Ed Yong, Science Writer

It’s not often that scientists make people watch the first episode of 24 in the name of science. It’s even rarer that they pick Jack Bauer’s exploits because they wanted to show volunteers something “more true to life”. Then again, as Jason Chan dryly says, “Some of the earlier episodes were not as far-fetched as the later ones”.

Chan’s study is the latest to show how easy it is to disrupt our memories, and supplant what we think we know with misinformation. In this case, he and colleague Jessica LaPaglia from Iowa State University showed volunteers the pilot episode of 24 and then selectively rewrote some of their memories of the show’s events. For example, some of the volunteers came to believe that an assassin (Mandy!) knocked out a flight attendant with a stun gun, when she actually used a hypodermic syringe.

It wasn’t just a simple matter of saying Mandy used a stun gun. That wouldn’t have worked. Instead, Chan and LaPaglia fed their volunteers with false information immediately after they had actively remembered what they had seen. Then, and only then, did the new memories overwrite their old ones.

The trick relies on a quirk of memory that has come to light in recent years. I’ve written about it before:

Every time we bring back an old memory, we run the risk of changing it. It’s more like opening a document on a computer – the old information enters a surprisingly vulnerable state when it can be edited, overwritten, or even deleted. It takes a while for the memory to become strengthened anew, through a process called reconsolidation. Memories aren’t just written once, but every time we remember them.

This means, somewhat ironically, that the remembering something creates a critical window in which memories can be erased or manipulated. Many scientists have done this in rodents and humans using drugs or conflicting information. But these experiments usually manipulate single simple memories, such as a drug craving or a fearful association between a colour and an electric shock.

Chan and LaPaglia have now used the reconsolidation window to change declarative memories—facts and knowledge that we consciously recall. “We have people forming a very complex memory of a story that lasts 40-50 minutes and changing specific details within that larger context,” says Chan. “This is what’s new. It’s a pretty important step for demonstrating the fundamental importance [of reconsolidation] in humans.”

After showing the pilot episode of 24 to 146 volunteers, Chan and LaPaglia asked them to either play Tetris or answer memory-testing questions about the video. Twenty minutes later, they listened to a short audio recording that supposedly recapped the episode, but that secretly changed some details—for example, swapping Mandy’s syringe for a stun gun. Five minutes later, everyone took a final true-or-false test about what they had originally seen.

In this final test, the volunteers were worse at accurately recalling details that were changed in the audio recap, but only if they had previously answered questions that made them recall the video. Those who played Tetris were unaffected.

So, taking the quiz destabilised the volunteers’ memories of what they were quizzed on, paving the way for the false recap to mess with their knowledge. This worked even when volunteers correctly remembered what happened in the episode during the first quiz—the incorrect audio still changed what they thought they knew.

Through repetitions and variations of this basic experiment, Chan and LaPaglia showed that the effect lasts a long time, even if the final test followed the audio recap by a day rather than 5 minutes. But for the trick to work, the false information needs to come quickly and be very specific. If 48 hours passed between the first quiz and the audio recap, rather than 20 minutes, the original memories stay unchanged. And if the recap involved a different scenario—say, an assassin knocking out a flight attendant in the context of drug trafficking rather than terrorism—the new info never overwrote the original memory. This explains why we’re not constantly upsetting our old memories even though we’re constantly exposed to new information.

Chan and LaPaglia also suspect that people need to believe that the new information accurately represents the old set, and not if they consciously detect a factual discrepancy. “If they think there’s misleading information in here, they’ll be much less susceptible to that effect,” says Chan.

Other studies on reconsolidation have found similar results, but this one shows that memory manipulation isn’t limited to the simple products of basic conditioning, but also more complicated bits of knowledge. It supports the work of psychologists like Elizabeth Loftus, who have shown how easy it is to implant people with false memories.

It also fits with a growing body of evidence showing that, despite what people believe, eyewitness testimony is often seriously unreliable. “Say you’ve been questioned by an investigator and you recall the event,” says Chan. “In the next 15-20 minutes, you could run into another eyewitness or overhear investigators talking to each other. Some inaccurate information could update your memory.”

More positively, the study could have implications for treating conditions that involve unwanted memories, such as phobias or post-traumatic stress disorder (PTSD). As Chan and LaPaglia, “Humans are notoriously inept at suppressing unwanted thoughts.” If we try not to think about something, we usually end up thinking about it all the more. Instead, it may be more productive to actively remember what’s troubling us and reinterpret that in a new light, relying on reconsolidation to remake the old memories in a less disqueting way.

Acceptance and commitment therapies for PTSD work along similar lines, but it’s often assumed that they help people to put the past behind them or to disconnect their experiences from negative feelings. But Chan and LaPaglia suggest that such techniques might actually be exploiting the reconsolidation effect to actually rewrite the past, rather than just severing our connections from it.

Reference: Chan & LaPaglia. 2013. Impairing existing declarative memory in humans by disrupting reconsolidation. PNAS http://dx.doi.org/10.1073/pnas.1218472110

PS: I love that reference 55 of this paper is “24 12:00 a.m.–1:00 a.m. [dvd]. Fox Television Studio, producer; 60 min, sound, color”. And reference 56 is “Neave P (2009) Tetris N-Blox (Tetris Holding, LLC, Hawaii).”

