December 11, 2013
It’s long been known that carnivorous plants lure their insect prey in a range of ways: irresistible nectars, vivid colors and alluring scents that range from rose to rotten flesh.
But recently, a group of scientists at the Jawaharlal Nehru Tropical Botanic Garden and Research Institute in India discovered a previously hidden means of beckoning among the most ruthless of greenery. Some carnivorous plants, they discovered, lure insects to their death with a fluorescent glow invisible to the human eye.
Scientists believe that insects are attracted to carnivorous plants by the their odors and colors, but hard evidence as to what exactly lures the bugs to their deaths was previously unknown. In a stroke of serendipity, a team of scientists led by botanist Sabulal Baby put several carnivorous plants they’d been using for unrelated experiments under ultraviolet light, including Nepenthes khasiana, a rare pitcher plant native to India, and photographed what they saw.
“To our great surprise, we found a blue ring on on the pitcher rim,” Baby says. “Then, we looked at other Nepenthes species and the prey traps of other carnivorous plants, including the Venus flytrap, and we consistently found UV-induced blue emissions.” These colors, found in a total of twenty carnivorous plant species and documented in a study published in Plant Biology, were the first time such distinct fluorescent emissions were ever detected in the plant kingdom.
Under normal light, these bright, glowing rims would look green to humans. But an ant—which can’t see red, but is extremely sensitive to blue and violet light—would see rings of blue florescence, the result of metabolic compounds in the plant that absorb UV radiation from the Sun and re-emit it as visible light. Putting the plants under a UV light in an otherwise dark room, as Baby’s team did, amplifies the effect, allowing humans to more clearly see the blue emissions.
To prove that these emissions were involved in the plants’ predation, the scientists constructed an elegant experiment. They monitored live pitcher plants in the field for a ten-day period, cutting them open afterward and seeing how many ants each one caught. Some of the plants, though, were painted with an acetone extract that blocks fluorescent emissions. It’s not clear exactly why the ants would be attracted to the blue light, but the results, produced several times and in several different locations, pretty clearly indicate that it’s the case:
He has yet to test the idea, but Baby says that the plants might use their fluorescence for other purposes as well. Recent field studies in Borneo indicated that some species of pitchers may have a symbiotic relationship with small nocturnal mammals, such as rats, bats and tree shrews—these mammals come and drink nectar from the plants, and deposit nutritious feces nearby, which serve as a fertilizer. “Fluorescence emissions by Nepenthes traps could be acting as major visual cues luring these mammals towards them,” Baby says.
These sorts of normally invisible signals could be way more prevalent in the plant kingdom than we previously realized. A recent study by British scientists, for instance, revealed that bumblebees can detect electric fields produced by flowers, adding another layer of communication to the symbiotic relationship between these two types of organisms. “There could be many other forms of signaling out there, waiting to be found,” Baby says.
November 27, 2013
When we think of ants as builders, we normally imagine them digging intricate tunnel networks as part of underground colonies.
But David Hu, Nathan Mlot and a team of other researchers at Georgia Tech are studying a very different type of building behavior specific to one ant species: The ability of Solenopsis invicta to construct bridges, rafts and even temporary shelters using their own bodies as building material.
“Fire ants are capable of building what we call ‘self-aggregations,’” Hu says. “They can build little boats, little houses called bivouacs and even bridges to cross streams by being the building material, linking their bodies together and forming strong networks.”
The ants are now considered an invasive species in 25 states, Asia and Australia, but their unusual behavior is a survival strategy shaped by their native environment: a particular area of wetlands in western Brazil that are flooded frequently. “The ants live underground, but when it begins to flood, they have to gather the colony members, pull them out of the ground and build a floating raft,” Hu says.
When this raft hits land, the ants keep building. To cross small streams during their subsequent migration, they make living bridges that allow the entire colony to scramble to safety. Afterward, using their bodies, they construct a temporary aboveground encampment to provide shelter for the few days it takes to re-dig underground tunnels. All the while, the ants that form the temporary shelter are continuously moving, but still preserving the structure. “It’s really living architecture—it has well-constructed, organized tunnels, brooding rooms,” Hu says. At least for the ants in the inside, this provides protection against hostile weather or predators.
Hu, an engineer, is primarily interested in studying the swarming ants as a novel material with unprecedented characteristics. As part of his group’s recent research, presented yesterday at an annual meeting of the American Physical Society, he and colleagues considered the ants within the context of other “active materials”—substances that can respond to changing conditions, such as self-healing cements that can use the energy in sunlight to expand and fill their own fractures.
“We wanted to characterize what kind of material it is—is it a fluid, or is it a solid, and how does it respond to stress?” he says. “In nature, for instance, these rafts might float down a river and bump into rocks, or raindrops might hit them.”
