Ed Yong, Science Writer

You will probably not be able to read this piece without feeling a little itchy. I apologise in advance.

In a laboratory at the National Institutes of Health, Santosh Mishra and Mark Hoon have bred a group of mice with an enviable super-power—they’re immune to itching. You can dab their skin with substances that would send most of us into a scratching frenzy, and they’ll be completely unfazed.

Compared to normal mice, these rodents are missing just one gene called Nppb. It produces a similarly named neuropeptide—a protein fragment that neurons use to communicate with each other. If you inject mice with Nppb, they scratch furiously. If you remove the gene for it or kill the neurons that make it, the mice never itch again. Their other sensations are untouched. They can still feel their own body parts, the touch of others, painful substances, or heat. They just don’t itch.

Mishra and Hoon think that neurons that produce Nppb are the root of itching. They’re the first to detect itchy substances on the skin. When this happens, they use Nppb to trigger other neurons, creating a relay of signals that ends in the brain and creates the perception of an itch.

Itching probably evolved to protect us from parasites and other threats on our skin. By reacting in the instinctive way—having a good scratch—we remove the danger. But even though itchiness is a universal sensation, we’ve only recently started to understand how it works.

For the longest time, scientists regarded itching as a milder cousin of pain. But Zhou-Feng Chen’s group at Washington University buried that idea. In 2009, they found itch-specific neurons in the spines of mice, which produce another neuropeptide called gastrin-releasing peptide (GRP). When they deleted the gene for GRP or removed the neurons that make it, mice never scratched but could still feel pain, heat, pressure and inflammation.

It looked like the team had found the root of itching, but Mishra and Hoon disagree. They believe that Nppb comes first. “The papers on GRP were a huge breakthrough and 95% of their data still hold, but they over-reached in interpretation,” says Hoon. “It was thought that GFP was the primary neurotransmitter. It’s not; it’s the secondary one.” In the itching relay, GRP certainly carries the baton but Nppb that starts the race.

Mishra and Hoon’s study began with a broader aim: They wanted to understand how we tell the difference between different sensations on our skin, like heat, pain or itchiness. They had previously engineered mice that couldn’t register any of these feelings, because none of their neurons had a protein called TRPV1. Mishra and Hoon wanted to know if some of them were specific to particular sensations. For example, are some of the TRPV1 neurons devoted itch sensors?

The answer was yes. A small subset of these neurons produces large amounts of Nppb. Without this peptide, mice became completely insensitive to a wide range of itch-inducing chemicals, even though they could still feel their other sensations. And when the duo injected Nppb back into the rodents, they regained the ability to itch.

Buoyed by these experiments, Mishra and Hoon started to outline the path that itch signals take from the skin to the brain. So far, they’ve worked out the first three “stations” on the way.

The Nppb neurons are the first stop. They sit in nodules called the dorsal root ganglia, which are found on either side of the spine. From there, they send long branches to skin, muscle and other parts of the body. When these branches detect something itchy landing on the skin, the neurons release Nppb.

This peptide travels deeper into the spine. It docks at a protein called Npra, which is found on neurons within the dorsal horn—a routing station where sensory information gets collated and sent to the brain. This is the second stop. (Again, if Mishra and Hoon selectively killed off any neurons carrying Npra, they removed the ability to itch).

Here’s where GRP comes in–Mishra and Hoon think that the Npra neurons release GRP, which carries the signals onwards. That’s the third stop.

They base that conclusion on two lines of evidence. First, if you knock out Nppb, you can still make mice itchy by injecting them with GRP. But this doesn’t work the other way round—Nppb does nothing for mice that can’t make GRP. This implies that Nppb comes first. Also, they only found tiny amounts of GRP in the dorsal root ganglia—the first stop on the path between skin and brain—but lots within the spine itself. So, it can’t be part of the primary itch sensors.

But Chen (who published the GRP papers) is not convinced. “GRP is definitely [found] in dorsal root ganglion neurons,” he says. “The fact that they don’t see it doesn’t mean that what others observed is wrong.” Besides, he notes, a peptide doesn’t need to be present in large amounts to effectively transmit signals between nerve cells. A little will do.

Chen also says that other studies have shown that Nppb is involved in sensing pain in the context of inflammation—something that Mishra and Hoon didn’t test for. So, perhaps Nppb isn’t an itch-specific messenger after all.

