The Composer and the Cassowary: An Appreciation of Mistakes

High in a church balcony last weekend, waiting to perform a solo for Palm Sunday and trying not to panic, I thought about cars being hit with hammers. I'm not sure this is the kind of visualization recommended for singers. But sometimes genetics asserts itself.

A college biology professor once told my class that genetic mutation is like whacking a car with a hammer. You will almost never improve your car this way. More often, you'll damage it. If you're lucky the damage will be only superficial: a change in the silent portion of your genome, or maybe a few funny feathers.

The piece my choir was getting ready to sing, Gregorio Allegri's Miserere, has experienced some mutations in its own DNA over the centuries. Allegri composed the piece way back in the early 1600s, and after that it was sung exclusively during Holy Week at the Sistine Chapel. Even though people had to attend a 3 AM service in Rome to hear it, the Miserere became famous. The Vatican, wanting to keep the piece to itself, threatened excommunication for anyone who copied down the score.

As secrets and life forms tend to do, though, the music leaked out. In the late 18th century, a certain precocious teenager with the last name of Mozart spent Holy Week in Rome with his father. After hearing the Miserere at the Sistine Chapel, young Wolfgang sat down and transcribed the whole thing from memory. He returned for a second performance to double-check his work. From there, the score got into the hands of a music historian who published it.

If the music had really been genetic material, Mozart would have been DNA polymerase, a molecular machine that copies DNA. The polymerase molecule grasps a DNA strand and crawls along, letter by letter, building a matching strand as it goes.

Like Mozart, the enzyme is good at what it does. It proofreads. But sometimes it slips up: A single letter of DNA might be swapped for another one. A section of the code might be flipped backward. One or more letters might be inserted or deleted. (Even one letter lost or gained can cause a major change, since the DNA code is read in three-letter words. In English, imagine losing a letter from the sentence "SHE ATE THE RED BUG" and ending up with "SEA TET HER EDB UG." Some words are still there, but the meaning of the sentence is destroyed.)

Even if DNA polymerase is performing well, damage to the genome can come from outside sources such as UV radiation. But a large fraction of your DNA seems to do nothing at all. If a mutation happens here, you won't know the difference. If a slip-up creates a synonymous change in a gene—the code allows for some words to be spelled in multiple ways—you'll also be fine. And if the mutation does something horrible, it will remove you from the gene pool.

Evolution doesn't care much about any of this. It only notices the rare constructive strokes of the hammer, and it only sees them if they happen in the cells that will become your sperm and eggs (called the "germ line"). If you have DNA damage in the skin of your back from too much tanning, you can't pass it on to your children.

Back when Allegri's Miserere was being sung in the Sistine Chapel, the choirs were made up of men and boys. In choirs like mine, women sing the alto and soprano parts. But that's only a superficial mutation; we singers are the flesh of the piece.

The germ line mutation came in the 19th century. Someone who copied the piece apparently made a mistake, shifting a whole repeated section up by a fourth. What started out as a normal soprano solo now rocketed all the way to a high C, a preposterous note that humans are almost never asked to sing.*

Natural selection didn't weed out this mutation. Once the change had happened and been passed to new generations of the musical score, it stayed in place—even after the error was discovered. We continue to sing the mutated piece because, simply, it's awesome this way. Here's a video. You'll know when the boy soprano hits the high C: it's the note you hear through the bones of your spine instead of your ears.

It's not an overstatement to say that what happened to Allegri's music represents the whole history of life on Earth. Every new development has come from a mistake, small or egregious, that was allowed to stick around for one reason or another. Life started as tiny blobs, then whoops—heads! Legs! Oops again—tulips! Uncorrected errors became tree bark, snail shells, lungs, fur, resistance to antibiotics. Inching along mistake by mistake, life forms developed the machinery to make blood, slime, deadly venom, and spider silk.

Some living things have come together so elegantly that they bring an audience to its feet. There are racing cheetahs, swooping owls, orchids that mimic bees. But even the giant, gut-colored flower that stinks like a corpse to attract flies is a success in its family line. The cassowary is a bird that made so many mistakes, it traded the ability to fly for tree-trunk legs and a head with a sail on top. Even the cassowary, though, is doing something right. Errors become the high notes.

Postscript: My choir director turns out to have a son who, at age three, actually took a hammer to the family car while it was in the garage. The car was not improved. 

Images: Top, cassowary from The New Student's Reference Work and Gregorio Allegri, both via Wikimedia Commons. Bottom, cassowary by Peter Nijenhuis via Flickr.

*Plot clarification, in case anybody is worrying about me up there in the loft: this is not the part I sang.

Fishing Yanks the Best Parents from the (Gene) Pool

A fishing rod and reel aren't just gear for human recreation: they're the tools of evolution. The difference between fish we pull out of lakes or commercial fisheries by their lips and those we leave behind can drive change in entire fish populations. And that change may be for the worse. In at least some species, the fittest fish are the ones that end up on our hooks.

The largemouth bass (Micropterus salmoides) lives all over the United States and is a popular target of recreational anglers. You wouldn't guess it from the bug eyes and mailbox mouth, but M. salmoides males are also doting dads. For several days after the female lays her eggs and before they hatch, the male stays close to the nest. He fans the eggs with his tail and chases off any other creatures who come looking for a snack.

The more aggressively a male largemouth bass attacks intruders near his nest, the more of his offspring are likely to survive. But when fending off threats, a bass doesn't necessarily notice the difference between a hungry fish and a dangling lure. So the fish that guard their nests most aggressively might also be the most likely to bite into a fishhook.

David Sutter, a PhD student at the University of Illinois at Urbana-Champaign, and other researchers used specially bred largemouth bass in artificial ponds to investigate this question. Their fish had been bred into two lines: one that's especially likely to attack a fishhook, and one that's especially unlikely.

(Vulnerability to being caught on a rod and line is heritable, Sutter explains—a kind of personality trait for fish. Largemouth bass were first bred this way starting in the late 1970s. Researchers kept the bass in a reservoir where any fish that got caught were marked and rereleased. Eventually researchers drained the reservoir, revealing some fish with multiple marks and others that had never been caught. These extremes were separated into new ponds where the experiment was repeated. After a few generations of this, the researchers had created one line of fish that was consistently catchable and a second line that was consistently hard to catch.)