More on memory:

• Rewriting fearful memories by bringing them back to mind
• Scientists create mice that automatically label new memories for easy reactivation
• Five myths about memory (and why they matter in court)
• Memory improves when neurons fire in youthful surroundings
• The extended mind – how Google affects our memories
• Beta-blocker drug erases the emotion of fearful memories
• Memories can be strengthened while we sleep by providing the right triggers
• The guardians of fear – molecules that provide safety nets for scary memories
• Erasing a memory reveals the neurons that encode it
• Drugs and stimulating environments reverse memory loss in brain-damaged mice

More on memory:

·         Rewriting fearful memories by bringing them back to mind

·         Scientists create mice that automatically label new memories for easy reactivation

·         Five myths about memory (and why they matter in court)

·         Memory improves when neurons fire in youthful surroundings

·         The extended mind – how Google affects our memories       

·         Beta-blocker drug erases the emotion of fearful memories

·         Memories can be strengthened while we sleep by providing the right triggers

·         The guardians of fear – molecules that provide safety nets for scary memories

·         Erasing a memory reveals the neurons that encode it

·         Drugs and stimulating environments reverse memory loss in brain-damaged mice

If animals and plants can’t defend themselves, they often form partnerships with bodyguards. Wasps use zombified caterpillars. Corals recruit goby fish. And acacia trees hire ants. The ants defend the trees against hungry mouths by biting and stinging any invading plant-eaters. Some are so ferocious that they can deter elephants. In return, the trees pay their bodyguards by providing shelter in the form of swollen thorns, and food in the form of nectar or nutritious parcels called “food bodies”.

This alliance between ants and acacias is a staple of textbooks, but it’s even more intimate than anyone suspected. Some acacias don’t just supply their ants with any old food. They offer the biological equivalent of a cheque—a reward that only the ants can cash.

Every partnership is vulnerable to thieves. The acacia’s bright, nutritious food bodies could easily be pilfered by any insect quick enough to avoid the patrolling ants. But insects that steal them are in for a poor and possibly dangerous meal.

Domanicar Orona-Tamayo from CINVESTAV-Irapuato in Mexico and Natalie Wielsch from the Max Planck Institute for Chemical Ecology in Germany found that the food bodies of two acacia species are loaded with enzymes called protease inhibitors. As their name suggests, these block other enzymes called proteases, which animals use to digest the protein in their food.

These acacia enzymes were extremely good at neutralising the proteases of two species of seed-eating beetles, slashing their protein-busting abilities by more than 98 percent.

Pseudomyrmex ferruginea—one of the ants that guards the acacia—has no such problems. Its guts are dominated by a special protease called chymotrypsin-1, which the acacia’s protease inhibitors do not inhibit. When these bodyguards eat the food bodies, they get a nutritious reward. When beetles try to do the same, they get indigestion.

The protease inhibitors aren’t found throughout the acacia, just in the food bodies. They are security measures that protect the tree’s rewards by harming would-be thieves. Only the ants can bypass these defences, and only the right ants at that.

Orona-Tamayo and Wielsch found that Pseudomyrmex gracilis—a species that exploits the acacia’s rewards without ever lifting a mandible to defend it—isn’t quite as well-equipped as the P.ferrugineus. It has some chymotrypsin-1, but also plenty of other proteases that are inactivated by the acacia’s neutralising enzymes.  It gets something out of the food bodies, but not as much as the tree’s true partner.

There are other examples in the natural world of alliances where partners lock each other into exclusive contracts. Some do it physically. Many flowers hide their nectar at the bottom of long tubes that only the right pollinators can reach them, whether they’re long-billed hummingbirds or long-tongued flies.

In these cases, it’s clear that the flowers and their pollinators evolved alongside one another. As nectar tubes got longer, so did bills and tongues, until both fit together like locks and keys. Is the same true for the acacia and the ant? It’s possible, but the team suspects that both partners came prepared for exclusivity.

The acacia uses the same protease inhibitors as many other related plants, and many ants and spiders* have chymotrypsin-1 in their guts. The tree eventually concentrated its inhibitors into its food bodies, while its ant partners emphasised chymotrypsin-1 and downplayed other proteases. They were already a good match from the start. They just became closer over time.

*This might be why the world’s only vegetarian spider, Bagheera kiplingi­­, can get away with eating acacia food bodies.

Reference: Orona-Tamayo, Wielsch, Blanco-Labra, Svatos, Farias-Rodriguez & Heil. 2013. Exclusive rewards in mutualisms: ant proteases and plant protease inhibitors create a lock–key system to protect Acacia food bodies from exploitation. Molecular Ecology http://dx.doi.org/10.1111/mec.12320

More on ants and acacias:

• Slackers and parasites can sometimes make the best partners
• Threatened by elephants? Try recruiting ants

A female strawberry poison frog faces an abundance of choice when it comes time to breed. The forest floor is full of bright red males trying to attract her with their songs, and wrestling with other males to defend their territories. She could pick a suitor based on his size or health. She could weigh up the quality of his territory. She could judge him on the depth, volume or length of his croaking, any of which could indicate how strong he is.

Or she could just mate with the first male she finds.

That, rather anticlimactically, is exactly what happens. For all the effort that males put into attracting a partner, the only factor that seems to matter to the females is who’s nearest. And according to Ivonne Meuche from the University of Veterinary Medicine in Hanover, this strategy makes perfect sense for these frogs.

The strawberry poison frog (Oophaga pumilio) has become something of a celebrity among scientists studying frog behaviour. It’s easy to find because of its bright colours and tendency to hop about in the day. And it has lots of sex. On average, a female will only go for 4 to 5 days between partners.