Given that our understanding of itching is still in its infancy, future studies may flip, tweak or strike out the suggested roles of GRP and Nppb. But for the moment, Xinzhong Dong at Johns Hopkins University School of Medicine, another researcher in the field, is impressed by the new study. “It’s very interesting and important,” he says. “Just like in all research, more experiments are needed to be done to support the “3-station” itch circuit model, but the findings definitely offer new molecular targets to treat the chronic itch that many patients suffer.”

He’s referring to cases like “M”, a woman who features in Atul Gawande’s astonishing New Yorker story about chronic itching. He describes it as “a constant, relentless itch [that] crawled along her scalp, and no matter how much she scratched… would not go away.” The condition is so bad that one night, M scratched through her skull, all the way into her brain.  Cases like these show that itch circuits can malfunction in spectacular fashion, with life or death consequences.

The Nppb discovery doesn’t mean that treatments are around the corner. In the brain, the peptide may only be involved in itching. But beyond the brain, it also helps to control blood pressure in the heart, kidneys and other organs. If you knock it out, you could get lots of unwanted side effects. Hoon hopes that by tracing the rest of the itch circuit, all the way to the brain, he’ll be able to find other potential ways of interrupting it, in people like “M” with the greatest need.

For more on itching, I highly recommend Atul Gawande’s piece.

Reference: Mishra & Hoon. 2013. The Cells and Circuitry for Itch Responses in Mice. Science http://dx.doi.org/10.1126/science.1233765

White tigers were first recorded in India in the 1500s, but the last wild one was shot in 1958. Still, this spectral animal thrives in captivity. Its captivating white coat and blue eyes have made it a popular mainstay of zoos, and a small number of individuals have been repeatedly bred with each other to boost captive numbers. There were just a few dozen in the 1970s. Now, there are hundreds.

The white tiger isn’t a species in its own right, or even a subspecies. Instead, it’s a mutant version of the Bengal tiger, whose orange coat has whitened thanks to an extremely rare recessive gene. If a tiger inherits two copies of this recessive variant, one from each parent, it’s white. If it has even one normal copy, it’s orange.

Back in the 1970s, Roy Robinson suggested that the gene in question was tyrosinase (TYR). It’s involved in making melanin—a pigment responsible for black, brown, red and yellow colours. If individuals have faulty versions of TYR, they are born without melanin and have pale hair, skin and eyes—they’re called albinos.

The white tiger isn’t a true albino since it still has black pigment in its stripes and eyes. Instead, Robinson thought that it carries chinchilla—a version of the TYR gene that only removes the type of melanin behind yellow and red colours. Without this, the orange coat becomes white, but the black bits stay black. Mystery solved.

You’ll still find this explanation all over the internet, but Xiao Xu from Peking University showed that Robinson was wrong. White tigers have the same version of TYR as orange ones. They also carry identical variants of four other genes that affect the colour of mammal coats. These include MC1R, the gene responsible the white coats of “snow coyotes” and “spirit bears”.

To find the real culprit behind the white coats, Xu’s team compared the DNA of 7 white tigers and 9 orange ones, living in China’s Chimelong Safari Park. They’re all related, and you can see their family tree below. The team sequenced the entire genomes of the three parents, identified more than 170,000 places where their DNA varied between individuals, and sequenced these locations in the rest of the animals.

Gradually, they homed in on seven genes that consistently differed in the white and orange animals. And by looking at these genes in 130 more tigers, from several unrelated sources, the team narrowed their list down to just one.

It has the tremendously catchy name of SLC45A2. It’s also involved in making melanin, although no one is entirely sure how. Variations in the gene have been linked to lighter skin or hair in mice, horses, chickens, medaka fish and humans. It’s associated with light skin colour in modern Europeans, as well as one type of albinism.

The SLC45A2 gene makes a protein of the same name, which consists of 560 amino acids. A single mutation in the gene—a change in just one DNA letter—switches one of those 560 amino acids from an alanine to a valine. This distorts the protein’s shape, and potentially prevents it from taking part in the creation of red-yellow melanin. Every white tiger has two copies of this mutated gene, and can only make the distorted protein. That’s all it takes to change their coats from orange to white.

Greg Barsh from the HudsonAlpha Institute of Biotechnology thinks that Xu’s team have found the right gene, and their results might eventually help to explain exactly what SLC45A2 does. In other species, mutations in the gene usually interfere with both the red-yellow and brown-black types of melanin. But in the tigers, they just disrupt the red-yellow pigments. Mutations in the TYR gene can sometimes do the same—remember chinchilla?—so even though Robinson was wrong about the gene behind the white coats, it’s still possible that SLC45A2 somehow interacts with TYR.

