November 20, 2009
Category: Memory • Neuroscience • Sleep
In my final year of university, with exam deadlines looming and time increasingly fleeting, I considered recording some of my notes and playing them over while I was asleep. The concept of effectively gaining 6 extra hours of revision was appealing, but the idea didn't stick - it took too long to record the information and the noise stopped me from sleeping in the first place. And the whole thing had a vague hint of daftness about it. But a new experiment suggests that the idea actually has some merit, showing that you can indeed strengthen individual memories by reactivating them as you snooze.
Sleep is a boon to newborn memories. Several experiments have shown that sleep can act as a mental cement that consolidates fragile memories into stable ones. But John Rudoy from Northwestern University wanted to see if this process could be taken even further by replaying newly learned information while people slept.
He asked a dozen volunteers to remember the positions of 50 different objects as they appeared on a screen. The items, from kittens to kettles, were all accompanied by a relevant noise, like a meow or a whistle. Shortly after, the recruits all had a short nap. As they slept, Rudoy played them the sounds for 25 of the objects, against a background of white noise. When the volunteers woke up, they had to place each of the 50 objects in the right position, and they were marked on how close they came to the actual target.
The results were very clear - the volunteers positioned the objects around 15% more accurately if they'd heard the relevant sounds while they slept. Although the sleep sounds didn't work for everyone, the majority of the participants - 10 out of 12 - benefited in some way. And none of them knew they heard anything at all while they slept. When they were told this and asked to guess which sounds they heard, they didn't do any better than chance.
To show that this isn't just a general benefit of revision, whether conscious or not, Rudoy did a similar experiment. This time, his volunteers heard the noises after they had first seen the objects but while they were still awake. This group proved to be no better at remembering the items' locations than those who didn't hear the second round of sounds.
Finally, to understand what was going on in the brains of the slumbering recruits, Rudoy used electroencephalograms (EEG) to measure the electrical activity in the heads of 12 fresh volunteers. He showed that people who were better at remembering the objects' positions after their nap were also those who showed the most brain activity when they heard the sounds Rudoy thinks that hearing the sounds during sleep prompted the brain to rehearse and strengthen associations between the objects and their locations.
Some people think that sleep improves memories in a general way, by making our brains more flexible and easing the incorporation of new information. But these simple experiments show that the benefits can be very specific indeed. It's not only possible to strengthen specific and individual memories by providing the right triggers, but we get the opportunity to do so every single night.
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Posted by Ed Yong at 9:20 AM • 3 Comments • 0 TrackBacks
November 19, 2009
Category: Palaeontology
Around 15,000 years ago, North American was home to a wide menagerie of giant mammals - mammoths and mastodons, giant ground sloths, camels, short-faced bears, American lions, dire wolves, and more. But by 10,000 years ago, these "megafauna" had been wiped out. Thirty-four entire genera went extinct, including every species that weighed over a tonne, leaving the bison as the continent's largest animal.
In trying to explain these extinctions, the scientific prosecution has examined suspects including early human hunters, climate change and even a meteor strike. But cracking the case has proved difficult, because most of these events happened at roughly the same time. To sort out this muddled chronology, Jacquelyn Gill has approached the problem from a fresh angle. Her team have tried to understand the final days of these giant beasts by studying a tiny organism, small enough to be dwarfed by their dung - a fungus called Sporormiella.
Sporormiella grows in the droppings of large plant-eating mammals and birds, and it leaves tell-tale spores in its wake. More spores mean more dung, so Sporormiella acts as a rough indicator of the number of herbivores in a given area. The fall of these beasts is reflected in falling numbers of spores.
Gill counted these spores in the sediment of Indiana's Appleman Lake, and compared them to counts of fossilised pollen and charcoal from the same soil. That allowed her to match the numbers of plant-eaters at any given time with the local plant species and the frequency of forest fires.
Using this fungal index, Gill has produced a detailed timeline of the changes in the Pleistocene. Her revised history argues against a role of climate change or alien rocks, but fails to clear early humans of the blame. More importantly, it suggests that many events that happened around the same time, such as an upheaval in the local plant communities and a rise in large infernos, were the result of the beasts' decline, rather than the cause of them.
The spores revealed that the fall of the megafauna began in earnest around 14,800 years ago. By the 13,700 year mark, their numbers had fallen to less than 2% of their former glory. They never recovered, but it clearly took a few more millennia for the stragglers to succumb - the last bones of the great beasts date to around 11,500 years ago.
Changes in the local vegetation happened after the beasts started disappearing, around 13,700 years ago. Before this point, the environment was open grassland with the odd tree. Fires were a rarity. But without the suppressive mouths of the big plant-eaters, trees grew unchecked, producing a combo of vegetation you just don't see today. Large numbers of temperate deciduous trees like elm and ash happily coexisted with cold-loving conifers like larch and spruce.
And with them came fires, large infernos that broke out around 14,000 years ago and returned every century or so for the next few millennia. The pollen and charcoal of Appleman Lake tell the story of these changes, and also show that they came after the beasts' disappearance.