The frogs practice ‘lekking’—a style of mating where many males call at the same time, allowing females to choose between them. Each male defend a small territory, and each female wanders across many of these. When she chooses a mate, the two partners face in opposite directions while she lays eggs and he fertilises them.

Meuche’s team followed 20 female frogs in the rainforests of Costa Rica to see which males they mated with. They compared the qualities of these victors to those of every other male within the females’ home ranges. They also compared the two males that were closest to the females on the morning of their egg-laying days.

In an earlier study, one of the team, Hieke Prohl, suggested that males mated with more females if they called more often and at a lower pitch. But this time, they found that females were completely oblivious to the males’ territory size, weight, length, health or calls. Instead, they just went straight for the nearest one who was calling.

You could argue that females are making pickier choices the night before, so that they’re waking up near their favoured partners on egg-laying days. But in other studies, the team showed that the females’ whereabouts don’t depend on the males but on the availability of food.

They also checked their results by using two speakers to play recordings of males with different call rates and pitches. Forty-five females heard these calls and none of them seem to care about the calls themselves. They just went for the closest speaker.

This is unusual. Lekking is almost synonymous with female choosiness, although some other frogs also use a “closest-male-wins” strategy. It presumably means that they sometimes mate with dud partners while there are prime specimens calling a bit further away.

But Meuche thinks that the females aren’t fussy because there are big costs to shopping around. In this corner of Costa Rica, female strawberry poison frogs outnumber the males. Males are in short supply, and if they’re with another female, they stay silent and cannot be found. If a female rejects a male, she might not be able to find another partner, much less a better one. If this happens, she’ll lose an entire clutch. On her egg-laying days, she has to find a mate within a certain time or she’ll just lay unfertilised eggs that never develop.

The team also found that the males are all much of a muchness. They compete so intensely for territories that those with good ones, which put them closest to as many females as possible, will probably also have good genes. Females have a good chance of getting a high-quality mate even if they grab the closest one.

Reference: Meuche, Brusa, Linesenmair, Keller & Prohl. 2013. Only distance matters – non-choosy females in a poison frog population. Frontiers in Zoology http://dx.doi.org/10.1186/1742-9994-10-29

More on frog sex:

• Male Frog Extracts and Fertilises Eggs From Dead Female
• Wolverine frogs fights & grabs mates with bony thumb-spikes
• Tree frogs shake their bums to send threatening vibes

Top picks

Commander Chris Hadfield ended his amazing run on the International Space Station with this beautiful video of him singing Space Oddity. When he croons “floating in a most peculiar way”, and he *actually is because he’s in space*, it’s pretty much the best thing ever. (And is this the most expensive pop video ever?) And Megan Garber looks at what made Hadfield’s run on the ISS so unique.

The ScienceSeeker award winners are out, and they’re great. Massive congrats to Ginny Hughes and others. For some of the best science blogging out there, start here.

Maia Szalavitz’s five (maybe six) diagnoses of mental illness show what’s right and wrong with the DSM. An amazing, brave, insightful post.

This. Is. Fascinating. Could DNA databases curb human trafficking? By Virginia Hughes

Bravo, Alice Bell. “Politics doesn’t distract from the science. An over-emphasis on decontextualised science is used to distract from the politics.”

Antibiotics for back pain? Authors involved in setting up for-profit clinics and stand to make money from them.

Industrial scale rat-killing on the Galapagos – great feature by Henry Nicholls

Mosses Make Two Different Plants From Same Genome: Single Gene Can Make the Difference. By Jennifer Frazer.

How post-disaster therapy is a disaster by Vaughan Bell.

More than half of the world’s population lives inside this circle (which is mostly water)

No, wi-fi doesn’t make people sick, but it’s pretty easy to convince someone that it does. By Elizabeth Preston.

Canadian mine may host an ecosystem that’s been isolated for 2.6 billion years

Your frontal lobe is decidedly average. It’s vanilla. Nothing special. Just like mine.

Good piece on BRCA1 and breast cancer, with some carefully laid-out stats, by Henry Scowcroft. A very good piece on Jolie, Minogue & reactions to celebrity health decisions, by Hilda Bastian. And a look at BRCA1’s history, by Carl Zimmer.

Something often lost in the controversy about replication in psychology: how much people are doing to fix it.

Psychological Science article titles start a nerdy in-joke that keeps on going and going.

I’ve got a new feature in Scientific American (subscription required) about stereotype threat.

“The evolutionary race is not in fact won by the perfect, but by the good-enough.” – Carl Zimmer on mediocre adaptations.

This post on a monster dandelion, by Malcolm Campbell, is a marvellous example of how biology enriches one’s world-view

Science/news/writing

This “scrappy, open-source project” to build a virtual worm began with a tweet.

Awesome headline: “This disease’s deadliest weapon is the fact you’ve never heard of it”

New research on malaria-directed mosquitoes arose from dumb-sounding, Ig-Nobel-winning study. Science needs the silly.

How A Virus Hid In Our Genome For Six Million Years

Brain-controlling magnets: how do they work?

Study claims that electrical stimulation of the brain can boost maths skills. It looked at 13 people, and the long-term results are based on 6 people. This post on underpowered neuroscience experiments seems apposite.

Johnny Depp immortalized in name of extinct creature with ‘scissor hand-like’ claws

Why do bees like hexagons?

