Three Earth-sized planets orbiting a star practically next-door might be a good place to hunt for alien life — or at least check out some worlds that are different from anything in our solar system.

The planets orbit a dim, cool star just 39 light-years away in the constellation Aquarius. Each is outside or possibly on the edge of the star’s habitable zone — where average temperatures are just right for liquid water. But there could be niche locales on these worlds where alien life might thrive, Michaël Gillon, an astrophysicist at University of Liège in Belgium, and colleagues report online May 2 in Nature.
A year on the two inner planets lasts just a couple of days. Data on the third world are sparse; it could take anywhere between 4.5 and 72.8 days to trek around its sun. The star, designated 2MASS J23062928−0502285, is roughly the size of Jupiter — about one-tenth as wide as our sun — and about 3,200 degrees Celsius cooler than the sun. Such runts make up about 15 percent of the stars in the galaxy, though astronomers had not found planets around one before. All three planets were discovered as periodic dips in starlight in late 2015 using TRAPPIST, a telescope at La Silla Observatory in Chile.

If anything does crawl or grow on these worlds, it bathes in mostly infrared light. The innermost planets receive several times as much energy from their star as Earth does from our sun, which technically puts them outside the star’s habitable zone (SN: 4/30/16, p. 36). But the planets are huddled up so close to the star that gravity might keep them from spinning, creating a temperate zone along the line where day turns to night, the researchers suggest.

Faint red stars such as this one are the best place to look for warm rocky planets, says Nicolas Cowan, an astronomer at McGill University in Montreal. Planets, even small ones, are easier to see around these dim bulbs rather than sunlike stars. NASA’s planet-hunting Kepler space telescope has already shown that planets exist around similar stars, but those are too far away to investigate further. “This [study] finds a nearby example,” says Cowan.

Being nearby is important for studying the atmospheres of such worlds, or learning whether they have atmospheres at all. They may not. Red dwarf stars take a long time to form; planets arise while their sun is still a puffy, temperamental ball of contracting gas. “That might bake off all the water and the atmosphere,” Cowan says. Astronomers won’t know, though, until they point some big telescopes toward these worlds.

The Hubble Space Telescope might be able to get a crude look. But NASA’s James Webb Space Telescope, scheduled to launch in 2018, could gaze at these planets and measure how much starlight is being absorbed by molecules in their atmospheres. If there is an atmosphere, James Webb could look for such gases as oxygen and methane (SN: 4/30/16, p. 32). On Earth, at least, those gases are produced by plants and microbes.

Whether or not life has found a home on these worlds, all offer a peek at unfamiliar environments. The two planets closest to the star, for example, are bombarded with more energy than Venus, notes Lisa Kaltenegger, an astronomer at Cornell University. “How would Venus evolve if you heat it up even more?” she asks. “We don’t have such planets in our own solar system, so it is really interesting to find out what such planets can be like.”

New sperm-catching beads could someday help prevent pregnancy — or enable it.

Researchers created microscopic polymer beads that mimic unfertilized eggs and trap passing sperm. The beads are coated in the sperm-binding section of a protein called ZP2. In mammals, ZP2 is found in membranes around unfertilized eggs; sperm must bind to the protein before entering the egg.

The beads could be used as short-term contraceptives, Jurrien Dean of the National Institutes of Health in Bethesda, Md., and colleagues report in the April 27 Science Translational Medicine. In the laboratory, human sperm attached to the beads within five minutes. The researchers then mixed 100,000 human sperm with 1.5 million beads and 28 mouse eggs containing human ZP2 proteins. After 16 hours, only one sperm reached an egg.
In another experiment, beads coated with mouse ZP2 delayed pregnancy when injected into the uteruses of mating female mice. Bead-free mice took just over 28 days, on average, to conceive and give birth; bead-treated mice didn’t have babies for nearly 73 days on average. The beads didn’t appear to cause swelling or damage, and treated mice were able to give birth again within five months.

The beads could also help combat infertility. In an egg-penetration test, researchers gently detached bead-captured sperm and pitted those sperm against a control batch of sperm that had not been exposed to the beads. More than half of eggs (mouse eggs with human ZP2) exposed to the bead-selected sperm ended up with three or more sperm attached to them; none of the eggs exposed to the control group snagged three or more sperm. In fact, the control group failed to penetrate 38 out of 50 eggs. So the beads could someday be used to select healthy sperm for assisted reproduction, the researchers say.