Right away, this timeline rules out the possibility that a collision with a large space object killed the megafauna. The proponents of that theory place the collision at around 13,000 years ago, after the giants had started to decline. And it's clear that extinctions were long, drawn-out affairs, rather than the relatively rapid annihilations you'd expect from an extraterrestrial impact.
Likewise, changing climate becomes an unlikelier suspect. The megafaunal extinction predated a rapid, millennium-long chill called the Younger Dryas that took place around 11,500 and 12,800 years ago. When the megafauna started dying, the Earth was going through a warming phase. That might well have affected them, but it didn't do so through the most obvious method - changing the plants they ate. After all, Gill's work tells us that the beasts' disappearance changed the plants, not the other way round.
What about humans, those pesky slayers of animals? Some scientists believed that North America's Clovis people specialised in hunting big mammals, causing a "blitzkrieg" of spear-throwing that drove many species to extinction. But these hunters only arrive in North America between 13,300 and 12,900 years ago, around a thousand years after the population crashes had begun.
If people were responsible, they must have been pre-Clovis settlers. There's growing evidence that such humans were around, but they weren't common or specialised. They may have contributed to the beasts' downfall, while Clovis hunting technology delivered a coup de grace to already faltering populati0ons.
By analysing the sediment at Appleman lake - spores, pollen, charcoal and all - Gill has replayed the history of the site, spanning the last 17,000 years. Her data rule out a few theories, but as she says, they "[do] not conclusively resolve the debate" about climate causes versus human ones. It's possible that similar studies at different sites and other continents will help to provide more clues.
Meanwhile, her study certainly tells us more about what happened in Earth's recent history, when a large swathe of hefty plant-eaters died off - a change from savannah to woodland, and more fires. This isn't just a matter of historical interest. The same events might be playing out today, as the largest modern land mammals suppress fires by eating flammable plants, and are facing a very real threat of extinction. History could well repeat itself.
Reference: Science 10.1126/science.1179504
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November 18, 2009
Category: Journalism
News journalism relies on a tried-and-tested model of inverted storytelling. Contrary to the introduction-middle-end style of writing that pervades school essays and scientific papers, most news stories shove all the key facts into the first paragraphs, leaving the rest of the prose to present background, details and other paraphernalia in descending order of importance. The idea behind this inverted pyramid is that a story can be shortened by whatever degree without losing what are presumed to be the key facts.
But recently, several writers have argued that this model is outdated and needs to give way to a new system where context is king, Jason Fry argues that this "upside-down storytelling" is broken and while his piece primarily deals with sports reporting, his arguments equally apply to other areas.
"Arrive at the latest newspaper story about, say, the health-care debate and you'll be told what's new at the top, then given various snippets of background that you're supposed to use to orient yourself. Which is serviceable if you've been following the story (though in that case you'll know the background and stop reading), but if you're new you'll be utterly lost."
Fry cites an excellent article by Matt Thompson at Nieman Reports, which compares the reading of modern news to "requiring a decoder ring, attainable only through years of reading news stories and looking for patterns, accumulating knowledge". Both writers make excellent points that are especially problematic for bigger stories, where rolling coverage drives audiences deeper into the latest minutiae and further away from the context needed to make sense of it all. The problem isn't limited to old media - blogs often send readers on interminable trails of links and archived posts to the start of a debate or topic.
These issues are highly relevant to science journalism. Here, context is vital for placing new findings against the body of research that inspires, supports or contradicts it. It shows you the giant shoulders that each new discovery stands upon.
Take the widely reported news about FOXP2, the so-called "language gene" last week. The human version of FOXP2 encodes a protein that's just two amino acids away from its chimp counterpart. FOXP2 is an executive gene that controls the activity of many others; a new study in Nature showed that the two changes that separate the human and chimp proteins give FOXP2 control over a different network of minions. This could have been an important step in the evolution of human speech.
Cue the headlines saying that the human speech gene had been found and that one gene prevents chimps from talking. One site even claimed that one gene tweak could make chimps talk. But human speech is a complicated business, involving radical changes to both our brains and our anatomy. FOXP2 may have been an important driver of these changes but the odds of there being a single language gene are about as high as there being a gene for penning fatuous headlines or writing in an inverted-pyramid style. And experiments in mice, birds and even bats have suggested that if it's a gene for anything, it's for learning coordinated movements.
When I saw the press copy of the paper, I knew that it was going to be big and that I wanted to cover it. But I wanted to try something different. Last year, I wrote a long feature for New Scientist about the FOXP2 story, from the gene's discovery to the erosion of its "language gene" moniker. Instead of covering the paper fresh, I decided to re-edit the feature, incorporating the new discoveries (and others that had come out in the last year) into the narrative I'd already crafted. The result is a living story, an up-to-date version of the FOXP2 tale, kitted out in this season's colours. The new stuff is there, but you hopefully get the nuances that are necessary to appreciate their significance. I'm pleased with the result and I want to do more.