Some people have suggested that the genes behind the white coat also cause other defects, which have become more prominent because the captive animals are so inbred. These include club feet, crossed eyes, cleft palates, and hip or spine problems.

But Xu’s team argue that the white coat is the result of a pigmentation problem, and nothing more. After all, white tigers did once exist in the wild, and those that were captured or shot were often mature adults. This suggests that they’re capable of surviving in the wild despite their mutation—possibly because they hunt colour-blind prey.

Barsh disagrees. “Many humans and other animals with SLC45A2 mutations have severe visual problems,” he says, and he notes that previous studies have found abnormal visual connections between the tigers’ eyes and brains. This might explain the crossed eyes of the captive animals, and probably means that the mutation did affect the white tigers’ survival in the wild.

All of this feeds into a longstanding debate about the role that these white beasts should play in tiger conservation. Writing in Slate, Jackson Landers argues that white tigers should play no role in breeding programmes or reintroduction efforts, and should be allowed to “disappear into memory”. Every zoo enclosure that houses one is an enclosure that isn’t preserving one of the genuinely endangered tiger subspecies, whose numbers and genetic diversity are dwindling.

Xu’s team argues, based on their results, that the white tiger “should be considered a part of the genetic diversity of tigers that is worth conserving”. They argue that both white and orange tigers should be used to boost the Bengal population, and that reintroductions are possible.

It’s hard to see how their results address that issue, though. Given the past existence of wild white tigers, it’s clear that the white mutation was indeed a naturally occurring one—we just know which gene it affects now. Identifying SLC45A2 doesn’t change the fact that white tigers do suffer from several abnormalities, thanks to generations of inbreeding.

And with fewer than 3,200 tigers left in the wild, it’s perhaps a distraction to worry about conserving this one mutant gene. As John Seidensticker form the Smithsonian National Zoological Park bluntly puts it, “We have much more pressing tiger conservation problems.”

Reference: Xu, Dong, Hu, Miao, Zhang, Zhang, Yang, Zhang, Zou, Zhang, Zhuang, Bhak, Cho, Dai, Jiang, Xie, Li & Luo. 2013. The Genetic Basis of White Tigers. Current Biology. http://dx.doi.org/10.1016/j.cub.2013.04.054

More on cat genes:

• One way to skin a cat – same genes behind blotches of tabbies and king cheetahs

Sculpture is all about deliberation. You painstakingly chip marble from a block, or slowly assemble Lego bricks into a shape, or carefully pile clay upon clay. But we’re now entering a world where people can sculpt with proteins, creating amazingly intricate nano-scale shapes just a few billionths of a metre across. And when it comes to these nano-sculptures, the deliberation lies in selecting your materials in the first place. Once that’s done, you throw them all together and watch them assemble themselves.

Masaru Kanekiyo and Gary Nabel used this approach to create a new breed of flu vaccine that (in animal tests) provides better and broader protection than the ones we currently have. I’ve written more about this over at Nature, so head over there for the details.

Over here, I’m going to lay out exactly how the vaccine is built because it’s just so damn cool.

Flu vaccines are caught in a seemingly endless struggle against an ever-changing enemy. Flu viruses mutate all the time, and every year brings a slightly different set of seasonal strains. Immunising against one strain won’t necessarily protect against the others, so flu vaccines must be re-made every year to protect against the (usually three) strains that are predicted to cause the most problems in the upcoming season.

The traditional vaccine uses actual flu viruses that have been killed or inactivated. The idea is to give the immune system a sneak preview of next year’s likely blockbuster strains, so it can prepare by raising an army of defensive antibodies. Kanekiyo’s vaccine trains the immune system in the same way, but does it much more effectively. And it uses faux-viruses.

It’s made of two proteins. The first—haemagglutinin (HA)—is used by flu viruses to recognise and break into our cells. It studs the outer coat of a flu virus like pins in a pincushion. Each pin is made of three HA molecules, which line up in parallel to form a three-sided cylinder.

The second protein—ferritin—is involved in shuttling and storing iron molecules. It’s completely irrelevant to flu infections; it’s there for its handy ability to assemble into a sphere. Each sphere looks a bit like a volleyball and is made from 24 ferritin molecules.