Sutter and his colleagues put the two kinds of male bigmouth bass together in a pond, along with ordinary females. Once the fish had spawned, snorkelers visited their nests to count their eggs. By spying on the fish remotely, researchers could observe how attentive the fish dads were to their nests—and how aggressive they were to "intruders," which in this case were hookless fishing lures.

The fish bred for catchability, as expected, attacked the fishing lures more often than other fish. In addition to chasing these imaginary predators away from their eggs, they also spent more time hanging out near the nest and fanning their eggs with their tails. By comparison, the fish bred to ignore fishhooks spent more time away from the nest and didn't bother chasing away intruding lures. Overall, as the authors report in PNAS, the easiest-to-catch largemouth bass are also the best dads.

Hooking one of these fish from a body of water obviously removes him—and his good-dad DNA—from that population's gene pool. It also dooms any eggs he was guarding, which carry those same genes, to become food for roving predators.

There's another way fishing fouls up the next generation of fish. The researchers found that females spent more of their eggs on aggressive males, especially large ones. Apparently the female fish can tell which males will guard a nest well. When these sexy bass are removed from a pond, they leave behind more eggs (and more potential young) than a smaller and less aggressive male would.

All this means that humans can drive the evolution of a whole fish population. Thanks to our fishing lines, male largemouth bass (or species with similar behaviors) can become less aggressive, less capable as parents, and less attractive to females. And, of course, less catchable by us. The authors suspect these changes are already happening in popular angling spots, though it hasn't been studied yet.

Sutter says fisheries might be able to prevent the problem by leaving largemouth bass alone during their spawning season. "It would probably be best to allow fish to successfully reproduce and minimize disturbances," he says—by disturbances he means fishhooks—"especially in areas where fish only have limited opportunities to reproduce." Otherwise, the only fish that are left alive may be the deadbeats.


David A. H. Sutter, Cory D. Suski, David P. Philipp, Thomas Klefoth, David H. Wahl, Petra Kersten, Steven J. Cooke, & Robert Arlinghaus (2012). Recreational fishing selectively captures individuals with the highest fitness potential PNAS : 10.1073/pnas.1212536109

Image: (Not a largemouth bass) by Blake Facey (Flickr)

Belly Button Safari: Who's Living in There?

"We are covered in an ecological wonderland," declares Rob Dunn, a man with a strange idea of a wonderland. In the wild bacterial jungle that is our skin, Dunn has been studying an especially dark cave: the belly button. He's found out which microorganisms are the big game, which are the rare birds, and which ones may take up residence in your navel if you stop bathing.

Dunn is a biologist at North Carolina State University who studies the tiny life forms that share our personal space, from insects in our yards and houses to microbes on our bodies. The organisms we live with can affect our health, for better or worse. Yet researchers are only beginning to explore the various ecosystems we carry on ourselves. From our intestines to our faces to the bottoms of our feet, each of us holds a planet's worth of different habitats.

Out of all these bacterial habitats, the belly button is especially convenient to study. Everyone has one. Its shape and size don't change dramatically from person to person (among innies, anyway). And it's hard to scrub clean, making it a relatively undisturbed environment on the body. A national park, if you will.

The belly button also has crowd appeal, which is important for Dunn's citizen-science approach. He's interested in projects that involve unsqueamish members of the public. For his belly button research, Dunn recruited crowds at two 2011 events: One was Darwin Day at the Museum of Natural Sciences in Raleigh, North Carolina, and the other was the annual Science Online conference in Raleigh.

In total, 60 volunteers had their navels swabbed. Researchers extracted the bacterial DNA from each sample, sequenced it, and searched it for matches to particular species.

What the team found was diversity, and lots of it, as they report today in PLOS ONE. With a median of 67 different bacterial species per person, Dunn says the navel is at least as diverse as the other skin areas studied so far. That diversity varied widely; some people housed more than 3 times as many species in their belly buttons as others.

Out of the thousands of bacterial species the researchers found overall, the vast majority showed up in only a few people, or in just one person. Even though this habitat looks similar from one person to the next, we all have very different collections of rare critters running around in the undergrowth. No one bacterial species appeared in every belly button.

But there are common belly button denizens, too. On our umbilical safari, these are big obvious trees and loud monkeys that show up in most people's jungles. Eight species of bacteria were present in more than 70% of subjects. And wherever these species show up, they do so in large numbers. If you could dump the bacteria from everyone's belly buttons into one pile, members of the 8 king-of-the-jungle species would make up nearly half the heap.

Extending this group to the 23 most common bacterial species, the researchers looked at how the group's DNA compared to rarer bacteria. They found that the ruling bacteria were more closely related to each other than randomly selected groups of bacteria were—sort of a royal family. This suggests that the most common belly button bacteria share evolved traits that help them thrive in this environment.

The most surprising thing about the belly button bacteria, Dunn says, is their ultimate predictability. Even though thousands of species turned up in his study, he now knows which ones are most likely to live in someone's navel. "I expected that the common species would be far more random," he says. "But the truth was otherwise." There are only a few bacteria ruling the belly button jungle, and a diverse throng of others that make up their subjects. Dunn thinks we might be able to study what goes on in our skin's ecosystem by focusing on these few common bacteria.

Dunn hopes that eventually he'll be able to predict the specific bacteria living in someone's belly button based on their age, gender, habits, and history. "But I'll admit we are having an interesting struggle," he says. The research shows that people can be sorted into two or three "bacteriotypes," like blood types, based on the clusters of bacteria that inhabit their navels. But as to why a person is one type or another? "So far we can't explain what causes those differences," Dunn says. "It is a real mystery."

He's getting a little help in this area from one Science Online participant who claimed not to have showered or bathed in "several years." This subject's belly button swab turned up two species of archaea—single-celled organisms, entirely separate from bacteria, that often live in extreme environments. Until now, no one had found archaea on human skin.

This social non-conformer might represent the kinds of bacteria that our ancestors carried around. "Historically, no one washed very often," Dunn says. "This colleague of yours may be far more representative of how our bodies were for thousands, or even millions, of years than are most folks."

He adds, "That isn't saying I'm encouraging everyone to abandon washing."

Dunn suspects that belly button depth, too, might influence what species live there. But he's had a hard time studying this. "No one really wants to answer a question about the depth of their innie, no matter how anonymous we make the process," he says. However, his group's next study will look at a larger group of people, including outies.