Opportunity just broke NASA’s record for miles driven in space

Did eyes really stare down bicycle crime in Newcastle?

On the difficulties of sci-comm when your message (and research) is a huge downer.

The Trouble With “Limitations” In Science

A slug of very little brain manages to learn something

Half of researchers have reported trouble reproducing published findings: MD Anderson survey

Has a Lidar survey found a lost city in Central America?

Attendees at the World Conf on Research Integrity search for ways to tackle misconduct and sloppy science

Human cloning successfully makes embryonic stem cells. I’m underwhelmed, but Paul Knoepfler has a good bit of analysis.

Science communication is at a tipping point, and it’s the community that matters. Good post by Liz Neeley.

Very interesting and helpful critique of Temple Grandin’s “The Autistic Brain”

Ants protect aphids from predators and parasites. Except these ants. These ants are rubbish.

There’s no us in uterus. Al Dove on embryonic cannibalism. I especially appreciate the final image.

“That’s only [a factor of] 35 million away” from the target”

The Sun says these huge radiation eruptions happen to every star and it’s insensitive to go on about them

Surprising discovery: Species of male spiders eat females

Is Galileo really a good example of admitting when you’re wrong? No.

Why everything you know about wolf packs is wrong; the alpha wolf doesn’t exist—at least not in the wild.

What is Wrong With Dissections? Not what you think.

Skyping with some elephants

Heh/wow/huh

Don’t play the Star Trek lens flare drinking game

Now is the printer of our discontent: A 3D-printed model of Richard III’s head

World’s most comprehensive guide to primates – in pictures

Oh, Nature. See also: the standfirst.

The Japanese have a word for “the act of buying books and not reading them, leaving them to pile up”

Distance to different stars, as measured by the pop culture memes that have just reached them

What’s up with the British accents in Game of Thrones?

“There’s two ways we can do this.” “Is one of them the easy way?” “No.”

“An earlier version of the headline suggested humans have the same genome as the western painted turtle”

Steven Poole’s review of Dan Brown’s new book, written in the style of Dan Brown

Journalism/internet/society

Bizarre op/ed pretends that “infotainment” & “critical” science journalism are discrete, opposing things. Brian Clegg’s comment says it all.

Publisher threatens librarian blogger with $1bn lawsuit

New Yorker introduces Strongbox, a way for sources to share info anonymously w/ journos

“For everyone on the client side who must approve your work, add 12% to the fee.” Freelancer guidelines

So This Is How It Begins: Guy Refuses to Stop Drone-Spying on Seattle Woman

The umbrella has to be one of the best examples of terrible yet long-lasting design

This is the best moment to be in journalism

How Transformers are made

When Europeans arrived in the New World, they brought devastating diseases like smallpox, which killed more native Americans than guns and other weapons. Infections go the other way too: When grey squirrels from North America arrived in the UK, they brought a squirrel pox virus that decimated the local red squirrels. Time and again, animals have invaded new regions and killed the locals by inadvertently bringing biological weapons with them.

Now, Andreas Vilcinskas from Justus-Liebig-University of Giessen has found that one the world’s most invasive insects—the harlequin ladybird—also belongs in the biological weapons club.

It hails from central Asia, but was willingly introduced to Europe, North America, and other parts of the world, by people who were seemingly undeterred by the outcomes of bringing cane toads to Australia or mongooses to Hawaii. Like those other invaders, the harlequin has brought ruin to local ladybirds, many of which have declined dramatically since its incursion.

There are probably many reasons for that. Perhaps it simply outcompete other species for food, or eats them directly. It carries a potent slew of antibacterial chemicals in its blood (or haemolymph) that makes it remarkably resistant to disease. For example, it can shrug off a deadly fungus that kills other ladybirds.

One of these antibacterials is a toxic chemical called harmonine. Many scientists suspected that this substance was poisoning other ladybirds that tried to eat the harlequin’s eggs. But Vilcinskas found that harmonine doesn’t affect native species at all. When he injected the seven-spot ladybird with high doses of the stuff, they were fine. But when he shot them up with the harlequin’s unfiltered haemolymph, they died. The invader clearly has something in its blood that’s deadly to other ladybirds, but it’s not harmonine.

Vilcinskas found the culprit by looking at harlequin haemolymph under a microscope. He found it swarming with microscporidians—a type of single-celled parasitic fungus. These parasites are found in every harlequin that the team examined, but don’t seem to do any harm. They stay in an inactive state and their genes are completely inactive. “I have worked on insect immunity for 20 years, and I had never [before] seen a haemolymph sample that was full of microsporidians that do not harm the carrier,” says Vilcinskas.

It’s possible that harmonine and other antibacterials allow the harlequin to tolerate its parasite. But the native seven-spot ladybird isn’t so well-defended. When Vilcinskas injected them with the microsporidians, they all died within two weeks.

This might be why so many native ladybirds die when the harlequin invades. Since all ladybirds eat each other’s eggs, those that chomp on the harlequin’s young could get a mouthful of lethal microsporidians.

Of course, they need to actually prove that. Helen Roy, who leads the UK Ladybird Survey, says that injecting seven-spots with microsporidians is a far cry from showing that they actually get infected in the field. For a start, she says that seven-spots very rarely eat harlequin eggs, so their chances of getting infected by microsporidians would be few and far between. Then again, seven-spots seem to be holding their own against the invaders, and are unusual among British ladybirds in showing no population declines. Perhaps other species are more wanton in their feeding habits and pay the price?