To test these self-aggregations, Hu’s team used a few techniques, comparing live ant structures to clumped dead ants as a control. Using a rheometer—a device that can precisely measure the stress response and flow of a fluid, and is often applied in industrial situations (such as the development of a new shampoo)—they found that the ants continuously reorganize their structure to maintain stability.
Many materials behave like a solid when stressed by forces moving at certain speeds, and a fluid when stressed by slowed ones. Water, for instance, behaves like a fluid when you stick your hand in it, but a solid when hit by a human body jumping off a diving board—the reason that a belly flop hurts so much.
But the ant structures are a combination of solid and fluid when stressed by forces at all speeds, the researchers found. They actively deform their structure to accommodate a stress (like a fluid) but then bounce back into place afterward (like a solid). Check out what happens when one of their structures is compressed by a petri dish, for instance:
“This makes sense, based on their natural environment,” Hu says. “If they’re floating in a raft down a river, they have no control over where it floats, so if there’s something in the way—say, a twig—you see respond and flow around the twig, kind of like an amoeba.”
The ants’ sheer resiliency and buoyancy is also remarkable. When the researchers tried to push the floating rafts below the water’s surface, they found they could resist a significant amount of force and float back up:
This is enabled, in part, by the ants’ exoskeletons, which are naturally hydrophobic (i.e. they chemically repel water). When many ants clump together to form a structure, water doesn’t penetrate into the gaps between then, so when they’re forced underwater, the air that remains in these cavities helps them float.
Perhaps the biggest mystery of these ants’ remarkable living structures is how the creatures communicate to build them. Most ant communication is based on trails of pheromones left on the ground, but in such an interconnected form, that type of communication seems unlikely. Microscopic examination reveals that the ants grasp each other using both their jaws and little claws on the end of their legs. Noting this, Hu adds, ”We think they’re communicating through touch, but we really don’t understand it yet.”
November 25, 2013
Once upon a time, scientists thought that the human brain was a rigid, predictable organ, not tremendously different from the lungs or liver. Based on a person’s genetics, it developed in a predetermined way, endowing an individual with a particular level of learning capabilities, problem-solving abilities and baseline intelligence.
Now, though, as part of emerging research into brain plasticity, neuroscientists are recognizing that the brain is a responsive, constantly evolving organ that can change at both the cellular and large-scale levels due to environmental influences and experiences. Much of this research is hopeful: It’s shown how in people with impaired vision, for instance, areas of the brain normally devoted to processing sights can be repurposed to analyze sound.
Over the past few months, though, a series of studies have emphasized that the brain can change for worse, as well as for the better. A child’s brain, not surprisingly, is especially vulnerable to such effects—and this research has shown that growing up in difficult circumstances dictated by poverty can wreak damage to a child’s cognitive skills that last a lifetime.
An October study by researchers from the University of Michigan, for instance, used fMRI (functional magnetic resonance imaging)—which detects blood flow in various areas of the brain as a reflection of brain activity—to study the regulation of emotions in young adults who were part of a long-term study on poverty. They compared a participant’s family income at age 9 (based on survey data collected at the time) with his or her current neural activity in different brain regions, and found that those who grew up in poverty showed increased activity in the amygdala (believed to be involved in anxiety, fear and emotional disorders) and decreased activity in the prefrontal cortex (which limits the influence of the amygdala, putting long-term decision making over impulse) when the participants were shown emotionally-upsetting images.
It’s impossible to know for sure, but the researchers suspect that a range of chronic stresses that can accompany growing up in poverty—things like crowding, noise, violence, family turmoil or separation—impact the development of the brain in childhood and adolescence, potentially explaining this correlation.
Another October study, meanwhile, took a more basic approach, examining the relationship between nurturing during childhood and the growth of brain tissue in children between the ages of six and 12. In it, Washington University in St. Louis researchers found that among the 145 children studied, those whose parents had poor nurturing skills had slowed growth in white matter, grey matter and the volumes of several different areas of the brain involved with learning skills and coping with stress. Based on the differing growth rates between children who resembled each other in terms of other key factors, it seemed as though the experience of growing up with adults with less nurturing skills effectively set back their mental development a year or two. And impoverished parents, they found, were more likely to have poor nurturing skills.
Sure, attempting to objectively evaluate the parenting styles of the adults in this study might be a bit heavy-handed, but the study identified chronic stresses experienced by the children as a key element as well: Children who grew up in poverty but had fewer stressful life events (as part of a larger program, they’d gone through annual assessments from the age of three onward) demonstrated smaller reductions in neural development.