Future safaris into our bodies' ecosystems might help scientists understand skin allergies and other health issues. Although belly button sampling is over for now, Dunn encourages people who want to get involved to join the mailing list at yourwildlife.org. He's currently looking at camel crickets in basements, ants in yards, and bacteria in bedrooms and kitchens.

"Armpits," Dunn adds—or perhaps threatens—"are also on the horizon."


Jiri Hulcr, Andrew M. Latimer, Jessica B. Henley, Nina R. Rountree, Noah Fierer, Andrea Lucky, Margaret D. Lowman, & Robert R. Dunn (2012). A Jungle in There: Bacteria in Belly Buttons are Highly Diverse, but Predictable PLOS ONE : 10.1371/journal.pone.0047712

Images: Copyright Belly Button Biodiversity.

Urinating Through Your Mouth Is Great. Ask This Turtle.

Even if you did ask the Chinese soft-shelled turtle what's so great about excreting bodily waste through one's mouth, you would probably just get gurgling in reply. The animal spends a lot of time with its face underwater. But its unusual strategy may be what allowed it to move into its favorite swamps and ponds in the first place.

Pelodiscus sinensis lives in China and other parts of Asia, as well as more remote spots, such as Hawaii, where it was introduced by turtle-soup-eating immigrants. It spends time both out of water and underwater, coming to the surface to breathe air into its lungs. When it has to stay submerged for long stretches, though, the turtle can breathe almost like a fish. It fills its mouth with water and empties it out again while rhythmically pulsing its throat, a maneuver that lets the turtle get all the oxygen it needs via specialized surfaces inside its mouth.

Scientists in Singapore observed that a soft-shelled turtle on land will occasionally dunk its head into a puddle for no clear reason. It may stay this way for an hour and a half or more. While in this position, the turtle makes the same throat-pulsing motion, which led the scientists to wonder whether the turtle's specialized underwater-breathing equipment had some other role as well.

Yuen Kwong Ip at the National University of Singapore, along with other scientists, investigated organs at the back of P. sinensis's mouth called the buccopharyngeal villiform processes (BVPs, if you prefer). These look sort of like gills and are on the roof and bottom of the mouth, near the throat.

To find out exactly what materials were entering and exiting the soft-shelled turtle, the researchers performed a series of tests. They restrained turtles for several days on a dry platform, with a box of water in front of their heads for drinking and whatever else it was they were doing. A second container waited under the turtles' tail ends to collect urine that came out the traditional way.

Urinating is a way for animals to dispose of the waste products their cells constantly generate. Nitrogen, one of these waste products, is filtered out of the blood and sent on its way—in P. sinensis and in many other animals, including mammals—as a molecule called urea. It's usually collected by the kidneys and dumped in the urine.

But when the researchers observed their soft-shelled turtles' waste production, they found that although some wastes showed up in the urine, most urea came out through the mouth.

Ip writes in the Journal of Experimental Biology that turtles on dry land dunked their heads in water for 20 to 100 minutes at a time. While submerged, they repeatedly "rinsed" their mouths with water while rhythmically pulsing their throats. He discovered that this motion simultaneously pulled oxygen out of the water, so the turtles could keep breathing, and expelled urea into it.

Looking at the turtle's DNA, the researchers found what looked like a gene for a urea transporter, a protein that carries urea molecules across membranes. The gene was active in the turtle's mouth and the gill-like BVPs, but not—as it would be in humans or almost any other vertebrate animal—in the kidneys.

Ip thinks the Chinese soft-shelled turtle's strategy is not, unlike most cases of misplaced urine, an accident. He notes that P. sinensis and other soft-shelled turtles often live in salty marshes and swamps, or even in the sea. If they excreted urea in the usual way, they would need to continuously drink the water around them to make urine. But like human castaways in the ocean, the turtles would be ill-advised to drink this water; their kidneys can't handle that much salt. So instead, P. sinensis—perhaps along with the other soft-shelled turtles—sends urea back toward its mouth after filtering it from its blood. To dispose of the urea, the turtle only has to rinse its mouth with water, not drink it.

Chinese soft-shelled turtles aren't the only animals that know the taste of urea. Cows and other ruminant animals excrete some urea into their saliva. Their reasons are quite different: they use nitrogen in urea to feed the friendly bacteria that live in their guts and help them digest plant matter. By swallowing their urea-carrying saliva, cows send it to their stomach and keep their microbes alive.

You may find this trick unappealing, but to Ip it's inspirational. Hypothetically, he says, doctors could one day treat patients who have kidney failure by turning on genes for urea excretion in their mouths, just as these genes are turned on in turtles. "Urea excretion can still occur through rinsing the mouth with water, just like the soft-shelled turtle," he says, "without having to go through blood dialysis." Then we'll be able to ask them just how great it is.


Yuen K. Ip, Ai M. Loong, Serene M. L. Lee, Jasmine L. Y. Ong, Wai P. Wong, & Shit F. Chew (2012). The Chinese soft-shelled turtle, Pelodiscus sinensis, excretes urea mainly through the mouth instead of the kidney Journal of Experimental Biology DOI: 10.1242/jeb.068916

Image: Chinese soft-shelled turtle by muzina_shanghai (Flickr)

Close Look at Bison DNA Reveals Our Dirty Fingerprints

We really owe the American bison an apology. But where do you buy a card that says, "Sorry we wiped out nearly your entire species, then muddied your DNA by forcing you to mate with cows"? Would flowers be better?

In the 19th century Americans slaughtered bison (also referred to as buffaloes) with impunity. We killed them to sell their skins, to get them out of the way of our new trains, and to make life harder for Native Americans. It wasn't a shining moment. By the end of the 1800s the bison were nearly gone, reduced to perhaps as few as 100 animals in several small herds.

Even as Americans worked to restore bison in the early 20th century, we botched their genetics by breeding the animals with domestic cattle. Breeders wanted to make their cattle beefier and hardier. But the crossing wasn't easy, since the two species are separated by 1 to 2 million years of evolution. In addition to the question of genetic incompatibility, there was one of attraction: female bison refused to mate with male cattle.