I've touched on the idea of living stories in my write-ups of the World Conference of Science Journalists. There Krishna Bharat, founder of Google News, cited the Wikipedia page on swine flu as an example of a "timeless resource", constantly updated as statistics changed and discoveries were revealed. The page provided a valuable insight into a rapidly developing topic without simply setting new statistics adrift in a barren and featureless sea.
Fry and Thompson also cite Wikipedia as an example of how it should be done, and they quote an interview with co-founder Jimmy Wales, who notes that the online encyclopaedia is now a major attraction for news-hungry readers. On Wikipedia, the latest goings-on are added, but they're never allowed to ride shotgun at the expense of context. Clearly, something about the model is working, and "topic pages" are an emerging trend in the world of online news. The New York Times has introduced them. New Scientist has them. The Associated Press are following suit.
That's not to say that news pieces as we know them are journalistic dinosaurs. After all, people go to Wikipedia for summaries of newsworthy topics after finding out about them through more traditional channels. I doubt that many use the site as their primary news source. At a population level, a mix of approaches seems best - reporting of news alongside living resources that place them within a broader landscape.
This is especially needed when it comes to health-related stories, where new studies about Risk X and Disease Y must be weighed up against others of their ilk. Currently, this is a rarity - the focus on new news paints a picture of rapidly seesawing consensus, when the reality is more like a feather causing a weighted scale to teeter.
On an individual level, writers can also do more within the bounds of a single story, especially in the different environment offered by online media. Some selection pressures are the same - having important keywords in opening paragraphs pleases search engines and editorial conventions alike. But others are more relaxed - the inverted pyramid style may have been essential in a print environment where limited column space could hack a long piece to mere paragraphs but such unnecessary constrictions are irrelevant online. Here, pieces can find room to breathe, and Z-list elements like details and background can find their rightful place at a story's heart.
This is the approach that I try for in this blog, making news stories read more like mini-features. They're less inverted-pyramid and more factual oblongs. I try to get the important stuff in early for the attention-deficit among us, but there's no rush. I try to get a narrative in there without resorting to a straightforward school-essay structure. I hope it works, and I'm happy to take feedback. Meanwhile, I'm also considering adding topic pages for the pet issues that I find myself returning to time and again - horizontal gene transfer, embodied cognition, animal cooperation, transitional fossils... you know, the good stuff.
Thoughts?
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Posted by Ed Yong at 9:30 AM • 13 Comments • 0 TrackBacks
November 16, 2009
Category: Animal behaviour • Animal intelligence • Animals • Elephants • Evolution • Genetics • Human evolution • Mammals
At first glance, the African elephant doesn't look like it has much in common with us humans. We support around 70-80 kg of weight on two legs, while it carries around four to six tonnes on four. We grasp objects with opposable thumbs, while it uses its trunk. We need axes and chainsaws to knock down a tree, but it can just use its head. Yet among these differences, there is common ground. We're both long-lived animals with rich social lives. And we have very, very large brains (well, mostly).
But all that intelligence doesn't come cheaply. Large brains are gas-guzzling organs and they need a lot of energy. Faced with similarly pressing fuel demands, humans and elephants have developed similar adaptations in a set of genes used in our mitochondria - small power plants that supply energy to our cells. The genes in question are "aerobic energy metabolism (AEM)" genes - they govern how the mitochondria metabolise nutrients in food, in the presence of oxygen.
We already knew that the evolution of AEM genes has accelerated greatly since our ancestors split away from those of other monkeys and apes. While other mutations were reshaping our brain and nervous system, these altered AEM genes helped to provide our growing cortex with much-needed energy.
Now, Morris Goodman from Wayne State University has found evidence that the same thing happened in the evolution of modern elephants. It's a good thing too - our brain accounts for a fifth of our total demand for oxygen but the elephant's brain is even more demanding. It's the largest of any land mammal, it's four times the size of our own and it requires four times as much oxygen.
Goodman was only recently furnished with the tools that made his discovery possible - the full genome sequences of a number of oddball mammals, including the lesser hedgehog tenrec (Echinops telfairi). As its name suggests, the tenrec looks like a hedgehog, but it's actually more closely related to elephants. Both species belong to a major group of mammals called the afrotherians, which also include aardvarks and manatees.
Goodman compared the genomes of 15 species including humans, elephants, tenrecs and eight other mammals and looked for genetic signatures of adaptive evolution. The genetic code is such as that a gene can accumulate many changes that don't actually affect the structure of the protein it encodes. These are called "synonymous mutations" and they are effectively silent. Some genetic changes do, however, alter protein structure and these "non-synonymous mutations" are more significant and more dramatic, for even small tweaks to a protein's shape can greatly alter its effectiveness. A high ratio of non-synonymous mutations compared to synonymous ones is a telltale sign that a gene has been the target of natural selection.
And sure enough, elephants have more than twice as many genes with high ratios of non-synonymous mutations to synonymous ones than tenrecs do, particularly among the AEM genes used in the mitochondria. In the same way, humans have more of such genes compared to mice (which are as closely related to us, as tenrecs are to elephants).