Others have even looked into very specific behavioral effects of poverty. A recent Northwestern University study found a link that children with lower socioeconomic status tended to have less efficient auditory processing abilities—that is, the area of their brains responsible for processing sound showed more response to distracting noise and less activity as a result of a speaker’s voice than control participants. This might be an effect, the researchers say, of the known correlation between low income and the amount of noise exposure in urban populations.
Of course, most of these are limited by the very nature of a longitudinal study in that they’re correlations, rather than causations—ethics aside, it’s impossible to actively alter a person’s childhood circumstances in a controlled manner and then check the results, so researchers are forced to observe what happens in the real world and draw conclusions. Additionally, in most of these cases, it’s unknown whether the effects are temporary or permanent—whether children exposed to poverty are permanently left behind their peers, or whether they’re able to catch up if given the chance.
But the fact that correlations between poverty and altered mental function when stressed has been repeatedly observed across a range of study designs, circumstances and research groups makes it likely that these effects aren’t aberrations. Additionally, even if they are temporary effects that can be resolved by changing a child’s environment, there’s other recent research that dishearteningly reveals a neurological mechanism that helps to perpetuate poverty, by making it difficult for parent to make choices that change these circumstances.
An August study in Science found that being preoccupied with the all-consuming concerns of poverty—struggling to pay medical bills, for instance—taxes the brain, leaving less extra bandwidth to solve complex cognitive problems and harming long-term decision making ability. In a pair of study groups (shoppers in a New Jersey mall and sugar cane farmers in rural India), simply getting the participants thinking about economic problems (asking them what they’d do if they had to pay $1500 to repair their car, for instance) caused them to perform more poorly on tests that measure IQ and impulse control than otherwise.
The bandwidth problem they identified is temporary, not permanent, but it does explain how making the difficult decisions that might allow someone to get ahead are harder for a person immersed in poverty. It also highlights yet another stressor for parents seeking to ensure that their children escape poverty—they might be inadvertently contributing to an environment that keeps their children from rising above their circumstances.
November 21, 2013
Over the course of 1700 miles, they sampled the water for small pieces of plastic more than 100 times. Every single time, they found a high concentration of tiny plastic particles. “It doesn’t look like a garbage dump. It looks like beautiful ocean,” Miriam Goldstein, the chief scientist of the vessel sent by Scripps Institution of Oceanography, said afterward. “But then when you put the nets in the water, you see all the little pieces.”
In the years since, a lot of public attention has been justifiably paid to the physical effects of this debris on animals’ bodies. Nearly all of the dead albatrosses sampled on Midway island, for instance, were found to have stomachs filled with plastic objects that likely killed them.
But surprisingly little attention has been paid to the more insidious chemical consequences of this plastic on food webs—including our own. “We’d look over the bow of the boat and try to count how many visible pieces of plastic were there, but eventually, we got to the point that there were so many pieces that we simply couldn’t count them,” says Chelsea Rochman, who was aboard the expedition’s Scripps vessel and is now a PhD student at San Diego State University. “And one time, I was standing there and thinking about how they’re small enough that many organisms can eat them, and the toxins in them, and at that point I suddenly got goosebumps and had to sit down.”
“This problem is completely different from how it’s portrayed,” she remembers thinking. “And, from my perspective, potentially much worse.”
In the years since, Rochman has shown how plastics can absorb dangerous water-borne toxins, such as industrial byproducts like PCB (a coolant) and PBDE (a flame retardant). Consequently, even plastics that contain no toxic substances themselves, such as polyethylene—the most widely used plastic, found in packaging and tons of other products—can serve as a medium for poisons to coalesce from the marine environment.
But what happens to these toxin-saturated plastics when they’re eaten by small fish? In a study published today in Scientific Reports, Rochman and colleagues fill in the picture, showing that the toxins readily transfer to small fish through plastics they ingest and cause liver stress.This is an unsettling development, given that we already know such pollutants concentrate further the more you move up the food chain, from these fish to the larger predatory fish that we eat on a regular basis.
In the study, researchers soaked small pellets of polyethylene in the waters of San Diego Bay for three months, then tested them and discovered that they’d absorbed toxins leached into the water from nearby industrial and military activities. Next, they put the pollution-soaked pellets in tanks (at concentrations lower than those found in the Great Pacific garbage patch) with a small, roughly one-inch-long species called Japanese rice fish. As a control, they also exposed some of the fish to virgin plastic pellets that hadn’t marinated in the Bay, and a third group of fish got no plastic in their tanks at all.
Researchers still aren’t sure why, but many small fish species will eat these sort of small plastic particles—perhaps because, when covered in bacteria, they resemble food, or perhaps because the fish simply aren’t very selective about what they put in their mouths. In either case, over the course of two months, the fish in the experiment consumed many plastic particles, and their health suffered as a result.