James Derr, a professor in the veterinary college at Texas A&M University, explains that the hopeful breeders could only get male bison to mate with female cattle. And their offspring were all female; the species' mismatched genes apparently couldn't create a surviving male. These female hybrids were mated with more male bison. The result was a population of cattle-bison hybrids whose mitochondrial DNA—a little loop of genetic material passed solely through mothers—was 100% cattle.

In today's restored population, many bison still carry cattle mitochondrial DNA left over from the two species' historical tryst. To find out whether that genetic souvenir has any effect on today's animals, James Derr led a study of bison living in the wild and on a feedlot.

The herd of wild bison Derr studied live on Santa Catalina Island, off the southern coast of California, where they were introduced in 1924 for the filming of a silent movie. (Oops, better add that to the card.)  Looking at their DNA, Derr found that almost half the bison carried mitochondrial DNA from cattle.

The second bison population in the study was a group living on a feedlot in Montana, preparing to become products such as bison burgers. (On second thought, maybe a card won't cut it.) In these animals, cattle mitochondrial DNA was much rarer, at 6 percent.

By comparing the animals from the two populations, Derr could look for the effects of cattle mitochondrial DNA in both a wild population with limited resources and a well-fed ranch population. The feedlot bison were clearly beefier; at age 2 the feedlot males had reached a size that the island bison wouldn't attain until they were 17 years old.

Despite the two very different body types in the study, cattle genes had a clear effect across populations. Derr reports in Conservation Biology that bison with cattle mitochondrial DNA were slightly but significantly smaller than bison with mitochondrial DNA from their own species.

Bison that are smaller because of their domestic cattle DNA might be at a disadvantage. Derr says it's not clear yet whether this is the case—smaller size might have no effect on the fitness of bison, or it might even help them in places with limited resources like Santa Catalina Island. He plans to answer that question in a separate study.

If it turns out that having mitochondrial DNA from cattle hurts bison, the next question will be whether conservationists should try to weed these genes out of the population. Overall, Derr says, about 6 percent of bison carry cattle mitochondrial DNA, though in individual herds that number can range from 0 to 100 percent. It may be that by restoring the bison's genome to what it once was, we can start to make amends.


Derr JN, Hedrick PW, Halbert ND, Plough L, Dobson LK, King J, Duncan C, Hunter DL, Cohen ND, & Hedgecock D (2012). Phenotypic Effects of Cattle Mitochondrial DNA in American Bison. Conservation biology : the journal of the Society for Conservation Biology PMID: 22862781

Image: Michael Lusk/Flickr

Mom's Genes Make Males Die Sooner

Men who make it to adulthood without succumbing to the male habit of dying in accidents shouldn't congratulate themselves too soon: their life expectancy still doesn't match a woman's. In industrialized countries, women at every age out-survive men. And it's not just humans. Males that die before females have been observed throughout the animal kingdom. It's even true of the lowly fruit fly, and it looks like harmful mutations in mothers' genes are to blame.

This idea, which has been put forward before, is called the Mother's Curse. It has to do with a little loop of DNA that's passed down in humans—and in most other animals—exclusively through the mother. This DNA hides inside the mitochondria, which are the cell's batteries, and doesn't get packaged up with the rest of the genetic material when sperm are made. Those tiny sperm will rendezvous (if they're lucky, of course) with an egg that supplies all its own mitochondria, along with their DNA.

The Mother's Curse theory says that since fathers don't get any say in the makeup of mitochondrial DNA, it could carry mutations that harm men without being weeded out by natural selection. These anti-male mutations might be the reason for males' shorter lifespans.

Researchers led by Florencia Camus at Monash University in Australia examined this question in fruit flies, an animal whose genes are well understood and easily fooled with. By crossbreeding different fly types, they created 13 lines of fruit flies that were identical except for their mitochondrial DNA. They watched these flies for differences in male and female lifespan. Then they sequenced the mitochondrial DNA itself to see what was driving those differences.

In a study published in Current Biology, the team found that males died sooner across all the fly types. They also saw wide variation in male longevity, while female lifespans were more consistent. Females in most of the lines lived for around 60 days; males were variable but never lived much longer than 50 days. Since their mitochondrial DNA was the only thing that differed between the flies, something in that DNA must have been responsible.

Looking at the actual letter-by-letter differences in the mitochondrial DNA, the researchers found that fly types that were farther from each other genetically also differed more in longevity. In other words, more mutations in the mitochondrial DNA led to more variability in lifespan. Together, these findings support the idea that mitochondrial mutations cause males to die early—in fruit flies, anyway.

Mutations that somehow harm males, but not females, are free to pile up in the DNA of mitochondria. Since females pass down this DNA on their own, evolution is essentially blind to its effect on males. It remains to be seen whether the same mechanism is at work in animals that aren't fruit flies, including humans. If so, men will be able to blame their mothers for their shorter life expectancies. They might want to find a more positive way, though, to fill their abbreviated time on Earth.



M. Florencia Camus, David J. Clancy, & Damian K. Dowling (2012). Mitochondria, Maternal Inheritance, and Male Aging. Current Biology DOI: 10.1016/j.cub.2012.07.018


Image: someecards.com

Flightless Giant's Flower Diet Revealed by Poop Fossils

If Big Bird had ever invited his weird armless cousin from Down Under to visit Sesame Street, American kids would have met the moa. These flightless birds lived in New Zealand until hungry humans arrived; the last moa species predictably went extinct around 1500. Thanks to fossilized droppings, though, scientists are learning how the hapless giants lived, what they ate, and what holes they left in the ecosystem by vanishing.

Here are some fossil turds. In polite company, you can refer to them as "coprolites."

Researchers led by Jamie Wood of Landcare Research in Canterbury, New Zealand, discovered about a hundred moa coprolites in the entrance to a remote cave. Thanks to the sunlight and breezy air, the desiccated droppings had been well preserved. They picked out 35 choice specimens (above) to take back to the lab.

To turn the rocky clumps into open books, the researchers used every tool they had. They carbon dated the coprolites to find out their ages. They cracked them open and looked for tiny bits of leaves or seeds that had been fossilized inside. They extracted DNA from the coprolites, both belonging to the moas that had left them behind and the plants those birds had eaten. And they dissolved their samples to get out pollen grains, which could be traced to plant species.