These changes have taken place against a background of less mutation, not more. Our lineage, and that of elephants, has seen slower rates of evolution among protein-coding genes, probably due to the fact that the duration of our lives and generations have increased. Goodman speculates that with lower mutation rates, we'd be less prone to developing costly faults in our DNA every time it was copied anew.
Overall, his conclusion was clear - in the animals with larger brains, a suite of AEM genes had gone through an accelerated burst of evolution compared to our mini-brained cousins. Six of our AEM genes that appear to have been strongly shaped by natural selection even have elephant counterparts that have gone through the same process.
Of course, humans and elephants are much larger than mice and tenrecs. But our genetic legacy isn't just a reflection of our bigger size, for Goodman confirmed that AEM genes hadn't gone through a similar evolutionary spurt in animals like cows and dogs.
Goodman's next challenge is to see what difference the substituted amino acids would have made to us and elephants and whether they make our brains more efficient at producing aerobic energy. He also wants to better understand the specific genes that have been shaped the convergent evolution of human and elephant brains over the course of evolution. That task should certainly become easier as more and more mammal genomes are published.
Reference: PNAS doi:10.1073/pnas.0911239106
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November 15, 2009
Category:
Hi folks,
A couple of housekeeping issues:
- ScienceBlogs have developed a set of funky widgets that allow you to share the headlines from your favourite blogs on other websites. You can find the one for Not Exactly Rocket Science here - just click Share, and then Install outside Netvibes.
- The deadline is looming for this year's Open Laboratory compilation of the science blogosphere's best offerings. If any posts in this blog have tickled your fancy, stretched your brain or stoked your loins (heaven forbid, but there are some strange people on the internet), submit them for consideration here. For full disclosure purposes, I am helping to judge this year's competition, but I will obviously not be judging my own work except in a non-competition, self-critical, tortured-soul, writery sort of way.
- Recently, due to overwhelming demand (n=2), I've changed the way that posts appear so that the full shebang appears above the fold rather than teasing readers and making you click for the payoff. It makes the front page a bit messier, but I'm told this is easier for people reading on phones. There hasn't been a noticeable drop in traffic. Is everyone happy with this change, are you for some reason against it, or have you actually failed to notice any difference whatsoever?
E
Posted by Ed Yong at 6:13 PM • 10 Comments • 0 TrackBacks
Category: Altruism • Bacteria • Cooperation
As a species, we hate cheaters. Just last month, I blogged about our innate desire to punish unfair play but it's a sad fact that cheaters are universal. Any attempt to cooperate for a common good creates windows of opportunity for slackers. Even bacteria colonies have their own layabouts. Recently, two new studies have found that some bacteria reap the benefits of communal living while contributing nothing in return.
Bacteria may not strike you as expert co-operators but at high concentrations, they pull together to build microscopic 'cities' called biofilms, where millions of individuals live among a slimy framework that they themselves secrete. These communities provide protection from antibiotics, among other benefits, and they require cooperation to build.
This only happens once a colony reaches a certain size. One individual can't build a biofilm on its own so it pays for a colony to be able to measure its own size. To do this, they use a method 'quorum sensing', where individuals send out signalling molecules in the presence of their own kind.
When another bacterium receives this signal, it sends out some of its own, so that once a population reaches a certain density, it sets off a chain reaction of communication that floods the area with chemical messages.
These messages provide orders that tell the bacteria to secrete a wide range of proteins and chemicals. Some are necessary for building biofilms, others allow them to infect hosts, others make their movements easier and yet others break down potential sources of food. They tell bacteria to start behaving cooperatively and also when it's worth doing so.
Steve Diggle and colleagues from the Universities of Nottingham and Edinburgh have found that bacterial slackers can exploit this system. They studied an opportunistic species called Pseudomonas aeruginosa, that preys on the weak. It's a major cause of hospital infections, setting up shop in burn victims, cystic fibrosis patients and others with weakened immune systems.
The bug's success hinges on quorum sensing, which allows it to thrive in limited environments by cooperating. When Diggle cultured the bacteria in a nutritionally poor liquid containing only proteins as the only food source, they grew happily nonetheless. That's because the chemical signals exchanged as part of quorum sensing also triggers the release of proteases, enzymes that can digest proteins.
Diggle then tested two mutant forms of P.aeruginosa that are commonly found in nature. The first - the 'signal-negative' version - can't produce signalling molecules but can react to them. It obeys orders to secretes the right chemicals but never passes the orders along. As such, it doesn't secrete enough proteases and grows poorly in a protein-only solution. However, it picked up the pace if it was artificially doused in signalling molecules to cope with its deficiency.
The 'signal-blind' mutant is even more of a slacker - it can't react to signals at all, so it doesn't help or communicate. This strain also grew poorly in the protein-only liquid and only matched the normal strain if it was artificially given extra proteases.
If quorum sensing provides such obvious benefits, you might expect all bacteria to take part. But there is a catch - it's also quite draining. Making signals and proteases takes up energy, and when Diggle placed the different strains in a rich, nutritious solution, the mutants vastly outgrew the normal strain. With an abundance of easily digested food, it was every bacterium for itself and the mutants, that weren't busy making expensive signals and proteases, did better.
