari came from a colloquialism in physics, which refers to the set of standard particles that make up the entire universe as the ‘particle zoo’,” explains Patrick Stevenson-Keating, the designer we enlisted to help us devise a new way to explore particle physics. “This scale of subatomic particles is so different to our everyday world that there are few comparisons you can really make, so it was challenging to visualise some of the concepts.”

The fact remains that these basic concepts lie beyond an easy cognitive grasp for most people (myself included). To the uninitiated, gluons, bosons, quarks and electrons are indistinctive pin pricks of light and matter. The distinctions can seem insignificant – or at least, difficult to remember.

So to lend the particles a bit of personality, we gave each a costume and a character: speedy golden electrons, polyamorous colourful cuddly quarks, and a grumpy obese Higgs boson.

“When I was first approached to take part, I did think it sounded a bit nuts actually, but in the end it worked out reasonably well in terms of the science – I think most people would at least remember that quarks come in threes, and they are difficult to pull apart,” says Dr James Monk of the University College London, a particle physicist who works on the Atlas experiment on the LHC, whom we enlisted as a scientific consultant. “These particles and forces are important to understand how the world works, and it wouldn’t be fitting if physicists said that we do all this fantastic research – but the rest of you can’t possibly understand it.”

Dr Monk was giving a short lecture about his research and the workings of subatomic particles when the safari tour guide (played by our physics presenter Steve Mould) burst into the tent to announce an unmissable sight in the next field.

“We decided to make it more memorable by getting people physically involved in the experience,” says Jen Wong, Guerilla Science’s creative director. ”It is challenging coordinating multiple elements so that everything and everyone is on the same page in a way that still represents the actual science: volunteer particles, a genuine particle physicist, props, costumes and a safari tour guide. It’s a bit scary when you have brought together lots of people, content and stuff into a muddy field – you have no idea how it will pan out.”

In the end, abstract scientific concepts, sleep-deprived actors and muddy fields worked together better than expected. As the Higgs roared resentfully onstage, one audience member’s comment will ring in my ears forever:

“Dubstep and science … who knew?”

The “explosive backpacks” of Neocapritermes taracua, described in Science today¹, grow throughout the lifetimes of the worker termites, filling with blue crystals secreted by a pair of glands on the insects’ abdomens. Older workers carry the largest and most toxic backpacks. Those individuals also, not coincidentally, are the least able to forage and tend for the colony: their mandibles become dull and worn as the termites age, because they cannot be sharpened by moulting.

“Older individuals are not as effective at foraging and nest maintenance as younger workers,” says Robert Hanus, who studies termite biology at the Institute of Organic Chemistry and Biochemistry in Prague, and led the study.

But when the workers are attacked, he says, “they can provide another service to the colony. It makes perfect sense to me because theories predict that social insects should perform low-risk, laborious tasks such as housekeeping in the first part of their life and risky tasks such as defence as they age.”

Self-destructive behaviour is common among the sterile worker castes of eusocial insects such as termites and honeybees. The workers forego reproduction, so they are free to evolve altruistic behaviours that benefit the colony as a whole rather than themselves as individuals. Defensive suicidal rupturing — termed autothysis — has evolved independently in a number of termite species, suggesting that the behaviour is highly adaptive.

Arms race

Looking at defence mechanisms in other species of termite shows how the explosive backpacks might have evolved, says Hanus. Many termites fight off enemies by simply defecating onto them, sometimes with remarkable accuracy from a distance.

Other species go a step further, by actively squeezing their own abdominal muscles until a specialized thin portion of abdominal wall explodes showering the enemy with excrement. In the next stage of suicidal rupturing, some species of termites produce a toxic chemical that showers the enemy when the abdomen ruptures.

N. taracua has added a yet another step, by using a reaction to make its defensive chemical even more toxic. The pouches holding the copper-containing blue crystals are located near to the salivary glands. When the termites are attacked, their enemies bites cause these swollen pouches burst and the crystals mix with salivary secretions, producing the toxic blue liquid.

“It is the two-component chemistry that underlies the exceptional toxicity in this species,” says Hanus.

His team dosed members of an enemy termite species with blue liquid from the older workers, white salivary gland liquid from younger workers, white liquid that had been treated with blue crystals, or liquid from the older workers with the blue crystal removed. The blue liquid from older workers proved the most toxic, followed by the white liquid that had been treated with blue crystals.

“The sophistication of this is remarkable: we have never seen an external pouch like this before that adds one substance that needs to be mixed with another substance,” says Olav Rueppell, an evolutionary biologist from the University of North Carolina Greensboro, who studies social evolution in honeybees. “This kind of adaptation would not evolve in a solitary context; this shows the power of eusociality, and why these insects are so successful.”

Coral reefs rely on algae to harvest sunlight - a co-operative, mutually beneficial, symbiotic relationship that all coral reefs depend upon.