There were 11 or so species of moa alive in the past, ranging from hefty to alarmingly large. The biggest were nearly twice the weight of a large ostrich today. However, the DNA sequences inside the coprolites revealed that they all belonged to just one species: the upland moa, Megalapteryx didinus. Jamie Wood says this was one of the smaller moa species, standing about three feet tall (minus the neck and head) and weighing around 80 pounds. "It had sharp claws and was feathered right down to the feet," he adds.

The upland moa was also the last one to go extinct. Carbon dating showed that the most recent fossil droppings were only dropped about 700 years ago. Other coprolites in the cave were closer to 6400 years old. Based on the pollen and moa DNA inside them, the authors think certain clusters of coprolites within their sample came from "a single defecation event." Nearly half their sample might be accounted for by just five birds, using this cave as a latrine at different points in history.

Plant DNA, pollen, and microscopic fossils inside the coprolites revealed what those historic birds had recently eaten. The upland moa wasn't picky: At least 67 types of plants were accounted for in the droppings. Some of the pollen may have blown onto the birds' food from elsewhere. But overall, the upland moa was an indiscriminate herbivore, eating whatever plants were around. In addition to trees, shrubs, and grasses, it likely ate the flowers of flax and fuchsia plants. (These nectar-filled treats are eaten by some living birds as well.)

The pollen and seeds inside the coprolites came from plants that flower in the spring and summer, which let the researchers infer that the birds moved to warmer forests during the winter months. And they squeezed a further bit of information from the stony droppings: Seeds from several plant species had survived intact inside them. This means the birds would have scattered these seeds—possibly to sprout again—wherever they did their business.

Certain regional plant species may have relied on the moas to distribute their seeds in this way. In evolutionary terms, the birds haven't been gone long; the authors point out that some very old trees alive today might have been planted by moas. Dominos tipped by the extinction of the moa may still be falling throughout the New Zealand ecosystem.

Jamie Wood says he and his colleagues still haven't exhausted the information that can be extracted from a fossil turd. In the future, they'd like to use DNA evidence to discover the sex of each dung-depositing moa. "Some moa species had vast size differences between sexes, so we are interested in working out whether the diets and habitat use also varied with the different sexes," he says.

Six-thousand-year-old poop might not have gone over well as a Sesame Street topic, even if Big Bird's extinct cousin had shown up. But for scientists, the fossils are providing an elementary education about a vanished species.

Jamie R. Wood, Janet M. Wilmshurst, Steven J. Wagstaff, Trevor H. Worthy, Nicolas J. Rawlence, & Alan Cooper (2012). High-Resolution Coproecology: Using Coprolites to Reconstruct the Habits and Habitats of New Zealand’s Extinct Upland Moa (Megalapteryx didinus) PLoS ONE : 10.1371/journal.pone.0040025


Images: Upland moa by George Edward Lodge/Wikipedia; coprolites Wood et al.

Rare Blooms

John pauses with his cursor over a photo of a dark yellow flower. He seems to be debating whether to say something. "I call this one the penis orchid," he admits.

I see it. The Coryanthes bears a bulbous, upright projection, behind which is a bucket-shaped area filled with fluid. Male euglossine bees tumble into the bucket while trying to collect the orchid's fragrance, which they use like a cologne to make themselves more attractive to females. As a male bee repeatedly falls into and crawls back out of these buckets, he unwittingly pollinates the flowers.

It's a great story, but the flower's endowment might be distracting to the middle- and high-schoolers who read the magazine I edit. "Yeah," I tell him, "my photo editor will never let that fly."

I'm visiting my friend John Osterhagen to research an article for kids about orchids. John works for an insurance company by day, but returns home to an apartment bursting with orchid plants. There are eighty or so, living in his bedroom on rows of shelves and windowsills, under special lamps or misting devices. John's cat, Keiko, likes to chew the leaves of just one plant, so he keeps it tucked in his farthest corner.

Flowers aren't John's only self-admittedly strange hobby. He loves early music, origami, and coloring with Crayolas. But none of his other hobbies lives and breathes in his home with him. "People say in the orchid world that you 'get the bug,'" he says. A few fussy but handsome potted plants become shelves full of exotic hybrids and a membership to the Orchid Society. "It's as if the orchids themselves are manipulating you."

John also has the bug for orchid taxonomy, which is always changing as genetic studies revise the family trees guessed at by past centuries' naturalists. He rattles off genus names: Paphiopedilum, Phragmipedium, Bulbophyllum. Sometimes a genus becomes empty and abandoned as taxonomists shift all its species into different groups. John keeps up on the research and edits Wikipedia pages where he can.

The magazine story I'm working on is about deception. Orchids thrive on lying. Some grow petals that look precisely like the back of a female bee or beetle or wasp; a male of the targeted species will try his hardest to mate with the unresponsive flower part while the orchid quietly glues its pollen onto his head. Other species trap their pollinators in well-like petals that can only be exited through a tunnel rigged with pollen. There are orchids that mimic other flowers to attract the pollinators that drink their nectar. (Most orchids don't make nectar, the usual lure for insects, at all.) Those that seek to attract carrion flies mimic rotting meat, emitting a stink from masses of gut-colored petals decorated with maggoty white streaks.

John shows me examples on his computer and on his shelves while Keiko paces around our ankles. A petite epiphytic orchid—a species that lives on trees with its roots dangling into the air—has bloomed just in time for me to see it. He points into the innards of another flower, where I can barely make out the trap door flanked with pollen blobs.

And he points out several species that bear a speckled pattern around their centers, as if a breeze has generously dusted them with their own pollen. In reality, the pollen is waiting elsewhere in a large mass to be attached to a pollinator. John has a strong suspicion that the speckles are another kind of deception, meant to attract insects that eat pollen. "I don't know whether it's been studied academically," he says.

The flowers bloom infrequently and on their own schedules, most often around December or January. Even after putting so much effort into dressing up for a pollinator, they seem not to care whether they get pollinated at all. John says he sometimes gets up in the morning to find that an orchid has tossed a new, perfectly formed blossom to the ground overnight.

The whole family of Orchidaceae, in fact, can appear bent on self-destruction. They grow slowly, sometimes taking years to reach maturity. They're "insanely specialized to their pollinators," many wagering all their future generations on a visit from a single species. If pollinated, they produce seeds that are nearly microscopic. And those seeds can't sprout unless they happen to cross paths with a fungus that will enter into a symbiotic relationship and provide the nutrients the orchid needs. "It seems like the odds are stacked against them," John says.