“We saw significantly greater concentrations of many toxic chemicals in the fish that were fed the plastic that had been in the ocean, compared to the fish that got either clean plastic or no plastic at all,” Rochman says. “So, is plastic a vector for these chemicals to transfer to fish or to our food chain? We’re now fairly confident that the answer is yes.”
These chemicals, of course, directly affected the fishes’ health. When the researchers examined the tiny creatures’ livers (which filter out toxins in the blood) they found that the animals exposed to the San Diego Bay-soaked plastic had significantly more indications of physiological stress: 74 percent showed severe depletion of glycogen, an energy store (compared to 46 percent of fish who’d eaten virgin plastic and zero percent of those not exposed to plastic), and 11 percent exhibited widespread death of individual liver cells. By contrast, the fish in the other treatments showed no widespread death of liver cells. One particular plastic-fed fish had even developed a liver tumor during the experimental period.
All this is bad news for the entire food webs that rest upon these small fish, which include us. “If these small fish are eating the plastic directly and getting exposed to these chemicals, and then a bigger fish comes up and eat five of them, they’re getting five times the dose, and then the next fish—say, a tuna—eats five of those and they have twenty-five times the dose,” Rochman explains. “This is called biomagnification, and it’s very well-known and well-understood.”
This is the same reason why the EPA advises people to limit their consumption of large predatory fish like tuna. Plastic pollution, whether found in high concentrations in the Great Pacific garbage patch or in the waters surrounding any coastal city, appears to be central to the problem, serving as a vehicle that carries toxins into the food chain in the first place.
November 20, 2013
In 1834, Charles Darwin discovered a strange animal during his exploration of Chile’s southern coast. The creature, a small frog, was shaped like a leaf with a pointed nose, but appeared puffed up as if had been blown full of air, like a balloon. As it turned out, those fat male frogs hadn’t been gorging themselves on too many mosquitoes, but instead were enacting duties that earn them distinction as one of nature’s best dads. They were incubating several of their squirming babies in their vocal sac.
These peculiar animals, known as Darwin’s frogs, are today divided into two species, one that occurs in northern Chile, and another that lives in southern Chile and Argentina. When a female Darwin’s frogs lay her eggs, her mate keep a careful watch until the tadpoles hatch. The eager dad then swallows his young, allowing the babies to safely grow within his vocal sac until they turn into frogs and are ready to strike out on their own. Here, you can see a dutiful papa frog seemingly vomit up his living young:
Northerly Darwin’s frogs, however, have not been spotted in the wild since 1980. Researchers are nearly certain the species is extinct. Meanwhile, their southerly cousins are in steep decline and seem to be heading down extinction’s death row as well. For once, it seems that humans are not entirely to blame for these biodiversity disasters (unlike the western black rhino, which bit the dust a couple years ago after enduring decades of poaching for its valuable but medicinally worthless horn, used as an ingredient in traditional Chinese medicine). Instead, the deadly amphibian chytrid fungus, researchers report today in PLoS One, is likely to blame.
The chytrid fungus has popped up in amphibians in North and South America, Europe and Australia. The fungus infects the animals’ skin, preventing them from absorbing water and other nutrients. The fungus can rapidly decimate amphibian populations it comes into contact with, and has been called (pdf) “the worst infectious disease ever recorded among vertebrates in terms of the number of species impacted, and its propensity to drive them to extinction” by the International Union for Conservation of Nature.
To identify chytrid as the likely culprit behind the Darwin’s frogs disappearance and decline, researchers from Chile, the UK and Germany conducted a bit of historical sleuthing. They dug up hundreds of archived specimens of Darwin’s frogs and closely related species dating from 1835 until 1989, and then tested them all for fungal spores (the problematic form of chytrid fungus was first recorded in the 1930s and reached epidemic-status around 1993, but researchers aren’t certain of when it first emerged). They also took around 800 skin swabs between 2008 and 2012 from 26 populations of still-living southern Darwin’s frogs and other similar frog species that live nearby.
Six of the old museum specimens, all collected between 1970 and 1978–just before the northern Darwin’s frog’s disappearance–tested positive for the disease. More than 12 percent of the living frogs tested positive for the fungal spores. In places where the Darwin’s frog has gone extinct or is experiencing drastic declines, however, rates of infection jumped to 30 percent in other amphibian species. Although these events don’t prove that the fungus killed the northern Darwin’s frogs and are now wiping out the southern species, the researchers strongly suspect that is the case.
Despite evidence that the disease has spread throughout the Darwin’s frog’s range, the researchers are not giving up on hope to save one of the world’s greatest dads from extinction. “We may have already lost one species, the Northern Darwin’s frog, but we cannot risk losing the other one,” Claudio Soto-Azat, the study’s lead author, said in a statement. ”There is still time to protect this incredible species.”