Imagine filming a movie hundreds of thousands of times with an infinitely patient crew. Every time you shoot it, you remove just one thing, be it an actor, a line of dialogue or a crew member. By comparing the resulting films, you’d soon work out which elements were vital to the movie’s success, and which could be lost without consequence. Beate Neumann, Thomas Walter and a group of scientists known as the Mitocheck Consortium have taken just such an approach to better understand one of the most fundamental processes of life.

Some directors employ inanimate objects like Keanu Reeves, but Neumann and Walter wanted to work with far more dramatic stars – DNA, proteins and the like. Their task was to work out which genes were vital for the process of mitosis, the immensely complicated operation where one cell divides into two. To do that, they systematically went through each of the 21,000 or so genes in the human genome and inactivated them, one by one, in different cells. They then filmed these subtly different actors as they divided in two.

This incredible library of around 190,000 films, all shot in time-lapse photography, is publicly available at the Mitocheck website. It’s a treasure trove of data, whose doors have been left for the entire scientific community to walk through, and no doubt they will. Name a gene, any gene, and with a couple of mouse clicks, you can find a movie that shows you what happens when it’s knocked out. You can work out if your favourite gene is essential to cell division, and you can even find other genes that have similar effects.

The study’s leader Jan Ellenberg says, “The response of human cells to silencing each gene is already pre-recorded and scientists can simply log in to our database to check the result, rather than spending weeks or months of time in the laboratory to obtain the data.”

The movies are certainly useful, but they are beautiful in their own right. For a daily and microscopic process, mitosis is an astonishingly beautiful dance. It begins with cells creating the right number of partners, by duplicating all of their chromosomes. At first, the dancers haphazardly mingle with each other but as things get underway, they separate and line up in a neat row. Then, dramatically, they shimmy across to opposite ends of the room, following long spindles of protein. Once the partners split up, the cell pinches down its middle and separates them forevermore. Without this courtly dance, you would never have been anything more than a fertilised egg. Life simply wouldn’t work.

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Ever prodded at an injury despite the fact you know it will hurt? Ever cook an incredibly spicy dish even though you know your digestive tract will suffer for it? If the answers are yes, you’re not alone. Pain is ostensibly a negative thing but we’re often drawn to it. Why?

According to Marta Andreatta from the University of Wurzburg, it’s a question of timing. After we experience pain, the lack of it is a relief. Andreatta thinks that if something happens during this pleasurable window immediately after a burst of pain, we come to associate it with the positive experience of pain relief rather than the negative feeling of the pain itself. The catch is that we don’t realise this has happened. We believe that the event, which occurred so closely to a flash of pain, must be a negative one. But our reflexes betray us.

Andreatta’s work builds on previous research with flies and mice. If flies smell a distinctive aroma just before feeling an electric shock, they’ll learn to avoid that smell. However, if the smell is released immediately after the shock, they’re actually drawn to it. Rather than danger, the smell was linked with safety. The same trick works in mice. But what about humans?

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In autumn, as green hues give way to yellows and oranges, some leaves develop mysterious green islands, where life apparently holds fast against the usual seasonal decay. These defiant patches still continue the business of photosynthesis long after the rest of the leaf has withered. They aren’t the tree’s doing. They are the work of tiny larval insects that live inside it – leaf-miners.

The larvae were laid within the leaf’s delicate layers by their mother. They depend on it for shelter and sustenance, and they can’t move away. If their home dies, they die, so they have a vested interest in keeping at least part of the leaf alive. These are the miniature landscape architects that create the green islands, and they don’t do it alone – to manipulate the plant, they wield bacteria.

Wilfried Kaiser and scientists from Rabelais University discovered this partnership after realising that some bacteria and fungi can also cause green islands. He reasoned that microbes might be helping insects to achieve the same ends. So he searched for them in one particular species, a tiny moth called the spotted tentiform leaf-miner, Phyllonorycter blancardella. Its larva makes its home in the leaves of apple trees.