Either way, Vilcinskas’s team need to show that wild ladybirds do eat harlequin eggs, that they contract microsporidian infections, and that this contributes to their downfall. “The next steps would be to assess ecological relevance,” says Roy. “What does this mean in the real world?”

Lori Lawson Handley, who also works on the UK Ladybird Project, wonders if the microsporidians could be travelling between species through a more grisly route. Some parasitic wasps, like Dinocampus coccinellae, lay their eggs in ladybirds, and they could be spreading the parasites from the harlequin to other species. Their stings could be the equivalent of dirty needles.

A version of this piece also appears at Nature News.

Reference: Vilcinskas, Stoecker, Schmidtberg, Rohrich & Vogel.  2013. Invasive Harlequin Ladybird Carries Biological Weapons Against Native Competitors. Science http://dx.doi.org/10.1126/science.1234032

“It’s like, how much more black could this be? And the answer is none. None more black.” – Nigel Tufnel, This is Spinal Tap.  

The Gaboon viper is a fairly docile creature, and that’s where the good news ends. It also has the longest fangs of any snake—2.2-inch-long weapons that swivel forwards like switchblades. The fangs are connected to such huge glands that they deliver more venom than any other snake—a cocktail of toxins that thin the blood, trigger massive internal bleeding, and can stop hearts.

And to make things much, much worse, the Gaboon viper is virtually impossible to see.

From above, its head looks like a dead leaf. Its five-foot-long body is patterned with rectangles and hourglasses, and shaded in cream, yellow, brown and black. Against the leaf litter of its forest home, the viper simply fades away.

Now, Marlene Spinner from Kiel University has discovered one of the secrets to the Gaboon viper’s exceptional camouflage: The black on its body is really, really black. Not just black, but black. Ultra-black. None more black.

These dark patches also have the texture of velvet, so they’re evenly black from every possible direction. There’s no gloss to them, which creates an illusion of depth. The patches don’t seem to be part of the same surface as the rest of the viper. This, together with the geometric shapes and sharply contrasting colours, break up the snake’s outline and aid its camouflage.

Spinner studied the West African Gaboon viper (Bitis rhinoceros). It’s one of two snakes that people thought were the same, until genetic studies showed that they are dissimilar enough to qualify as separate species.

She looked at the snake’s scales under a powerful electron microscope, which requires samples to be covered in a thin layer of gold. As a result, the pale parts of the viper’s scales developed a light metallic sheen. But the black areas still looked black. That’s a clue—it means that the colour isn’t just produced by a dark pigment, but also by the structures of the scales themselves.

Spinner caught a glimpse of these extraordinarily intricate structures down the microscope. The dark parts of the scale are covered in small ridges, like leaves standing on end (a, below). There are around 1,900 of these leaves in every square millimetre of scale, and each is just 30 micrometres (millionths of a metre) tall.

Spinner zoomed in a thousand times closer, and saw that each leaf was itself covered in a network of even thinner ridges, each just 60 nanometres (billionths of a metre) thick (c). They form a branching pattern like a fingerprint (b). And even the areas between the leaves are covered in hair-like projections (d). The gaboon viper’s black scales contain the most intricate of patterns, in spaces barely wider than a human hair.

When light hits the dark scales, it gets repeatedly reflected and scattered by the tiny leaves and ridges. As it bounces back and forth, it gets increasingly absorbed by dark pigments. In the end, less than 11 percent of any incoming light gets reflected away. This is why the viper’s black patches look so damn black, and evenly so from any viewing angle.

Other closely related vipers don’t use the same nano-scale trick, but there’s a butterfly that does. The Ulysses butterfly (Papilio ulysses) has wings with eye-catching electric blue centres, but their edges are ultra-black for the same reason as the Gaboon viper’s scales. They have a hierarchy of ridges upon ridges that repeatedly reflect incoming light onto absorbing pigments.

Spinner suggests that these tricks could be useful to engineers who work with machines that want to retain as much light as possible, such as solar panels. Admittedly, we have already created blacker-than-black materials that surpass even the viper’s scales. The current record-holder is a surface covered in carbon nanotubes that reflects just 0.045 percent of the light that falls on it. However, it’s extremely fragile. The Gaboon viper might reflect more light, but its black surfaces can cope with months of slithering through rough undergrowth.

Reference: Spinner, Kovalev, Gorb & Westhoff. 2013. Snake velvet black: Hierarchical micro and nanostructure enhances dark colouration in Bitis rhinoceros. Scientific Reports. http://dx.doi.org/10.1038/srep01846

Also: Credit to Alok Jha for the Spinal Tap reference

More on structural colours:

• The world’s shiniest living thing is an African fruit that looks like a pointillist bauble
• A shiny dinosaur –four-winged Microraptor gets colour and gloss
• Camouflaged communication – the secret signals of squid
• Forget butterflies – wasps and flies have hidden rainbows in their wings
• Bird of paradise creates colourful dance with microscopic mirrors in its feathers

In 2011, a team of palaeontologists led by Nancy Stevens, unearthed a single molar in Tanzania’s Rukwa Rift Basin. It was a tiny fossil, but its distinctive crests, cusps and clefts told Stevens that it belonged to a new species. What’s more, it belonged to the oldest known Old World monkey—the group that includes modern baboons, macaques and more. They called it Nsungwepithecus.