Here’s the beautiful bit. Kanekiyo fused the two proteins together at just the right point that when he mixed 24 of them together, they automatically assembled into a ferritin sphere surrounded by eight HA spikes. Once he got the components right, they could sculpt themselves.

It gets better. The ferritin sphere has eight small triangular gaps on its surface, which are exactly the same width as the HA spikes—28 nanometres, no more and no less. This means that the HA spikes don’t just attach themselves to the sphere in random places. Instead, they become evenly spaced out in very specific positions. Under the microscope, the finished nanoparticle looks like a jack.

Compared to a traditional vaccine (which, if you’ll remember, are actual viruses)., these nanoparticles raise anywhere from 10 to 40 times more antibodies against flu. And the antibodies work against a far more diverse range of strains.

It’s all in the presentation. A real flu virus has around 450 HA spikes crowding its surface, along with other proteins. The nanoparticles have just 8 HA spikes, which are regularly spaced and have nothing else getting in the way. It screams, “LEARN THIS!” to the immune system and then gives it a really good look.

Nanoparticles built using the HA from one particular strain seem to protect against many others. So, if they prove their worth in human test, the hope is that they won’t need to be updated so regularly, or could better prepare us against future pandemics. (Again, read more over at Nature.)

But for the moment, I’m just in awe of how neatly the numbers work. Twenty-four ferritin molecules make a sphere with eight 28-nanometre-wide gaps. Twenty-four HA molecules make eight spikes that are 28 nanometres wide, and fit onto that sphere in exactly the right places.

It’s a testament to the importance of structural biology—knowing the precise shapes of proteins. That knowledge was the key to designing this new vaccine.

Reference: Kanekiyo, Wei, Yassin, McTamney, Boyington, Whittle, Rao, Kong, Wang & Nabel. 2013. Self-assembling influenza nanoparticle vaccines elicit broadly neutralizing H1N1 antibodies. Nature http;//dx.doi.org/10.1038/nature12202

The daily business of science journalism includes getting independent comments on new studies, and (in my opinion) providing those comments is one of the most important ways in which scientists interact with the media.

But from talking to scientists on Twitter, I know that there’s a lot of nervousness about giving comments to journalists. And when I send papers out to people for comments, I often get replies that say, “Sure, but what do you want me to say?”

A straw poll, conducted this morning on Twitter, suggested that people would value a guide on doing this. So, here’s what I am looking for. (To clarify, this isn’t me asking about your own work. It’s me asking you to comment on someone else’s work.)

Let’s start with some assumptions.

These may not be true for all journalists, but they’ll be Standard Operating Procedure for the good ones.

A) I have read the paper that I sent you and understand it (or I’ve talked to the scientists in question and they’ve explained it to me).  So you don’t need to explain its contents back to me.

B) I’m coming to you because you are an expert in this field and you know lots of stuff about it that I don’t know. I want you to use that expertise to help me put the research into context for my readers, and to help me point out any flaws and strengths.

C) I genuinely want to know what you make of the paper. I am not just trying to fill my story with a random cutaway quote to make it look like I did my job and asked around.

D) I’m not here to present people with the totality of your views, so what you say will almost certainly end up getting cut and distilled. BUT, I won’t do that in a way that misquotes or misrepresents you. If you say, “I’m fascinated by this approach but I think it has serious flaws”, I won’t cut that to “I’m fascinated”. I’m a journalist; I’m not making a movie poster.

E) All the tips below apply to situations where I email you a paper and ask for comments. If we’re chatting on the phone, it’s my job to guide you through all of this, but it will obviously take less time for both of us if you know what I’m after. And I’m talking about written interviews. Some of these will apply to TV and radio too, but those have very different constraints.

So, here’s what I would find useful:

1)       Weaknesses. The most important things you can tell me about a study are its weaknesses. Are there inaccuracies in the paper? Statistical failings? Do you think the conclusions don’t hold water? The last thing I want to do is to credulously cover a weak study. But I don’t work in your field and my bullsh*t detector is probably less finely calibrated than yours. So I’m basically relying on you to help me not mislead my readers. Maybe your comments will persuade me to drop a story because it’s just that bad. Maybe your comments will help me to confront an editor and say: “We shouldn’t cover this story that you seem so insistent on. Look: all these scientists think it’s bunk.”

2)       Strengths. But hey, it’s not all doom and gloom! If you’re excited, I want to hear that! Go, science, etc.! But also, tell me the reasons for that excitement. Did they get an unprecedentedly big data set? Some cool new method? An unusual model organism? Innovative technique?

