This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.
Two people are dancing a waltz, and it is not going well. One is tall and the other short; one is graceful, the other flat-footed; and both are stepping to completely different rhythms. The result is chaos, and the dance falls apart. Their situation mirrors a problem faced by all complex life on Earth. Whether we’re animal or plant, fungus or alga, we all need two very different partners to dance in step with one another. A mismatch can be disastrous.

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

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

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

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

Read the rest of this entry »

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

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

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

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

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

Read the rest of this entry »

New Scientist had a great new feature on nine lost treasures that science wants back. I wrote about one of them – the bones of Peking Man.

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

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

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.
Over the last three years, a group of scientists have been going round two suburbs of Cairns, Australia, and asking local people if they could release mosquitoes on their properties. Ninety percent said yes. These were no ordinary mosquitoes. They had been loaded with bacteria that stop them from passing on the virus that causes dengue fever.

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

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

Read the rest of this entry »

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

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

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

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

Read the rest of this entry »

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

---

The wing of a fruit fly, viewed against a white background, looks very ordinary. It is transparent, with no obvious colours except for some small brownish spots. But looks can be deceptive. If you put the wing in front of a black background, it suddenly explodes in a kaleidoscope of colour. Oranges, blues, greens, violets – virtually the entire rainbow dances across the wing, except for red.

A French scientist called Claude Charles Goureau first noticed these vivid hues back in 1843. Since then, they have languished in obscurity, “apparently unnoticed by contemporary biologists”. Whenever new species of wasps or flies are described, their discoverers almost never mention the coloured patterns of the wings. The visible pigments have even been described as “evolution in black and white”. It’s like walking through an art gallery with a blindfold.

Now, Ekaterina Shevtsova from Lund University has taken off the blind. By photographing several species against dark backgrounds, she has revealed a world of hidden colour, rivalling that of more obviously beautiful insects. “The claim that fly and wasp wing patterns are no match for the incredible diversity of colourful butterfly wing patterns is obsolete,” she says.

Read the rest of this entry »

Top picks

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

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

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

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

The 20 Most Beautiful Bookshops in the world

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

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

This is what a scientist looks like – a Tumblr

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

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

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

The perks and pitfalls of scientific databases

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

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

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

News/science/writing

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

Why isn’t caffeine as addictive as cocaine?

Mammals get small 100x faster than they get big

Cultures of the past, brought low by changing climates

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

Paper denying HIV–AIDS link sparks resignation

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

The age of the great plant hunter continues

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

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

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

How do female insects keep sperm fresh for 30 years?

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

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

Improbable evolution: how life beats the odds.

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

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

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

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

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

Ancient DNA as anthrovoyeurism

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

Why gorillas “grin” when they play

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

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

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

True Confessions of a Dolphin-Loving Marine Biologist

Sea cucumber poo could save reefs from acidification

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

Waging war by killing scientists in Iran.

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

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

Heh/wow/huh

Gorgeous: desert rivers that look like trees

Parkour + trampolining = Wall trampolining = AWESOME

Behold: Etymology Man

Watch Lugnut the bear giving birth

No, CNN, London isn’t there.

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

Flying People in New York City

All the things Tyrannosaurus couldn’t do with those small

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

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

Journalism/internet/society

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

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

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

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

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

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

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

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

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

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

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

Slovenian library creates surprise book packs based on genre

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

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

I’ve written a few guest posts for the Faculty of 1000’s Naturally Selected blog, covering some interesting papers from last year that I missed here. There’s one about how eggs greet sperm, and another on how sleeping alone affects newborn babies. But the third post is one that I particularly want to draw attention to – it’s about a cancer paper that didn’t get much notice last year, but seems to deserve it. Here’s the first bit:

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

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

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

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

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

Image by Hakan Dahlstrom

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Some of you may remember that in September, I flew to Peru for a story I was writing for Wired UK. That story is finally out. It’s about Greg Asner, a scientist who is scanning the Amazon by air, in an effort to study and save it. Here’s how it starts:

A small twin-propeller plane flies over the Amazon rainforest in eastern Peru. The scale of the vegetation is staggering. The tree canopy stretches as far as our eyes can see – an endless array of broccoli florets bounded only by haze and horizon. Greg Asner, 43, Asner has seen the rainforest from this vantage point many times before, but he still stares out the window in rapt fascination.

This patch of forest in the Tambopata National Reserve is luxuriant with life even by the Amazon’s standards. A 50-hectare patch of forest – the size of as many rugby pitches – contains more plant species than the whole of North America. “We might as well be exploring Mars,” says Asner. “You’re looking at areas where no human has ever been. There’s no access.”

Access isn’t a problem for Asner. Behind him are three state-of-the-art sensors of his own devising which, as the plane flies along, takes the forest’s measure. “We’re trying to do something really new,” Asner says. “This world is changing and it requires science that isn’t incremental.” Using the technology he’s developed, Asner is mapping the shape and size of the trees down to individual branches from two kilometres overhead. He can measure the carbon stored in trunks, leaves and soil. He can even identify individual plant species based on the chemicals they contain. With wings and lasers, Asner is conducting one of the most ambitious ecology studies ever staged. He accumulates more data in a single hour than most ecologists glean in a lifetime. With this data, he means to influence governments, steer the course of climate-change treaties and save the forests over which he soars.

Asner’s high-flying science has roots on the ground. In 1994, Asner was working in Hawaii for Nature Conservancy, the environmental non-profit organisation. He was frustrated. His seemingly simple task of eliminating invasive plants was thwarted by an equally simple problem – he could not find them. “We were stumbling around in the dark. That’s how I started getting into this, thinking how we could get maps of this stuff.” Satellite data was too coarse and aerial photos uninformative. Eventually, during a PhD position at the University of Colorado, Asner found his answer – airborne sensors. Fifteen years and much head-scratching later, his team has developed AToMS (Airborne Taxonomic Mapping System), a suite of three plane-borne sensors that he describes as “probably the most advanced Earth-mapping system in the world”.

I’m really proud of the piece. It was my first true taste of field reporting, the science is interesting, and it’s a bit structurally more interesting than what I normally do.

For the moment, you’ll have to buy the issue (or subscribe to the iPad edition) to read it. I’d encourage you to do that (support science writing!) but for non-UK people, the story will be online by the end of the month, and I’ll stick a PDF up in a few weeks.