Kaiser found that the leaf-miners are host to just one detectable type of bacteria – Wolbachia. That’s hardly surprising. Wolbachia infects around 60% of the world’s insect species, making it a strong candidate for the title of world’s most successful parasite. Without exception, every leaf-miner that Kaiser tested, from all over the Loire Valley, carried Wolbachia in their tissues.

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Releasing a steady stream of urine to attract a mate and then fighting off anyone who still dares to approach you doesn’t seem like a great idea for getting sex. But this bizarre strategy is all part of the mating ritual of the signal crayfish. A female’s urine, strange as it sounds, is a powerful aphrodisiac to a male.

Fiona Berry and Thomas Breithaupt studied these courtship chemicals by organising blind speed-dates between male and female crayfish, whose eyes had been covered with tape. They also injected a fluorescent dye into the animals’ bodies, which accumulated in their bladders. Every time they urinated, a plume of green dispersed through the water.

If the duo blocked the female’s nephropores (her urine-producing glands), the males never showed her any interest. If they met, they did so aggressively. But when the duo injected female urine into the water, things took a more lustful turn, and the males quickly seized the females in an amorous grip. Female urine is clearly a turn-on for males.

But the female doesn’t want just any male – she’s after the best, and she makes her suitors prove their mettle by besting her in a test of strength. As he draws near, she responds aggressively, even though it was her who attracted him in the first place. No quarter is given in these fights. The female only stops resisting if the male can flip her over so that he can deposit his sperm on her underside.

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Today, the city of Angkor in Cambodia lies in ruins. But a thousand years ago, life there was very different. Then, Angkor was the heart of the Khmer empire and the largest preindustrial city of its day. It had a population of a million and an area that rivalled modern Los Angeles. And the key to this vast urban sprawl was water.

Radar images of the city by the Greater Angkor Project (GAP) revealed that Angkor was carefully designed to collect, store and distribute water. The “Hydraulic City” included miles of canals and dikes, irrigation channels for supplying crops, overflow channels to cope with a monsoon, massive storage areas (the largest of which was 16km² in area), and even a river diverted into a reservoir. Water was the city’s most precious resource, allowing it to thrive in the most unlikely of locations – the middle of a tropical forest.

But water, or rather a lack of it, may have been part of Angkor’s downfall. Brendan Buckley from Columbia University has reconstructed the climate of Angkor over the last 750 years, encompassing the final centuries of the Khmer Empire. The records show that Angkor was hit by two ferocious droughts in the mid-14^th and early-15^th century, each lasting for a few decades. Without a reliable source of water, the Hydraulic City’s aquatic network dried up. It may have been the coup de grace for a civilisation that was already in severe decline.

Many theories have been put forward for the downfall of Angkor, from war with the Siamese to erosion of the state religion. All of these ideas have proved difficult to back up, despite a century of research. Partly, that’s because the area hasn’t yielded much in the way of historical texts after the 13^th century. But texts aren’t the only way of studying Angkor’s history. Buckley’s reconstruction relies on a very different but more telling source of information – Fujian cypress trees.

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If anyone wants to find out a bit more about me, my background, my goals and my thoughts on online science communication, this is probably a good place to start.

Some background: following every ScienceOnline conference, Bora likes to pretend that he doesn’t already know everything about everyone by watching their internet habits on a gigantic bank of monitors, while cackling and stroking a cat. To that end, he does a series of interviews, where the conference participants say a bit about themselves. It’s now my turn, and we’re both posting this up at the same time. Given that I wrote this for Bora, it seems fitting that I was a bit more verbose than usual.

Welcome to A Blog Around The Clock. Would you, please, tell my readers a little bit more about yourself? Where are you coming from (both geographically and philosophically)? What is your (scientific) background?

I’m Ed, I talk to people about science and I do it in three main ways. I write a science blog called Not Exactly Rocket Science, I do a fair bit of freelance journalism for British press, and I work in a science communications role for a big UK cancer charity. Round about the time that swine flu was saturating the headlines, I started calling myself a triple-reassortant science writer, which is a seriously geeky affectation but worth it for the occasional person who gets it and sniggers.