But it’s not clear if the ability to bind to ZP2 necessarily indicates a healthy sperm, says Andrew La Barbera, chief scientific officer of the American Society for Reproductive Medicine in Birmingham, Ala. “Sperm selection is a very complex undertaking because of the fact that sperm are very complex,” he says. “We don’t know what makes a good sperm.”

Contraception might be a more reasonable future use for the beads, although allowing fertilization of one in 28 eggs is underwhelming, La Barbera says. Birth control should be closer to 99.9 percent effective. “It only takes one sperm to fertilize an egg,” he says. Still, the beads’ performance at blocking pregnancy in mice seems promising, La Barbera says. Future experiments would need to determine if the beads are safe and effective in women, and how many beads are needed to prevent conception.

Dean notes that the study is a proof of principle. Many unknowns must be evaluated before using the beads for birth control, including the side effects of long-term use, he says. “Although promising, we are a long way from translating these basic laboratory observations into useful clinical applications that provide people with better reproductive choices.”

During the rainy season in the Orinoco Llanos of Columbia and Venezuela, an odd landscape feature appears in places: mounds of grassy plants, as big as five meters across and two meters tall, surrounded by water. Traversing this landscape, called surales, requires either hopping from mound to mound or trudging through the boggy bits in between.

Locals and scientists have generally agreed that some kind of earthworm creates the mounds, but what species and how it does so has been a mystery. Now Anne Zangerlé of the Braunschweig University of Technology in Germany and colleagues report that they’ve found the culprit — giant Andiorrhinus earthworms, which can grow to a meter in length as juveniles. And the mounds themselves, the team reports May 11 in PLOS ONE, are actually made mostly of earthworm poop.

Zangerlé and her colleagues used Google Earth images to locate surales landscapes, finding that they come in the shape of both mounds and labyrinths. Leaving the complex labyrinths for a future study, the team studied the mounds and the lands on which they were found in both the rainy and dry seasons. They characterized the soil and the plants and worms living in and on the mounds. And then they pieced all of that information together to come up with a scenario that they think explains the construction of the mounds.
Andiorrhinus earthworms deposit feces, or casts, in towers that give the worms access to the air so they can breathe. The worms then return to the tower, depositing more and more material, building the tower into a mound. These young mounds, the researchers found, are dominated by Andiorrhinus earthworms. But over time, as the mounds get even bigger, other worm species begin to make their home there, as well as plants and, eventually, if the mounds get big enough, trees.

The Andiorrhinus earthworms tend to stay around the same mound because, as they build, they excavate soil from the region around the mound. That moat gets deeper and deeper until it becomes a barrier to the giant earthworm that created it.

The researchers don’t quite understand everything that is happening in the system. For example, there could be an as-yet-unknown end stage to mound development, or some kind of equilibrium state for the landscape. But they note that “these ecosystems are under threat from industrial agriculture, and are being leveled to make way for highly intensified commercial production of rice.” Because of that, they say, there is a risk that these wonderfully complex and mysterious systems could disappear before anyone fully understands what made them in the first place.

Earth’s plate tectonics could be a passing phase. After simulating rock and heat flow throughout a planet’s lifetime, researchers have proposed that plate tectonics is just one stage of a planet’s life cycle.

In the simulation, the Earth’s interior was too hot and runny at first to push around the giant chunks of crust, researchers report in the June Physics of the Earth and Planetary Interiors. After the interior cooled for around 400 million years, tectonic plates began shifting and sinking, though the process was stop-and-go for about 2 billion years. The simulation suggests that Earth now is nearly halfway through its tectonic life cycle, says study coauthor Craig O’Neill, a planetary scientist at Macquarie University in Sydney. In around 5 billion years, plate tectonics will grind to a halt as the planet chills.