Yet orchids are some of the most successful plants in the world. There are around 25,000 species, living on every continent except Antarctica and in nearly every kind of climate. They're either the largest or second-largest flowering plant family that exists, depending who does the counting.

The secret to their world dominance may be genetic. During the orchid's evolution, master genes that control the organization of the flower were duplicated. This gave the plant a huge amount of freedom to mutate. New flower shapes emerged to fill thousands, then tens of thousands, of ecological niches.

John doesn't breed his plants. With their expected pollinators never showing up, and John declining to pollinate them by hand, he says they're "the world's most sexually frustrated orchids."

But he does see plenty of mutants. The orchid tendency to create genetic monsters manifests even in his apartment. John shows me a plant that grows flowers with four parts instead of six, and another that has piles of unnecessary petals, "like a Frankenstein flower." He has a plant that can't keep its flowers' lips (the modified petals at the front and center) straight from its other petals. After the mottled fuchsia flowers open, the lips try to turn into petals while the petals start to curl like lips. In a photo, another flower grows an extra petal straight from its center, like an arm coming out of its face.

Orchid growers keep track of individual plants with an elaborate naming system that traces each plant's family history. Thanks to the finickiness of orchid growth, many of these species can't be cloned like other plants can. So their incarnations on John's shelves are one of a kind.

Whether they grow flawless blossoms or freaks, "that particular plant is unique in the whole world," he says. "Like a human."

All images by John Osterhagen. Top to bottom: An orchidarium; Paphiopedilum venustum (a Himalayan species species with a pattern that, John notes, looks like a brain); Jumellea comorense (native to the Comoros Islands in the Indian Ocean); and Dendrobium Negro (a hybrid of Southeast Asian Denbrobium species).

Memory-Improving Gene Tied to PTSD

A superior visual memory is the best friend of artists and competitive card memorizers. But to people who've lived through traumatic events, it might be the enemy.

Researchers in Switzerland and Germany guessed that people with a better memory might be more susceptible to post-traumatic stress disorder, their minds clinging stubbornly to horrific events in the past. But studying the memories of people living with a mental illness is difficult, since the disorder itself might affect their memory. So when the researchers went on a hunt for genes that are linked to both memory and PTSD, they began in a healthy population.

A group of more than 700 Swiss young adults, free of any mental illness, participated in the first part of the study. They viewed several dozen pictures that were meant to elicit either a positive emotional response, a negative emotional response, or a neutral one. After being distracted for 10 minutes, they were given a surprise quiz on how many of the pictures they could recall.

The subjects's DNA underwent testing too. The researchers checked 2,005 individual spots in each person's genes called SNPs (pronounced "snips"). These are bits of DNA that vary across a population, such that some people might have a T nucleotide where others have a G, for example. All of the 2,005 SNPs the researchers checked had to do with certain multitasking molecules called protein kinases that seem to be involved in memory formation.

Out of the 2,005 gene variants in this haystack, one needle emerged: a bit of DNA that was significantly linked to subjects' performance on the memory test. There are two versions (or alleles) of the gene in question, which makes a molecule called PKC alpha. People with one of these alleles--an A rather than a G--remembered more of the pictures they'd seen. Although researchers were especially interested in their subjects' recall of emotionally negative pictures, the effect seemed to extend to positive and neutral ones as well.

Brain scans showed a difference inside the heads of these high-performing memorizers. Subjects with A alleles had more activity in parts of the prefrontal cortex while looking at the negative images. These same regions, the authors say, have been linked to emotional memory storage in other studies.

Now that the researchers had found a gene of interest, they could study it in some actual traumatized people. They turned to a group of 347 Rwandan refugees who fled their country during the civil war. After being interviewed thoroughly, 134 of the refugees were found to meet criteria for post-traumatic stress disorder. Rwandans who had the better-memory gene variant from the first part of the study were more likely to be in the PTSD group. They were also more likely to have the symptom of reliving a traumatic memory over and and over.

Among the healthy Swiss population, the better-memory A allele was more common than the worse-memory G allele. But among the Rwandan refugees, the opposite was true: The better-memory gene variant was the rare one. If it were more common, PTSD symptoms might have been even more frequent among the displaced Rwandans.

The genetics of mental illness are tricky to untangle, and what merits a diagnosis in one culture might  be normal in another. Studies such as this one, though, could reveal who's most at risk for certain symptoms. And if scientists can figure out how exactly the genes in question are acting in the brain, we might see new drugs that can treat some of these symptoms--or prevent people's memories from turning against them in the first place.


de Quervain, D., Kolassa, I., Ackermann, S., Aerni, A., Boesiger, P., Demougin, P., Elbert, T., Ertl, V., Gschwind, L., Hadziselimovic, N., Hanser, E., Heck, A., Hieber, P., Huynh, K., Klarhofer, M., Luechinger, R., Rasch, B., Scheffler, K., Spalek, K., Stippich, C., Vogler, C., Vukojevic, V., Stetak, A., & Papassotiropoulos, A. (2012). PKC  is genetically linked to memory capacity in healthy subjects and to risk for posttraumatic stress disorder in genocide survivors Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1200857109


Image: Virginia Guard Public Affairs/Flickr

Hearing: Your Other Sense of Touch

Those of us without prehensile ears tend to think of our senses of hearing and touch as separate. But our sensory abilities overlap with each other more often than our kindergarten teachers let on. Our sense of smell gets help from our vision centers. Tasting food is mostly done with our noses. And a new study says hearing is just another sense of touch. The same genes can make you good--or deficient--at both.

Hearing a bird chirp and picking up a pencil from your desk, though they seem like wildly different tasks, are really the same trick performed by your body twice. Cells that receive physical input from the outside world (the edge of the pencil against your fingertips, or the vibration of sound waves rattling your inner ear) have to turn that information into an electrical signal and send it back to your brain.

So researchers in Germany guessed that the same genes affect both senses, in people as well as in other vertebrates. They used human subjects to ask the question in several different ways.

First, the team studied a group of more than 500 hearing subjects. In a battery of tests, people listened to tones and clicks, responded to tiny vibrations on their fingertips (measuring their touch sensitivity), and felt surfaces with narrow ridges (touch acuity).