In terms of my background, I did a degree in Natural Sciences at Cambridge, covering all sorts of fields from animal behaviour to experimental psychology. I assumed that research was going to be my calling and I spent a year or so as a PhD student before realising that I was apocalyptically bad at it. Mythically bad. People composed ballads about how much I sucked. If I didn’t destroy the world during my time in the lab, it’s only because that would probably have counted as a publishable result.

Thankfully, the insight that I sucked at doing science coincided nicely with the revelation that I wasn’t too bad at talking about it. Essentially, I can’t narrow my attentional spotlight on a single subject; I need broad vistas. I can’t derive motivation from rare but transcendental moments of success amid a long drought of failure; I need a more regular fix. And my hands are clumsy and inept when handling a Gilson; they’re much better at dancing on a keyboard. And thus concludes my origin story. Maybe I should have just lied and said something about being bitten by a radioactive David Attenborough.

Moving on to here and now, I’m constantly excited by the new discoveries that I read about and I’m keen to infect other people with the same enthusiasm. I just think that people will be better off if they have a deeper understanding of the world around them and if they’re motivated to sceptically seek out that knowledge in the first place. Telling awe-inspiring stories about science is one way of achieving both those ends. My own love for science was fuelled by masterful communicators and I want to carry on that tradition.

Oh, and I live in London, a great, beautiful, cosmopolitan, culturally vibrant city that has the god-awful problem of being full of Londoners.

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Not Exactly Pocket Science is a set of shorter write-ups on new stories with, where possible, links to more detailed takes elsewhere. It is meant to complement the usual fare of detailed pieces that are typical for this blog.

Live broadcasts of sperm races

Last week, I blogged about the sperm wars of ants and bees. Even after males have mated with a queen, their semen contains chemicals that have evolved to incapacitate the sperm of their rivals. But there’s more than one way of winning the sperm wars. Some insects do it through sheer numbers.

Mollie Manier managed to set up live broadcasts of the sperm wars. She engineered male flies whose sperm was loaded with proteins that glow either red or green. By following these glows with a special microscope, Manier captured astounding and beautiful videos of the sperm racing around the female’s genital tract at high speed, like miniature formula-one cars.

When fruit flies mate, the female stores the male’s sperm in a special pouch. Because of this, the last male to mate with her gets an advantage because his sperm can flush out those of earlier suitors. To facilitate this, males ejaculate far more sperm than is actually necessary to fill the female’s stores. That gives them the best chance of ousting as many rival cells as possible. But unlike the battles of ants and bees, the sperm of fruit flies don’t actually harm those of rivals. Once the number of racers has been set, it’s a fair fight.

Reference: Science http://dx.doi.org/10.1126/science.1187096

More from Jef Akst at The Scientist

Poisonous fungi unwittingly betray plants to voles

Meet the Southern vole – it looks unassuming but this little critter might just have a penchant for stealing biological weapons. As the vole eats grass, it sometimes gets mouthfuls of a fungus called Neotyphodium, which lives inside the stems. The fungus produces chemicals that poison plant-eaters trying to munch its home. Related species, like the field vole, lose weight and die earlier when they eat these poisons, but Susanna Saari found that the Southern voles seem to be immune. When they eat infected ryegrass, they’re perfectly healthy and neither their body weight nor their numbers fall.

If anything, they actually seem to benefit from the poisons, becoming less likely to fall prey to their greatest enemy, the least weasel. The reason for this protection is still unclear. Many animals steal biological weapons: the sea slug Glaucus protects itself with stinging cells taken from the jellyfish it eats; the tiger keelback snake eat toads to steal their poison; the hooded pitohui nicks poisons from beetles. But Saari thinks that the voles are different. Lleast weasels, which hunt by smell, couldn’t distinguish between the urine of voles that had fed on infected or uninfected grass. When the voles faced a weasel, those that were full of fungi were actually less active but despite this tendency to freeze, they were less likely to be captured by weasels. Perhaps by freezing in the face of danger rather than fleeing, they somehow protected themselves.