Quorum sensing may be good for the group, but for each individual bacterium, it pays to sit back and let your peers do all the work. Diggle demonstrated this by allowed the normal and mutant strains to compete in the protein-only liquid, in a real-time experiment in evolution. The mutant strains were engineered with luminescent genes so that the team could track their growth by the light they gave off.
At first, the signal-blind cheats made up just 1% of the population but after 2 days, they accounted for 45% of it. In a separate culture, the proportion of signal-negative cheats went from 3% to 66%. Among P.aeruginosa, cheaters can indeed prosper and then some - they outgrew their cooperating cousins by 60 to 80 times.
In a separate study with the same species, Kelsi Sandoz from Oregon State University found that cheaters evolve naturally. Like Diggle, she grew a normal strain of P.aeruginosa in conditions where they needed to make proteases to survive.
After 12 days, she managed to isolate specific colonies that weren't pulling their weight. All of them had developed mutations in a key gene involved in quorum sensing which meant that they were only secreting a very small amount of protease. Within 20 days, these cheats made up 40% of the cultures.
Why then, do any individuals bother cooperating at all? If slacking is so profitable, why doesn't everyone do it? For a start, cheating pays fewer dividends if you do it at the expense of your relatives who share your genes. This is especially true for bacteria colonies that reproduce asexually and spawn genetically identical clones.
In this case, helping your neighbour pays off because it ensures that your genes are passed on to the next generation. Diggle found that when the bacteria were very closely related to each other, mutants were much less likely to gain a foothold in a population of co-operators.
There is another reason though, and it's probably more important. Both studies found that as the proportion of cheaters increased, their growth rate dropped because the value of cheating diminished.
Slackers only prosper if they can cadge of a hard-working population - if every bacterium took the easy way, there would be no proteases and no food. Sandoz found that when this happened, the entire population suffered and overall growth plummeted. If there were enough cheaters, the signalling molecules became too dilute, the 'quorum' fell apart and the population crashed.
However, Sandoz also found that the bacteria usually evolved compensatory measures in time to stop this from happening. During her study, she saw that many cheaters developed further mutations that restored protease production. Faced with a sinking ship, there was strong evolutionary pressure for them to swap sides and start cooperating again.
References:
Diggle, S., Griffin, A., Campbell, G., West , S. (2007). Cooperation and conflict in quorum-sensing bacterial populations. Nature, 450, 411-415.
Sandoz, K., Mitzimberg, S., Schuster, M. (2007). Social cheating in Pseudomonas aeruginosa quorum sensing. . Proceedings of the National Academy of Sciences, 104(40), 15876-15881.
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Posted by Ed Yong at 10:00 AM • 3 Comments • 0 TrackBacks
November 14, 2009
Category: Animals • Mammals • South African wildlife
This is Tyson, a male leopard and one of the last animals we saw on our South African safari. We only took headshots of him but immediately, you can see that he's stockier and more powerfully built than Safari, the female leopard that I showed photos of a few weeks back. Tyson, earning his name, probably weighs around 80kg or so.
And yet while we watched, he pulled off a languid stretch that made him look for all the world like a giant house cat - paws outstretched, maw agape and back arched in a graceful curve.
As he walked off, he marked his territory with a scent gland on his rump. I'm told that leopard scent markings smell rather a lot like popcorn, leading our guide to advise us, "If you smell popcorn during the drive, please tell us and stay inside the jeep."
Posted by Ed Yong at 12:00 PM • 6 Comments • 0 TrackBacks
November 12, 2009
Category: Brain • Happiness • Learning • Neuroscience • Psychology
How would you fancy a holiday to Greece or Thailand? Would you like to buy an iPhone or a new pair of shoes? Would you be keen to accept that enticing job offer? Our lives are riddled with choices that force us to imagine our future state of mind. The decisions we make hinge upon this act of time travel and a new study suggests that our mental simulations of our future happiness are strongly affected by the chemical dopamine.
Dopamine is a neurotransmitter, a chemical that carries signals within the brain. Among its many duties is a crucial role in signalling the feelings of enjoyment we get out of life's pleasures. We need it to learn which experiences are rewarding and to actively seek them out. And it seems that we also depend on it when we imagine the future.
Tali Sharot from University College London found that if volunteers had more dopamine in their brains as they thought about events in their future, they would imagine those events to be more gratifying. It's the first direct evidence that dopamine influences how happy we expect ourselves to be.
When we learn about new experiences, neurons that secrete dopamine seem to record the difference between the rewards we expect and the ones we actually receive. In encoding the gap between hope and experience, these neurons help us to repeat rewarding actions.
This was clearly demonstrated in 2006, when Mathias Passiglione showed that people's ability to learn about rewards could be improved by giving them a drug called L-DOPA. It's a precursor to dopamine, a sort of parent molecule that can increase the concentrations of its offspring. Passiglione asked volunteers to learn links between different symbols and different financial rewards. He found that under the influence of L-DOPA, they were better at picking the symbols that earned them the most cash.