A year later, and 15 kilometres away, the team struck palaeontological gold again. They found another jawbone fragment, this one containing four teeth. Again, a new species. And again, an old and distinctive one. The teeth represent the oldest fossils of any hominoid or ‘ape’. They called it Rukwapithecus.

Together, these two new species fill in an important gap in primate evolution. Based on the genes of living species, we know that Old World monkeys and apes must have diverged from each other between 25 and 30 million years ago. But until now, there weren’t any fossils from either group during that window. The ones we found were all 20 million years old or younger.

But Nsungwepithecus and Rukwapithecus were both found in sediments that could be precisely dated to 25.2 million years ago. They imply that apes had already split away from Old World monkeys by that time. Finally, fossils had corroborated the story that genes were telling. And they suggested that the split between these two groups took place against a backdrop of geological upheaval.

I wrote about the discoveries for The Scientist so head over there for the full story.

Some people show more self-control than others. If a marshmallow is placed in front of me, I will probably eat it. You might exercise more restraint than me, or you might not. Either way, your actions will depend on thousands of neurons in your brain. It would make little sense to describe any one of these neurons as showing restraint. They’re just interacting with each other in simple ways, and restraint emerges from these interactions.

You can see the same emergent behaviours in an ant colony. The red harvester ant mainly eats seeds. Some colonies go out searching for seeds no matter the weather but others hold back on dry days when they risk death by dehydration. Deborah Gordon from Stanford University has found that these restrained colonies are actually more successful as those that forage come rain or shine. And they even pass on their reserved behaviour to the next generation.

But it’s not that each individual ant is showing lots of self-control, any more than a single neuron does. The worker isn’t not weighing up how much food the colony already has. It’s not making active decisions based on the weather.

Here’s all that happens: If workers bump into others who have returned to the nest with food, they’re more likely to go out on their own foraging trips. Every colony has its own bar for the number of interactions it takes to make a worker leave to find food. That’s it.

These rules, which Gordon discovered last year, are similar to protocols that control traffic on the Internet—the Anternet, as she calls it. They allow the harvesters to tune their behaviour to their environment without any conscious knowledge. If there’s lots of food around, more foragers will return with seeds, stimulating more nest-bound workers to venture out. If seeds are scarce, fewer ants leave the nest. The size of the foraging parties automatically change to fit the amount of food around.

Harvesters live in deserts and lose water whenever they leave the nest. But they can only gain water by finding seeds. “Colonies must spend water to get water,” explains Gordon. Colonies balance their water budget differently. In some, workers are slightly and consistently less likely to respond to incoming foragers when the humidity is low. “This adds up, year after year, to less foraging activity by that colony,” says Gordon. On some days, not a single ant will leave these nests.

Each ant is behaving like a neuron in a brain, part of a literal hive-mind. It’s just going about its business and interacting with its colony-mates according to extremely simple rules. From these connections, restraint emerges. It’s a collective behaviour that happens at the level of the colony.

What effect does this have in the long-term? That’s a difficult question since harvester colonies can live for 25 years, and produce daughter colonies for 20 of those. To understand how their foraging differences pay off in the long run, you’d need to study a group of harvesters for decades.

That’s exactly what Gordon has done. Since she was a graduate student in 1985, she has almost single-handedly kept an annual census of around 300 harvester colonies in an area of New Mexico (here’s her TED talk on the work). Her records showed that the colonies that hunker down on dry days are just as likely to survive as those that head out all the time. Even though they may stay indoors up to two-thirds of the time, they can find enough seeds on good days and lose fewer workers in the process. They even seem to produce more daughter colonies. “In much of foraging theory, it’s assumed that ‘bigger is better’ – the more food collected, the more successful the forager,” says Gordon. “These results show the opposite.”

Iain Couzin from Princeton University, who studies collective behaviour, calls the study a “remarkable feat” and is particularly impressed that the collective foraging strategies seem to be heritable. Daughter colonies forage in very similar way to their parents. “Due to the relatively large distance between parents and offspring, it is unlikely that such synchronization is based on cultural transmission of behaviour,” he says.

For decades, scientists have been studying how animal swarms, from locusts to fish to birds, move as one, and even think as one. (You can read more about this in my Wired feature on the science of swarms.) But recently, they’ve begun to look at not just how collective behaviours work, but how they evolve.

Couzin, for example, showed that shoals can evolve to fool predators, even if the prey animals don’t know they’re in danger. Another group showed that parasites can make shrimps gather in shoals so they’re more likely to be eaten.

Gordon’s study is slightly different – it’s not about how collective behaviour arose, but how it continues to evolve. “It’s the first study of how natural selection is acting on collective behaviour in a natural population,” she says.

More on collective behaviour:

• Heart of the Swarm – the Amazing Science of Shoals, Flocks, Hives and Brains
• Parasites Make Their Hosts Sociable So They Get Eaten
• The Real Wisdom of the Crowds
• What are you looking at? People follow each other’s gazes, but without a tipping point
• To work out why fish swim together, tempt a predator with virtual prey
• March of the locusts – individuals start moving to avoid cannibals

The transformation from caterpillar to butterfly is one of the most exquisite in the natural world. Within the chrysalis, an inching, cylindrical eating machine remakes itself into a beautiful flying creature that drinks through a straw.

This strategy—known as holometaboly, or complete metamorphosis—partitions youngsters and adults into completely different worlds, so that neither competes with the other. It’s such a successful way of life that it’s used by the majority of insects (and therefore, the majority of all animals). Butterflies, ants, beetles and flies all radically remodel their bodies within a pupa as they develop from larvae to adults.