There was plenty of variability in subjects' hearing and touch abilities. Both senses clearly grew worse with age. And in many of the tests, women outperformed men. These data let researchers chart how a healthy person's senses should act throughout their lives.

Then 100 pairs of twins came in for testing. Geneticists love twins: Identical sets have all the same genes, so any differences between them must come from somewhere outside their DNA. Fraternal sets share about half their genes, but are the same age and grew up (usually) in the same environment, so they can be easily compared to identical twins.

Subjecting the twin sets to the same tests, the researchers saw that touch sensitivity and touch acuity both have major genetic components, just like hearing does. And they saw that the two senses correspond to each other: People with good hearing are more likely to have good sense of touch too.

What about people with bad hearing? The researchers recruited another set of 39 teenagers and young adults from a school for the hearing impaired. About a fifth of the deaf subjects had "very poor touch performance."

There are plenty of genetic and non-genetic reasons people are born deaf, and the researchers don't know which of these factors were present in their subjects. But it seems that for some hearing-impaired people, whatever damaged their hearing did the same to their sense of touch. The simple explanation is that the same genetic mutation affects both senses.

Finally, the researchers examined a group of subjects with an illness called Usher syndrome that causes deafness and blindness. Scientists know of several genes that are involved--a mutation in any one of then can cause Usher syndrome. The German team found that patients with a certain Usher gene mutation also had significantly worse touch acuity than normal.

The twins and the deaf young adults showed that hearing and touch go along with each other, seeming to rely on shared genes. The Usher syndrome patients let researchers go a step further and identify one specific gene that affects both senses. "Both senses require cells that convert tiny changes in mechanical force into an electrical signal," said senior author Gary Lewin. "Genes may code for proteins that play a similar role in this process in the two types of cells." In other words, if our cells use the same genes for hearing and touch, they may also share a set of molecular tools.

I asked Lewin whether science is on the path to trimming down our number of senses. If we begin to understand hearing and touch as one mechanism, and if taste barely exists without smell, do we really have three senses? "No, I think we will stick with five and even more senses," Lewin said. "The cellular mechanisms and the way these different sensory cells are connected are highly unique."

Even so, our sensory skills continue to surprise us. Our kindergarten teachers may not have been wrong, but our understanding of human senses is growing up.


Frenzel, H., Bohlender, J., Pinsker, K., Wohlleben, B., Tank, J., Lechner, S., Schiska, D., Jaijo, T., Rüschendorf, F., Saar, K., Jordan, J., Millán, J., Gross, M., & Lewin, G. (2012). A Genetic Basis for Mechanosensory Traits in Humans PLoS Biology, 10 (5) DOI: 10.1371/journal.pbio.1001318

Image: AiyaHMPH/Flickr

How Stress Makes Oranges Better for You

Though Sicily may seem like a relaxing oasis, it's really a stressful climate where rogue elements can turn you bloody--whether you have a run-in with the mafia, or you're an orange. New research shows why the Italian blood orange prefers this hostile environment to your backyard. With a little coercion, though, we might someday convince this extra-healthy fruit to move abroad.

A variety of the sweet orange Citrus sinensis, the blood orange has eerie red flesh and is grown most successfully around Sicily. To develop their trademark color, the oranges need to ripen in a climate where the nights are much colder than the days. They're cultivated in a few other places outside of Italy, and their color can be enhanced by storing them in the cold after picking them. But in general, the blood orange is an inflexible character.

The blood orange's pickiness makes it hard to mass produce and get onto grocery store shelves. A team of researchers from the United Kingdom, Italy, and China (where another variety of blood orange grows) set out to find what makes the orange so finicky.

Pigments called anthocyanins give the fruit its gory look. These same pigments are responsible for the deep purplish hues of blueberries, eggplant peels, and Japanese maples. Combing through the blood orange's DNA, the researchers found a gene they named Ruby that turns on the fruit's anthocyanin machinery.

When Ruby is activated, the plant makes anthocyanin and the orange turns red. To demonstrate this, the researchers snuck the Ruby gene into a tobacco plant. Tobacco leaves normally make anthocyanin only in small amounts. But with Ruby added to their genes, tobacco plants cranked up the pigment's production and sprouted reddish leaves.

If Ruby is the foreman who hits the ON button at the anthocyanin factory, he apparently needs a cold snap to get him out of bed--because without cold nighttime temperatures, blood oranges don't turn bloody. The researchers discovered that the element waking Ruby up is a kind of rogue gene called a transposon.

Also called "jumping genes," transposons are chunks of DNA that can hop around a genome and insert themselves wherever they like. At some point in the blood orange's evolution, a tranposon stuck itself right in front of Ruby and became the on-switch for the on-switch.

Ordinarily, the plant suppresses the transposon. It's not a good idea, after all, to let wandering genes start bossing around the rest of your DNA. But transposons often get turned on when plants are stressed. Scientists think this may be a desperate trick plants evolved to use when times are tough: The normal order of business isn't working, so plants set their rogue genes free to see if they have any useful innovations. When blood orange trees are stressed by cold temperatures, they release their hold on the transposon in front of Ruby. The transposon wakes up the factory foreman, and you know the rest.

Now that we've found the secret to making blood oranges bloody, senior author Cathie Martin says genetic engineers could create a new variety that doesn't need the cold at all. Scientists could tweak the orange's genome so that Ruby is active all the time, keeping the pigment factory going in any temperature.

Imagining a job for a task force of tree psychologists, I asked Martin if we could grow unmodified blood orange trees in warm climates and just stress them out some other way. But she said that probably wouldn't work. You also can't create a blood orange by chilling regular "blonde" oranges or orange trees--this particular team of rogue gene and factory foreman is specific to this variety of Citrus sinensis.

Of course, you could always just stick to the fruits that grow easily in your climate. But Martin says blood oranges are even better for us than regular oranges. "There are many examples of...dietary anthocyanins having a beneficial effect on health," she says, "especially for cardiovascular disease and obesity." In mice, blood orange juice (but not regular orange juice) limits weight gain and prevents obesity.

If these pigments are as healthful as they seem--and especially if climate change is going to make the tree's home turf less comfortable--maybe it's worth pursuing a way to get the blood orange out of Sicily.