Passiglione's study was important, but his volunteers were forced to make a fairly artificial choice between two virtual symbols in a constrained lab setting. What happens in real life, when choices are complex and our decisions hinge on our ability to think about the future?
To answer that, Sharot recruited 61 volunteers and asked them to say how happy they'd feel if they visited one of 80 holiday destinations, from Greece to Thailand. All of the recruits were given a vitamin C supplement as a placebo and 40 minutes later, they had to imagine themselves on holiday at half of the possible locations. After this bout of fanciful daydreaming, they had to take another pill but this time, half of them were given L-DOPA instead of the placebo. Again, they had to imagine themselves in various holiday spots.
The next day, Sharot brought the volunteers back. By this time, they would have broken down all the L-DOPA in their system. She asked them to choose which of two destinations they'd like to go to, from the set that they had thought about the day before. Finally, they rated each destination again.
By the end of the experiments, they perceived their imaginary holidays to be more enjoyable if they had previously thought about the locations under the influence of L-DOPA (while vitamin C, as predicted, had no effect). The implication is clear: think about the future with more dopamine in the noggin and you'll imagine that you have a better time.
Critically, this wasn't because they were feeling happier in the actual moment. All the recruits filled in questionnaires about their emotional state every time they took a pill and these revealed that the dopamine boost didn't actually affect the present state of mind. All it did was change their predictions of their future state of mind. These happier predictions affected their choices too - more often than not, they chose to travel to destinations that they had envisioned through dopamine-tinted goggles.
How dopamine has its way is unclear. Sharot suggests that it could boost how much we want something when we imagine it. Its effects could also tie into its role in learning. When we imagine the future, this chemical strengthens the link between what we think about and any feelings of enjoyment we might gain from it. This model fits with the fact that some neurons in the striatum become more active the more pleasure we expect from an experience.
Either way, it's clear that our knowledge of dopamine's myriad roles is just beginning. Broadening that knowledge is important for understanding our own behaviour, which, as Sharot says, "is largely driven by estimations of future pleasure and pain".
Reference: Current Biology 10.1016/j.cub.2009.10.025
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November 11, 2009
Category: Evolution • Genes and behaviour • Genetics • Language
Today, a new paper published in Nature adds another chapter to the story of FOXP2, a gene with important roles in speech and language. The FOXP2 story is a fascinating tale that I covered in New Scientist last year. It's one of the pieces I'm proudest of so I'm reprinting it here with kind permission from Roger Highfield, and with edits incorporating new discoveries since the time of writing.
The FOXP2 Story (2009 edition)
Imagine an orchestra full of eager musicians which, thanks to an incompetent conductor, produces nothing more than an unrelieved cacophony. You're starting to appreciate the problem faced by a British family known as KE. About half of its members have severe difficulties with language. They have trouble with grammar, writing and comprehension, but above all they find it hard to coordinate the complex sequences of face and mouth movements necessary for fluid speech.
Thanks to a single genetic mutation, the conductor cannot conduct, and the result is linguistic chaos. In 2001, geneticists looking for the root of the problem tracked it down to a mutation in a gene they named FOXP2. Normally, FOXP2 coordinates the expression of other genes, but in affected members of the KE family, it was broken.
It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 "the language gene" or the "grammar gene". Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited - the discovery sparked a frenzy of research aiming to uncover the gene's role.
Several years on, and it is clear that talk of a "language gene" was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. "When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language," recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours. "It gives us a really important lesson," says Fisher. "Speech and language didn't just pop up out of nowhere. They're built on very highly conserved and evolutionarily ancient pathways."
Two amino acids, two hundred thousand years
The first team to compare FOXP2 in different species was led by Wolfgang Enard from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. In 2001, they looked at the protein that FOXP2 codes for, called FOXP2, and found that our version differs from those of chimpanzees, gorillas and rhesus macaques by two amino acids out of a total of 715, and from that of mice by three. This means that the human version of FOXP2 evolved recently and rapidly: only one amino acid changed in the 130 million years since the mouse lineage split from that of primates, but we have picked up two further differences since we diverged from chimps, and this seems to have happened only with the evolution of our own species at most 200,000 years ago.
The similarity between the human protein FOXP2 and that of other mammals puts it among the top 5 per cent of the most conserved of all our proteins. What's more, different human populations show virtually no variation in their FOXP2 gene sequences. Last year, Enard's colleague Svante Pääbo made the discovery that Neanderthals also had an identical gene, prompting questions over their linguistic abilities (see "Neanderthal echoes below).
"People sometimes think that the mutated FOXP2 in the KE family is a throwback to the chimpanzee version, but that's not the case," says Fisher. The KEs have the characteristically human form of the gene. Their mutation affects a part of the FOXP2 protein that interacts with DNA, which explains why it has trouble orchestrating the activity of other genes.
There must have been some evolutionary advantage associated with the human form of FOXP2, otherwise the two mutations would not have spread so quickly and comprehensively through the population. What this advantage was, and how it may have related to the rise of language, is more difficult to say. Nevertheless, clues are starting to emerge as we get a better picture of what FOXP2 does - not just in humans but in other animals too.