Meanwhile, the discovery could recast the relationship between the fungus and the grass. Neotyphodium infects 20-30% of all grass species and the two are typically viewed as accomplices, whose interests are aligned. The fungus doesn’t harm the health of the grass, and its toxins deter grazers. But if the fungus’s poisons are actually a boon to some grass-eaters, its presence might actually harm the grass by drawing hungry voles. In that case, the fungus would be less a beneficial tenant than a resident parasite.

Reference: PLoS ONE http://dx.doi.org/10.1371/journal.pone.0009845

And finally…

The biggest story of the last week was undoubtedly the tale of X-Woman’s Fingerbone. Unfortunately, the timing of the story coincided with the move to Discover and other things, which meant no time to cover the story in the depth that it clearly required. But that’s no big loss – there’ s little chance that anyone could have produced coverage as thorough and lucid as my co-blogger(!) Carl Zimmer. Go read his take.

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Folks, a few people who were subscribing to the NERS feed via ScienceBlogs have noted that the feed automatically updated when this blog moved to Discover.

This is true, but you still need to manually change the feed URL in your reader to http://feeds.feedburner.com/notrocketscience/

Basically, the Discover tech spirits have done something clever with Feedburner where the old ScienceBlogs feed has been redirected to the new Discover one. But this is just a temporary solution. If you check your readers, you’ll see that it’s still using the old feed URL. In a few weeks, that URL will stop working and Feedburner will send you a reminder asking you to update your readers to the new one. The Internet, it seems, is clever, but not that clever.

During our early childhoods, the vast majority of us are boarded by a stowaway that can stay with us for the rest of our lives. It can rear its head when we are at our weakest and it can wriggle its way down our family tree into our children and grandchildren. It’s a virus called human herpesvirus-6, or HHV-6 for short. It’s probably in your genome right now.

As its name suggests, HHV-6 is one of the herpesviruses. Unlike other members, it doesn’t actually cause herpes, but it is one of the most common infections in the Western world. It infiltrates the bodies of over 90% of children and it causes a near-universal disease called ‘exanthema subitum’, also known as roseola or three-day fever. The signs of infection soon clear out, but the virus stays put.

Like all herpesviruses, HHV-6 can enter a dormant phase called “latency”, where it stays in our cells after the initial infection has cleared. These stowaways can stay with us for our entire lives but they can sometimes be roused from their slumber to infect again, especially if their host’s immune system becomes compromised. HIV patients, for example, often experience recurring infections. After decades of symptomless dormancy, HHV-6’s reawakening can be severe and debilitating.

Now, Jesse Arbuckle from the University of South Florida College of Medicine has uncovered the virus’s hiding place. Most herpesviruses just leave their genome as a ring of DNA floating about in infected cells. But HHV-6 is a far sneaker infiltrator. It actually shoves its genes into the genome of its host and it targets special structures call telomeres, which sit at the ends of our chromosomes. Telomeres are like the plastic tags at the ends of your shoelaces – they stop long strands of DNA from fraying at the ends, losing valuable information and becoming incorrectly entangled.

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Dan, a scientist working on dangerous viruses, is giving a visitor a tour of his lab. Before this happens, all test tubes containing disease-causing agents must be sealed in a chamber with a flick of a switch. Unfortunately, the switch broke recently and it hasn’t been repaired yet. Entering the room means certain death. Dan knows this but still, he bids the visitor to enter. The inevitable happens; they become sick and they die.

Would you consider Dan’s actions to be immoral? What if, in a parallel universe, the visitor miraculously survived? Does that change your views of Dan’s deeds? What if Dan didn’t know about the broken switch? For most of us, the answers are clear. If Dan knew about the broken switch, he was wrong to send in the visitor to potential death, regardless of whether they actually perished. But bizarrely, not everyone would see it that way.

Liane Young from MIT found that people with brain damage in an area called the ventromedial prefrontal cortex (VMPC) are unusually likely to brush off failed attempts at harming other people. They frowned upon actual murder with the usual severity but compared to normal people, they were twice as likely to think that attempted murder was morally permissible. Young thinks that the VMPC is vital for our ability to deduce respond emotionally to the intentions of other people, an important skill when it comes to making moral judgments.

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