Butelli, E., Licciardello, C., Zhang, Y., Liu, J., Mackay, S., Bailey, P., Reforgiato-Recupero, G., & Martin, C. (2012). Retrotransposons Control Fruit-Specific, Cold-Dependent Accumulation of Anthocyanins in Blood Oranges THE PLANT CELL ONLINE DOI: 10.1105/tpc.111.095232


Image: ccharmon/Flickr

How to Slim Down, Manage Your Man, and Stay Tight with Your Girlfriends!

Who ever said science wasn't for us ladies? This week's research is full of tips on looking good, eating right, and taking care of your man! Plus: Don't miss a shocking true story about a girls' get-together turned deadly.


DIET
The calorie-free way to de-bland your diet

You try to eat right. But sometimes that low-sodium poached chicken breast on lettuce doesn't thrill your taste buds. What if merely looking at pictures of steak, pizza or pastries made your healthy meal taste heartier? New research from Switzerland says that just might work.

A group of Swiss scientists studied 14 healthy adults. The subjects held an electrode on their tongues while researchers flashed pictures of foods in front of them. The electrode gave off little buzzes of "electric taste," triggering subjects' taste buds with a neutral, slightly metallic taste.

People experienced a more pleasant flavor in their mouths when the electric taste was paired with a high-calorie food picture than a low-calorie one. The scientists say these images of forbidden foods light up the parts of our brains that go "Mmm!"

Could you try this trick in your own home? The researchers didn't study what happened when people ate actual food while looking at pictures. But if your gluten-free, high-fiber bread is blander than a piece of metal, staring at a picture of chocolate cake might make it seem tastier.


FITNESS
This surprising workout trick will have you handing back unwanted pounds!

If you're overweight, you might find exercise frustrating. Just a few minutes of exertion can leave you feeling overheated and sweaty. But research presented at an American Heart Association meeting may provide a solution to your problem: colder hands.

Researchers at Stanford University conducted a small study on obese women between the ages of 30 and 45. All the women participated in a 12-week exercise program that included push-ups, lunges, and using a treadmill. Half the women held their hands in cylinders of cold water while they were on the treadmill, while the other half kept their hands in body-temperature water.

Because the women who exercised with their hands in cold water stayed cool, they were less likely to get frustrated and drop out of the exercise program. (They even stuck it out through those dreaded push-ups!) These women lost more weight and got in better shape than the other group of women.

You probably don't have one of these cold-water exercise devices in your local gym. But you can still apply the findings to your own exercise routine. In the summer, why not freeze water bottles and hold them in your hands while you work out? And in colder months, get outside and ditch those gloves! After all, everyone can agree that a beach-ready body is worth a little numbness in the extremities.


MAN MANUAL
Are cheeseburgers turning your guy's swimmers into toast?

Bad news, drive-through lovers! Fertility specialist Jill Attaman says a diet high in saturated fat is bad for sperm counts.

Attaman studied the swimmers of 99 men who came to a fertility clinic. She also gathered data about the men's diets and divided them into three groups based on their fat intake. The men in the highest fat-consuming group had sperm counts 43 percent lower than men who consumed the least fat. That's news that will chill some men's hearts colder than a Shamrock Shake.

But it's not all bad news for fats. While saturated fats were tied to low sperm counts, healthy fats called omega-3's seem to be good for sperm. Men who were in the highest third for consumption of this kind of fat had healthier, better-formed swimmers. So next time you cook your burger king a thoughtful dinner, think of his own little sesame seeds and try salmon instead of steak.


TRUE LIFE READ
"I was part of a hot defensive bee ball"

Bertha,* a Japanese honeybee, was hard at work in her hive one day when she became aware of an intruder. A giant hornet, Vespa mandarinia japonica, was inside the entrance of the hive. Suddenly Bertha found herself swept up in a buzzing mass of bodies.

"I'd heard rumors about the hot defensive bee ball before," Bertha says, "but I'd never been a part of one myself." The sister honeybees clumped together in a tight swarm around the massive body of the hornet. (They don't call them giants for nothing. Check out some mug shots of these unpopular predators here.)

Vibrating their muscles to generate heat, the bees cranked the temperature in the swarm up to 46 degrees Celsius, or 115 degrees Fahrenheit. That's even hotter than your Bikram class! It was uncomfortable for Bertha--but for the hornet, it was worse.

Within an hour, the hornet was dead. The bees dispersed. And that's when they found themselves, instead of at the hive's entrance, inside a glass beaker. The attack had all been a ruse perpetrated by scientists. The hornet hadn't even been coming after the bees in earnest; researchers had shoved it inside the hive on a wire.

"I felt sort of used," Bertha says. "I was just swept up in the moment, and now I know I was manipulated into joining the bee ball. But at least it was for science." (Bertha was luckier than some of her sisters, who were forced to donate their heads to science as well.)

The researchers wanted to find out what genes were activated in bees' brains while they formed the hot defensive bee ball. They found one gene of note. But the same gene was active when bees were heated up outside of the bee ball. So it seems to be a response to the furnace-like environment the bees create, not a cause of the mysterious ball-forming impulse.

To find out what drives bees to form hot, deadly mobs in the first place, scientists--and Bertha--will have to wait.

*Some names have been changed.


Ohla, K., Toepel, U., le Coutre, J., & Hudry, J. (2012). Visual-Gustatory Interaction: Orbitofrontal and Insular Cortices Mediate the Effect of High-Calorie Visual Food Cues on Taste Pleasantness PLoS ONE, 7 (3) DOI: 10.1371/journal.pone.0032434 


Attaman, J., Toth, T., Furtado, J., Campos, H., Hauser, R., & Chavarro, J. (2012). Dietary fat and semen quality among men attending a fertility clinic Human Reproduction DOI: 10.1093/humrep/des065


Ugajin, A., Kiya, T., Kunieda, T., Ono, M., Yoshida, T., & Kubo, T. (2012). Detection of Neural Activity in the Brains of Japanese Honeybee Workers during the Formation of a “Hot Defensive Bee Ball” PLoS ONE, 7 (3) DOI: 10.1371/journal.pone.0032902 


Images: plates of food Ohla et al.; glove peanutian/Flickr; burger guy Mr. T. in DC/Flickr; bee klugi/Flickr