But what goes on inside a pupa? We know that a larva releases enzymes that break down many of its tissues into their constituent proteins. Textbooks will commonly talk about the insect dissolving into a kind of “soup”, but that’s not entirely accurate. Some organs stay intact. Others, like muscles, break down into clumps of cells that can be re-used, like a Lego sculpture decomposing into bricks. And some cells create imaginal discs—structures that produce adult body parts. There’s a pair for the antennae, a pair for the eyes, one for each leg and wing, and so on. So if the pupa contains a soup, it’s an organised broth full of chunky bits.

We know this because scientists have dissected lots of pupae, although they’ve mostly trained their scalpels on fruit flies and blowflies.  By its nature, such work always destroys the insect that’s being observed. It also only provides a snapshot in time. If you want to work out what happens as metamorphosis progresses, you need to cut open many pupae that you think are at different stages of development.

But now, two teams of scientists have started to captured intimate series of images showing the same caterpillars metamorphosing inside their pupae. Both teams used a technique called micro-CT, in which X-rays capture cross-sections of an object that can be combined into a three-dimensional virtual model.

By dissecting these models rather than the actual insects, the teams could see the structures of specific organs, like the guts or breathing tubes. They could also watch the organs change over time by repeatedly scanning the same chrysalis over many days. And since insects tolerate high doses of radiation, this procedure doesn’t seem to harm them, much less kill them.

One team analysed the caterpillar of the stunning blue morpho just before it started metamorphosis and a week into the process. They analysed the structure of the tracheae—the network of breathing tubes that carry oxygen throughout the insect’s body. Their work was done with the BBC as part of a documentary on metamorphosis—it was publicised in March but hasn’t been published yet.

The second project had its origins in crime-fighting. Thomas Simonsen from London’s Natural History Museum started using micro-CT to look at the pupae for blowflies. These insects lay their eggs on fresh corpses, whether it’s “someone who has been murdered or a deer in a forest”. They appear so predictably that you can estimate a body’s time of death based on where its blowflies are in their life cycle. This gets trickier once the flies turn into pupae, since those all look the same from the outside. But by scanning their insides using micro-CT, Simonsen hoped to get better estimates for how old they are.

From flies, he turned his attention to his favourite subjects—butterflies and moths. He worked with Tristan Rowe and Russell Garwood from the University of Manchester, who regularly scanned the cocoons of painted lady butterflies, some every day.

The scans showed that the caterpillar’s guts quickly change shape, becoming narrower, shorter and more convoluted. Meanwhile, the tracheal tubes become bigger, although their arrangement barely changes. The common wisdom is that “almost everything is massively reorganised in the pupa,” says Simonsen. That’s largely true, but not for the tracheal system. From its first day as a chrysalis, the painted lady already has the breathing tubes of an adult butterfly. “If there is remodelling, it happens very quickly in the first hours of pupation,” says Garwood. Alternatively, it happens when the butterfly is still a caterpillar.

This doesn’t drastically change what we knew about metamorphosis. There are some small insights—it seems that midway through the transformation, the big breathing tube that delivers oxygen to the flight muscles reattaches itself to a different set of openings on the insect’s torso. But the big picture stays the same. “I think it will provide instructive images for textbooks, but I don’t think it provided surprising new insights,” says David Champlin at the University of Southern Maine, who studies metamorphosis.

There are other limitations. The technique’s resolution is rather low. You cannot stain individual tissues or proteins with coloured molecules, while still keeping the animal alive. And the scanners can only pick up a limited number of organs. Brains and nerves, for example, are invisible to them, although Garwood hopes that new technological advances will overcome that hurdle.

Micro-CT scans may not revolutionise what we know about metamorphosis but Garwood hopes that their advantages will give scientists new options for their experiments. For example, the scans use up fewer individuals, since you can scan the same ones over time. This could free up insect specialists to move beyond the usual suspects like fruit flies, and study the development of rare or valuable species without harming them. They could look at how pesticides affect the development of bees, or how mutations in different genes change the process of metamorphosis. Champlin agrees. “It would be great to compare the normal animal with a variety of mutant strains defective for specific genes,” he says.

Reference: Lowe, Garwood, Simonsen, Bradley & Withers. 2013. Metamorphosis revealed: three-dimensional imaging inside a living chrysalis. Interface. http://dx.doi.org/10.1098/rsif.2013.0304

When Bob Paine chucked starfish into the Pacific Ocean in 1963, he was also throwing bombs into the heart of ecology. Back then, the prevailing view was that communities of animals and plants were fairly stable, provided that they contained a diverse set of members. But Paine showed that some species are disproportionately influential. Take the ochre starfish. When Paine prised them from a stretch of Washington shore and pitched them into the surf, the mussels that the starfish ate advanced over the shore like a black glacier. They crowded out other creatures and radically remodelled the coastline.

Paine described crucial species like the starfish as “keystones”, after the central stone that stops an arch from collapsing. The whole community matters but some species are particularly important. Or to borrow from Orwell, “All animals are equal, but some animals are more equal than others”.

Now, the same lessons are being learnt in an ecosystem that’s very different to the rocky Pacific coast—the intestine. The guts of humans and other mammals contain thriving trillions of bacteria and other microbes. This “microbiota” outnumbers the cells that make up our actual bodies. They are so numerous that they are usually studied en masse. Scientists collect samples—say, from faeces—and sequence all the DNA within them, piecing together the identities of the resident species and families.