During development, the gene is expressed in the lungs, oesophagus and heart, but what interests language researchers is its role in the brain. Here there is remarkable similarity across species: from humans to finches to crocodiles, FOXP2 is active in the same regions. With no shortage of animal models to work with, several teams have chosen songbirds due to the similarities between their songs and human language: both build complex sequences from basic components such as syllables and riffs, and both forms of vocalisation are learned through imitation and practice during critical windows of development.
Babbling birds
All bird species have very similar versions of FOXP2. In the zebra finch, its protein is 98 per cent identical to ours, differing by just eight amino acids. It is particularly active in a part of the basal ganglia dubbed "area X", which is involved in song learning. Constance Scharff at the Max Planck Institute for Molecular Genetics in Berlin, Germany, reported that finches' levels of FOXP2 expression in area X are highest during early life, which is when most of their song learning takes place. In canaries, which learn songs throughout their lives, levels of the protein shoot up annually and peak during the late summer months, which happens to be when they remodel their songs.
So what would happen to a bird's songs if levels of the FOXP2 protein in its area X were to plummet during a crucial learning window? Scharff found out by injecting young finches with a tailored piece of RNA that inhibited the expression of the FOXP2 gene. The birds had difficulties in developing new tunes and their songs became garbled: they contained the same component "syllables" as the tunes of their tutors, but with syllables rearranged, left out, repeated incorrectly or sung at the wrong pitch.
The cacophony produced by these finches bears uncanny similarities to the distorted speech of the afflicted KE family members, making it tempting to pigeonhole FOXP2 as a vocal learning gene - influencing the ability to learn new communication sounds by imitating others. But that is no more accurate than calling it a "language gene". For a start, songbird FOXP2 has no characteristic differences to the gene in non-songbirds. What's more, among other species that show vocal learning, such as whales, dolphins and elephants, there are no characteristic patterns of mutation in their FOXP2 that they all share.
Instead, consensus is emerging that FOXP2 probably plays a more fundamental role in the brain. Its presence in the basal ganglia and cerebellums of different animals provides a clue as to what that role might be. Both regions help to produce precise sequences of muscle movements. Not only that, they are also able to integrate information coming in from the senses with motor commands sent from other parts of the brain. Such basic sensory-motor coordination would be vital for both birdsong and human speech. So could this be the key to understanding FOXP2?
Moving mice
New work by Fisher and his colleagues supports this idea. In 2008, his team engineered mice to carry the same FOXP2 mutation that affects the KE family, rendering the protein useless. Mice with two copies of the dysfunctional FOXP2 had shortened lives, characterised by motor disorders, growth problems and small cerebellums. Mice with one normal copy of FOXP2 and one faulty copy (as is the case in the affected members of the KE family) seemed outwardly healthy and capable of vocalisation, but had subtle defects.
For example, they found it difficult to acquire new motor skills such as learning to run faster on a tilted running wheel. An examination of their brains revealed the problem. The synapses connecting neurons within the cerebellum, and those in a part of the basal ganglia called the striatum in particular, were severely flawed. The signals that crossed these synapses failed to develop the long-term changes that are crucial for memory and learning. The opposite happened when the team engineered mice to produce a version of FOXP2 with the two characteristically human mutations. Their basal ganglia had neurons with longer outgrowths (dendrites) that were better able to strengthen or weaken the connections between them.
A battery of over 300 physical and mental tests showed that the altered mice were generally healthy. While they couldn't speak like their cartoon equals, their central nervous system developed in different ways, and they showed changes in parts of the brain where FOXP2 is usually expressed (switched on) in humans.
Their squeaks were also subtly transformed. When mouse babies are moved away from their nest, they make ultrasonic distress calls that are too high for us to hear, but that their mothers pick up loudly and clearly. The altered Foxp2 gene subtly changed the structure of these alarm calls. We won't know what this means until we get a better understanding of the similarities between mouse calls and human speech.
For now, the two groups of engineered mice tentatively support the idea that human-specific changes to FOXP2 affect aspects of speech, and strongly support the idea that they affect aspects of learning. "This shows, for the first time, that the [human-specific] amino-acid changes do indeed have functional effects, and that they are particularly relevant to the brain," explains Fisher. "FOXP2 may have some deeply conserved role in neural circuits involved in learning and producing complex patterns of movement." He suspects that mutant versions of FOXP2 disrupt these circuits and cause different problems in different species.
Pääbo agrees. "Language defects may be where problems with motor coordination show up most clearly in humans, since articulation is the most complex set of movements we make in our daily life," he says. These circuits could underpin the origins of human speech, creating a biological platform for the evolution of both vocal learning in animals and spoken language in humans.
Holy diversity, Batman
The link between FOXP2 and sensory-motor coordination is bolstered further by research in bats. Sequencing the gene in 13 species of bats, Shuyi Zhang and colleagues from the East China Normal University in Shanghai discovered that it shows incredible diversity. Why would bats have such variable forms of FOXP2 when it is normally so unwavering in other species?