3)       Your reaction. When you read the paper, how did it make you feel? Were you excited? Impressed? Overwhelmed by a deep existential malaise?

4)       The past. The paper will probably have a paragraph that crushes decades of earlier work. You will know all of that; I won’t have had time to read all those earlier papers. So tell me: How does this new discovery fit with what has come before? Is this based on a radical new approach? A long slog? Something that people in the field have been anticipating? Is it just reinventing the wheel?

5)       The present. Have other people found similar things? Contradictory things? Is this one of many such studies, or something truly original? If this is, say, a new approach to fighting malaria, how does it compare to all the other approaches people are investigating?

6)       The future. So, new discovery. Great. But what does it mean? Does it change what we knew about X? Does it open up new avenues for investigating Y? Will it lead to treatments or diagnostic tools for Z?

7)       Detail. Opinions may differ on this, but I like detail and specifics. People sometimes send me quotes that are paragraphs long and “This is probably much more than you need”. That’s true, but I’d rather know all that stuff and have to condense it into something I can use, than to only have something boring, vanilla, and non-descriptive (see the list below).

8)       Simple language, in some cases. Look, I know I’m asking a lot here, and it’s a bit much to expect you to lay out all the strength, weaknesses and context of a study for me and have to worry about jargon while you’re doing it. (Could you also rub my shoulders while you’re at it? Thanks ever so.) Just bear in mind that if something is riddled with jargon, I can paraphrase it but I can’t really quote it. That’s a little riskier for you, because maybe I might inadvertently misinterpret something you say. It’s also less good for me. I want to put your words in quote marks because it can really brighten up a piece.

Note that a lot of this boils down to you telling me something interesting that I couldn’t have predicted. That’s why, when people ask me, “Do you have any specific questions?” the answer is often, “No.” What you have to tell me—what springs into your head—is probably going to be far more interesting that anything I’m expecting you to tell me. Hence, any questions I have will be really broad like, “What does this mean?” or “Do you buy it?” or “How does this fit with other stuff?” or “Science me up, nerd.”

Update: I love Tom Stafford’s extra tip of “Don’t be afraid to tell me what the real story is.” Note that this is different to simply summarising the paper.

Now, here’s what I don’t find useful:

1)       A summary of what the paper showed. Around half of comments start with this. I don’t need it. I already know what the paper showed, or will have talked to someone else who explained it.

2)       Boilerplate adjectives. Please don’t say “This study is interesting…” when you actually mean “dubious” or “boring”.

3)       And on that note, the world’s most banal quote is: “This research is interesting but more work needs to be done”. It’s everywhere. It had invaded science stories like some linguistic cane toad. Of course, more research needs to be done. Otherwise, y’know, science would stop. But what research? What needs to be done? If you were doing that research, what experiments would you do? And if by “More work needs to be done” you really mean, “…because this impossibly flawed study tells us nowt”, then say that. Other banal quotes include, “We welcome any research that takes us further down the road towards [hand-wavy goal]” or “This adds to our understanding of [thingy]”.

4)       Publication politics. “I don’t know why this paper was published in Nature/Science/FEBS Letters” and other such comments are (usually) not useful. My readers don’t really know, or care about, publication hierarchies. “This paper should never have been published” can be useful for indicating strength of opinion, but I’d always want to know specifics about why. Isolated outrage makes for fun quotes, but not informative quotes.

5)       Citation politics. “The authors should have cited this paper instead of that paper.” Again, if an entire body of relevant work has been ignored, then let’s talk about that. But I’m not that bothered about whether reference 55 is the wrong reference 55.

And finally, a note on going off-the record.

Going off-the-record isn’t really a formal, enshrined, binding thing, but if you send me off-the-record comments, I won’t use them. However, my soul will ache when I see “This is off-the-record” followed by a long list of flaws and weaknesses and then “And now on-the-record” followed by something banal.

I get it. If you criticise a study, you risk angering colleagues who work in your field—the same people who you meet at conferences and review your papers. I’m not unsympathetic to that. But as I said, critical comments are probably the most useful variety that we get. You’re in a better position to criticise than I am. And it will probably carry more weight for a reader to see those words coming from the mouth of an expert in the field, than from some journalist. Critical comments do carry personal risk, but they also help us to fight credulous and uncritical science reporting.

Fellow journalists may totally disagree with any and all of this, in which case, have your say in the comments.

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

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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.

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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