It’s a powerful approach, which has already taught us much about our gut passengers. Studies have show how these communities change as we get grow older, eat different diets, or take courses of antibiotics. Unsavoury but impressive studies have shown that people can be cured of life-threatening gut infections by being implanted with someone else’s faeces. And many scientists have found links between our gut bacteria and obesity.

For example, in 2007, Ruth Ley, Peter Turnbaugh and Jeffrey Gordon showed that a group of bacteria called the Bacteroidetes are rarer in the guts of obese mice and humans, while a rival group—the Firmicutes—are more common. And a few months ago, Turnbaugh and Lee Kaplan showed that gastric bypass surgery (at least, in mice) might lead to weight loss because it changes an individual’s gut microbe society. Antibiotics might lead to obesity by creating similar upheavals.

The whole community matters but, again, some species are particularly important. One of these Very Important Prokaryotes is called Akkermansia muciniphila. Willem de Vos from Waginingen University first discovered it in 2004 but humans have been carrying it for much longer. Akkermansia accounts for 3 to 5 percent of the bacteria in a normal gut, making it one of our more common intestinal microbes. And it seems to wield a strong influence on our body weight.

Amandine Everard and Patrice Cani from the Catholic University of Louvain have been working with de Vos to understand how this microbe gives its host the guts to stave off the pounds.

They found that Akkermansia is 3,300 times less common in the guts of mice that are genetically predisposed to being obese than in normal rodents. Also, its numbers fall by 100 times when any mouse eats a high-fat diet. This mirrors the results of surveys in humans—if people have lots of Akkermansia in their guts, they tend to be slimmer.

But boost the microbe’s faltering numbers, and you can reverse several of the problems associated with obesity. When team fed their mice with a dose of Akkermansia, they put on less weight and body fat after eating a high-fat diet. They also showed fewer signs of type 2 diabetes. For example, their climbing levels of sugar in their blood completely reversed, and they became less resistant to insulin—the hormone that controls blood sugar.

When the team fed their mice with dead bacteria, nothing happened, proving that the bacteria need to be alive to exert their weight-controlling influence. They don’t, however, need any help. Everard found that a high-fat diet changes the entire community of bacteria in a mouse’s gut, but the addition of Akkermansia doesn’t. Whatever it does, it does it by itself. The whole community matters but some species are particularly important.

Akkermansia feeds upon the delectable mucus that covers our intestines—its species name, muciniphila, is Latin for “mucus lover”. This mucus comes in two layers. The inner one is a barrier that keeps harmful microbes out. The outer one is a meeting room, where our cells parlay with helpful species like Akkermansia.

As mice gain weight, their mucus layer gets thinner, but Akkermansia seems to prevent this erosion. By shoring up the mucus, it could prevent other microbes from inflaming the gut and triggering other changes that cause disease. And there’s probably more. Everard’s team also found evidence that Akkermansia could also affect the division of its host’s gut cells. It also persuades its host to release molecules that kill competing bacteria and reduce inflammation.

Cani sees the relationship between the microbe and its host as a mutually beneficial one. “The host provides energy and a habitat to Akkermansia and, in turn, Akkermansia protects its host from invading microbes.”

Akkermansia might eventually help us to control our weight or reduce the risk of diabetes, but that will take a lot more research. This study was done in mice, and Cani wants to check that the same relationships happen in the human gut. But since this microbe actually lives inside the mucus layer, it has a lot more potential for affecting our bodies than a lot of other “probiotics”. Indeed, when Everard’s team repeated their experiments with Lactobacillus plantarum—a “helpful” microbe commonly used in probiotic foods—it did nothing for the fat mice.

This is a reminder that our gut bacteria are not stowaways. They’re an intimate part of our lives. They contribute to the huge network of proteins and hormones that controls how hungry we get when we don’t eat or how full we feel when we do. They affect how much fat we store and how much sugar builds up in our blood. They influence our immune system, and how we decide which microbes to tolerate and which to attack.

We’re only starting to understand the conversations that happen between our guts and the microbes within them. And we’re only starting to identify the most important species among the vast hordes—the gut equivalents of Paine’s starfish. Rob Knight from the University of Boulder in Colorado, who studies the microbiota, thinks that research in the future will “likely shift back and forth between studies of individual microbes, like this one, and whole-community studies that allow us to generate hypotheses about which other key players in the gut they interact with.”

Reference: Everard, Belzer, Geurts, Ouwerkerk, Druart, Bindels, Guiot, Derrien, Muccioli, Delzenne, de Vos & Cani. 2013. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity.

More on gut bacteria:

• An introduction to the microbiome
• Antibiotics fuel obesity by creating microbe upheavals
• Are those the gut microbes of an unhealthy person, or a pregnant one?
• Three nations divided by common gut bacteria
• Infectious bacteria in your gut create black market for weapons
• What happens to your gut bacteria when you eat a yoghurt?
• Beneficial gut bacteria can become virus collaborators
• From guts to brains – eating probiotic bacteria changes behaviour in mice
• Gut bacteria steer the development of the young brain
• You are what you eat – how your diet defines you in trillions of ways
• Gut bacteria in Japanese people borrowed sushi-digesting genes from ocean bacteria
• Infusion of pseudo-poo cures gut infections in two women
• Gut Microbes Contribute to Mysterious Malnutrition
• Faecal transplants beat antibiotics in clinical trial