If I asked you to imagine what evolutionary biologists have to say about human nature, the phrases “selfish gene”, “survival of the fittest” and “red in tooth and claw” might spring to mind. Perhaps you would imagine explanations for why human history is a catalogue of war, conquest and strife. We are greedy and violent, because the greediest and most violent ancestors triumphed. We must overcome our biology in order to coexist.

Not quite, says David Sloan-Wilson, Distinguished Professor of Biological sciences and anthropology at Binghamton University in New York state. “It’s impossible to explain society only in terms of self-interest, because we are undeniably a co-operative species,” he says. “We are the only primate super-organism.”

Throughout human history we can see co-operation as the driving force – in the formation of complex societies, in building monumental architecture, in industrial agriculture and in organized religion. Neuroscientists think that the cornerstones of the human mind – language, empathy, “theory of mind”, and perhaps even consciousness – evolved partly out of a need to function in large groups.

But the popular understanding of evolution is still dominated by two words: “selfish genes”, coined by the British biologist richard Dawkins, who attempted to explain all evolutionary change in terms of the survival of single genes. ‘What people don’t understand is that “selfish genes” doesn’t necessarily mean selfish individuals – our genes can cause us to co-operate,” stresses Sloan-Wilson.

It all comes down to the power of “group selection”, he argues: survival of the fittest groups, rather than the fittest individuals. Groups that are composed of co-operative individuals will always out-compete groups of selfish individuals.

Our undeniably co-operative nature also has a dark side. Without our co-operative roots we could never wage war, make nuclear weapons or commit genocide. “Some people think group selection proponents wear rose-tinted glasses – but the truth is nothing of the sort,” says Sloan Wilson.

This concept of group selection is as old as the theory of natural selection itself. Charles Darwin himself suggested the idea:

An advancement in the standard of morality will certainly give an immense advantage to one tribe over another. A tribe including many members who, from possessing in a high degree the spirit of patriotism, fidelity, obedience, courage, and sympathy, were always ready to aid one another, and to sacrifice themselves for the common good, would be victorious over most other tribes; and this would be natural selection.

Surprisingly, none of those famous phrases mentioned at the start of this piece can be attributed to Darwin, though most people would think those to be his words. “Red in tooth and claw” comes from Alfred Lord Tennyson’s poem In Memoriam A. H. H. “Survival of the fittest” – though later quoted by Darwin – was actually coined by Herbert Spencer.

Darwin, counter to the later “neo-Darwinists”, was fascinated by the prevalence of altruistic and co-operative behaviour throughout the animal kingdom and believed group selection could be a powerful force. There was widespread support for the idea until the 1950s, but individualistic and neoliberal ideas came to dominate many intellectual fields, from sociology to history, political science and of course, economics.

“The scientific story is embedded in the larger cultural story,” says Sloan-Wilson. “The ethos of the rugged individualist made it alluring to think we can explain everything in terms of self-interest.”

“Part of the problem is that Darwin struggled to explain the widespread phenomenon of co-operative behaviour because at the time there was no mathematical machinery to do that,” explains Martin Nowak, who teaches biology and mathematics at Harvard University.

Our own bodies are ecosystems

When scientists attempted to revive the idea of group selection in the 1960s, the concept was widely rejected.

Fellow biologist George C Williams flatly wrote in his 1966 tome, Adaptation and Natural Selection: “Group-related adaptations do not, in fact, exist.” Discussion over. The concept of group-selection became virtually taboo. Dawkins likened the search for evidence of group selection to efforts to create a perpetual motion machine in his 1982 book, The Extended Phenotype.

“For many years, Sloan Wilson stood alone defending the concept of group selection – and he turned out to be right,” says Martin Nowak.

In a highly cited paper published in the journal Science in 2006, Nowak used computer modeling, mathematics and rigorous experiments to identify five mechanisms that lead to co-operation, including group selection.

“Co-operation exists everywhere in nature,” asserts Nowak, from the flocking of birds to the giant hives of termites. And it can be a powerful force. Insect colonies such as those of bees, ants and termites, in which the members of a colony give up reproducing so a single queen can produce all the young, account for half of the total weight of all the insects on earth.

Co-operation between different species, not just between individuals of the same species, is of paramount importance to life in every corner of the planet. Plants depend on pollinators to reproduce; coral reefs rely on symbiotic algae to harvest sunlight; trees use networks of soil fungi to communicate. Our own bodies are ecosystems: for every one human cell we possess ten bacterial cells, many of which we are dependent upon for our survival, such as the germs in our guts.

In fact, many of life’s key innovations – going back three billion years – are simple forms of co-operation. The progression from single-celled organisms to multicellular entities is entirely reliant upon co-operation. Even the networking of chemicals was needed for the dawn of life.

As Sloan Wilson puts it: “Today’s individuals are yesterdays groups.”

The academic struggle for these ideas has rarely been easy. Scientists now believe that some structures inside our cells – mitochondria, the power houses of animal cells; or chloroplasts, the energy factories of plant cells – were once individual microbes which became co-opted by larger cells. But when the now famed biologist Lynn Margulis first proposed the “endosymbiotic” theory, “her ideas were considered heresy,” according to Steven Rose from Britain’s Open University.