Zhang suspects that the answer lies in echolocation. He notes that the different versions seem to correspond with different systems of sonar navigation used by the various bat species. Although other mammals that use echolocation, such as whales and dolphins, do not have special versions of FOXP2, he points out that since they emit their sonar through their foreheads, these navigation systems have fewer moving parts. Furthermore, they need far less sensory-motor coordination than flying bats, which vocalise their ultrasonic pulses and adjust their flight every few milliseconds, based on their interpretation of the echoes they receive.
These bats suggest that FOXP2 is no more specific to basic communication than it is to language, and findings from other species tell a similar tale. Nevertheless, the discovery that this is an ancient gene that has assumed a variety of roles does nothing to diminish the importance of its latest incarnation in humans.
Since its discovery, no other gene has been convincingly implicated in overt language disorders. FOXP2 remains our only solid lead into the genetics of language. "It's a molecular window into those kinds of pathways - but just one of a whole range of different genes that might be involved," says Fisher. "It's a starting point for us, but it's not the whole story." He has already used FOXP2 to hunt down other key players in language.
The executive's minions
FOXP2 is a transcription factor, which activates some genes while suppressing others. Identifying its targets, particularly in the human brain, is the next obvious step. Working with Daniel Geschwind at the University of California, Los Angeles, Fisher has been trying to do just that, and their preliminary results indicate just what a massive job lies ahead. On their first foray alone, the team looked at about 5000 different genes and found that FOXP2 potentially regulates hundreds of these.
Some of these target genes control brain development in embryos and its continuing function in adults. Some affect the structural pattern of the developing brain and the growth of neurons. Others are involved in chemical signalling and the long-term changes in neural connections that enable to learning and adaptive behaviour. Some of the targets are of particular interest, including 47 genes that are expressed differently in human and chimpanzee brains, and a slightly overlapping set of 14 targets that have evolved particularly rapidly in humans.
Most intriguingly, Fisher says, "we have evidence that some FOXP2 targets are also implicated in language impairment." Last year, Sonja Vernes in his group showed that FOXP2 switches off CNTNAP2, a gene involved in not one but two language disorders - specific language impairment (SLI) and autism. Both affect children, and both involve difficulties in picking up spoken language skills. The protein encoded by CNTNAP2 is deployed by nerve cells in the developing brain. It affects the connections between these cells and is particularly abundant in neural circuits that are involved in language.
Verne's discovery is a sign that the true promise of FOXP2's discovery is being fulfilled - the gene itself has been overly hyped, but its true worth lies in opening a door for more research into genes involved in language. It was the valuable clue that threw the case wide open. CNTNAP2 may be the first language disorder culprit revealed through FOXP2 and it's unlikely to be the last.
Most recently, Dan Geschwind compared the network of genes that are targeted by FOXP2 in both chimps and humans. He found that the two human-specific amino acids within this executive protein have radically altered the set of genetic minions that it controls.
The genes that are directed by human FOXP2 are a varied cast of players that influence the development of the head and face, parts of the brain involved in motor skills, the growth of cartilage and connective tissues, and the development of the nervous system. All those roles fit with the idea that our version of FOXP2 has been a lynchpin in evolving the neural circuits and physical structures that are important for speech and language.
The FOXP2 story is far from complete, and every new discovery raises fresh questions just as it answers old ones. Already, this gene has already taught us important lessons about evolution and our place in the natural world. It shows that our much vaunted linguistic skills are more the result of genetic redeployment than out-and-out innovation. It seems that a quest to understand how we stand apart from other animals is instead leading to a deeper appreciation of what unites us.
Box - Neanderthal echoes
The unique human version of the FOXP2 gives us a surprising link with one extinct species. Last year, Svante Pääbo's group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from the bones of two Neanderthals, one of the first instances of geneticists exploring ancient skeletons for specific genes. They found that Neanderthal FOXP2 carries the same two mutations as those carried by us - mutations accrued since our lineage split from chimps between 6 and 5 million years ago.
Pääbo admits that he "struggled" to interpret the finding: the Neanderthal DNA suggests that the modern human's version of FOXP2 arose much earlier than previously thought. Comparisons of gene sequences of modern humans with other living species had put the origins of human FOXP2 between 200,000 and 100,000 years ago, which matches archaeological estimates for the emergence of spoken language. However, Neanderthals split with humans around 400,000 years ago, so the discovery that they share our version of FOXP2 pushes the date of its emergence back at least that far.
"We believe there were two things that happened in the evolution of human FOXP2," says Pääbo. "The two amino acid changes - which happened before the Neanderthal-human split - and some other change which we don't know about that caused the selective sweep more recently." In other words, the characteristic mutations that we see in human FOXP2 may indeed be more ancient than expected, but the mutated gene only became widespread and uniform later in human history. While many have interpreted Pääbo's findings as evidence that Neanderthals could talk, he is more cautious. "There's no reason to assume that they weren't capable of spoken language, but there must be many other genes involved in speech that we yet don't know about in Neanderthals."
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