“The controversy over co-operation arose particularly because of the extreme reductionism within which neo-Darwinism was formulated,” says Rose.

Those simplified explanations have penetrated deeply into popular consciousness. Sloan Wilson, Rose and Nowak all agree: everyone should be interested in this debate. Though theoretical biology can involve dense jargon and abstract mathematical equations, the basic concepts are not difficult.

“We don’t need big words to explain this – we all talk about altruism and selfishness all the time,” says Sloan Wilson. “Moral discourse by its nature is about the consequences of our actions as individuals and as groups.”

And the implications extend far beyond the philosophical. “The survival of intelligent life depends on whether we learn to co-operate with each other before we destroy the ecosystems of the planet,” argues Nowak.

“There is no technological solution. The solution requires a behavioural change.”

Meanwhile, Sloan Wilson has set up The Evolution Institute in his hometown of Binghamton, New York – an attempt to use biological science to influence society. “The idea that a thinktank could inform public policy from an evolutionary perspective is exciting,” he adds.

Rose is more sceptical: “Just because a group of wise scientists form a thinktank doesn’t mean we can solve all of society’s problems.”

That will take some time. And for now, “survival of the fittest” and “selfish genes” still reign in the public consciousness.

But at the very least, it’s worth reflecting on the etymology of the word “competition” which comes from the Latin compere, which means not “to defeat” – but “to strive together”.

Spiders can exert an influence on the biogeochemical processes of the ecosystems in which they live, simply through their very presence.

The presence of predators in an ecosystem can have a significant impact on soil ecology simply through the stress they cause in their prey.

Writing in Science today¹, ecologist Dror Hawlena of the Hebrew University of Jerusalem and his colleagues show that when stressed grasshoppers die, the chemical differences in their bodies indirectly affect how quickly the surrounding dead plant material is broken down by soil microbes, with knock-on effects for nutrient cycling in ecosystems.

“We were interested in bridging two subfields of ecology — organism ecology and biogeochemistry — in a way to make predictions about how food web structure can affect nutrient cycling,” says Hawlena.

Previous studies have shown that stress causes animals to change their diet by eating more carbohydrates to meet their heightened energy requirements. Switching to food that contains less nitrogen leaves a chemical signature in the bodies of stressed animals². In turn, their nitrogen-poor corpses affect the metabolism of soil microbes, because bacteria require nitrogen to produce their decomposing enzymes.

Living in fear

To investigate these effects, Hawlena and his team first reared grasshoppers in field cages with predatory spiders that had had their mouthparts glued shut — a way to measure the impact of fear on the grasshoppers without the spiders eating them. When the grasshoppers eventually died, the researchers added their decomposed remains to soil samples in the lab, and then added leaf litter to see how quickly the plant material would be decomposed by soil microbes and to “test for the legacy effects of fear” on soil microbe communities.

The indirect effects of predatory stress on soil microbes had a lasting effect. When the researchers added leaf litter to the soil samples that had been treated with stressed grasshoppers, the extent of decomposition of the plant litter 93 days later was 200% less than in samples treated with dead grasshoppers reared without spiders in their cage.

“We were surprised at how big the effect was,” says Hawlena. “The traditional view is that plants and microbes are the main players linking the biotic and the abiotic world, but here we have shown that predators can actually regulate microbes by affecting the chemical composition of their own prey.”

It is well established that predators can have significant impacts on both plant and soil microbe communities by reducing herbivore numbers as well as by depositing nutrients through their waste. But this study shows how predators can impact soil microbe communities and the cycling of nutrients in ways other than by simply eating their prey.

Tangled food webs

“The study is very clever and the results and the implications — that predators cause their prey to have less nitrogen and this cascades to affect decomposition — are not immediately obvious,” says ecologist Rudy Boonstra of the University of Toronto in Canada, who studies the effects of predators on stress physiology.

“This adds to a growing number of studies that show a whole range of other knock-on effects that organisms can have on the way the ecosystem functions, such as soil fertility, plant growth and nutrition,” adds soil ecologist David Wardle at the Swedish University of Agricultural Sciences in Umeå, who studies the links between above- and below-ground microbial communities in the boreal forests of Sweden and the rainforests of New Zealand.

Crucially, says Wardle, this points to the many roles predators can have in regulating ecosystems. “Top-level [apex] predators are extremely vulnerable to extinction, and when you lose apex predators there will be a whole range of effects on the way the ecosystem functions — including effects we don’t even know about,” says Wardle.

It is hard to speculate how losing top-level predators through human-induced changes will affect soil ecology and biodiversity globally, but Hawlena says that demonstrating that predators can have “dramatic effects” on biogeochemical processes has profound implications.

“This is a whole new component to the story of how anthropogenic changes can impact ecosystems,” he says.