The long delay before full-blown plate tectonics hints that the process could one day begin on currently stagnant planets, says Julian Lowman, a geodynamicist at the University of Toronto who was not involved in the research. “There is a possibility that plate tectonics could start up on Venus if conditions were right,” he says.
Plate tectonics regulates a planet’s climate by adding and removing carbon dioxide from the atmosphere. This climate control helps maintain Earth’s habitability. Plate movement is driven by heat flow through the planet’s interior. Simulating that heat flow requires complex calculations. Previous simulations were simplified and typically considered only snapshots of Earth’s history and missed how plate tectonics evolves over time.

O’Neill and colleagues simulated Earth’s full tectonic life span, starting with the planet’s formation around 4.5 billion years ago and looking ahead to around 10 billion years in the future. Even using a supercomputer and simulating only a two-dimensional cross section of the planet, the calculations took weeks.

The new timeline suggests that Earth’s plate tectonics is just a midpoint in the planet’s evolution between two stagnant states. Planets with different starting temperatures than Earth’s follow different trajectories, the team found. Colder planets may exhibit plate tectonics throughout their history while hotter planets could go for billions of years without plate tectonics.

Just because a planet currently lacks plate tectonics doesn’t make it uninhabitable, O’Neill says. Life potentially appeared on Earth as early as around 4.1 billion years ago (SN Online: 10/19/2015), a time when the new simulation suggests that Earth lacked full-blown plate tectonics. “Stagnant planets, depending on when they are in their history, can be equally likely of supporting habitable conditions” as planets with plate tectonics, O’Neill says.

Childhood fears are common, normal — Some behavior, such as nail biting, bed-wetting and fearfulness, may actually represent a temporary phase in normal development…. A most important finding [in a recent study] was that the fearful or anxious children, defined … as those with seven or more worries, did not seem to be in any particular psychological trouble.…Anxieties may be part of normal child development. — Science News, June 25, 1966

UPDATE
Actually, there is reason to worry about anxious children. Kids with anxiety disorders, depression or behavioral problems are especially likely to develop a range of difficulties as young adults, say researchers who conducted a long-term study published in 2015. The same goes for kids whose anxiety, mood or behavior issues cause daily problems but don’t qualify as psychiatric ailments. Problems that later dogged the study’s troubled youngsters, who grew up in rural North Carolina, included drug addiction, teenage parenthood, dropping out of high school and criminal arrests.

A mosquito’s spit can be worse than its bite alone. In some cases, the insect’s saliva makes the viral disease dengue fever more severe, a new study finds.

In mice, scientists found that mosquito spit weakened blood vessels, making them more permeable, or “leaky.” Easier exchange between the blood and tissues may help the virus spread faster — and increase the severity of disease — immunologist Michael Schmid and colleagues report online June 16 in PLOS Pathogens.

Dengue virus enters the bloodstreams of nearly 400 million people a year, through the sharp proboscises of tropical Aedes mosquitoes, which also deliver a spit-load of other molecules as they slurp a meal. There are four strains of dengue, which can cause bone and muscle aches, high fever and, in severe cases, death. Overcoming one type of dengue doesn’t protect the host from the other three strains. In fact, subsequent infections are often worse (SN: 6/15/16, p. 22).

Immune cells fight off the first dengue infection, and the body develops antibodies to that strain. But during a subsequent episode with a different variety of dengue, the antibodies from the first infection don’t kill the second — they amplify it. They pull new virus into healthy cells.

Scientists have studied this strange immune trap for three decades, “but what we didn’t know was that saliva could exacerbate it,” says Schmid, now at the University of Leuven in Belgium.
Investigating spit is important, says virologist Eva Harris of the University of California, Berkeley, a coauthor of the study. Molecules in mosquito saliva “can modify and modulate the infection process,” she says. Saliva’s role is well-studied in other viral diseases, like West Nile, but not for dengue.

Schmid’s team inoculated mice either with virus, saliva, or both virus and saliva, during primary and secondary dengue infections. In primary infections, the severity of the disease did not differ substantially between treatments. Symptoms were mild, at most. But in secondary infections, the combination of virus and saliva was lethal to more than half of the mouse population. Without the saliva, mortality was much lower.

To understand why, the researchers ran experiments to track viral spread through the circulatory system. In mouse ears, a molecule about the size of the dengue virus moved farther, and faster, when packaged with mosquito spit. And in the lab, human endothelial cells lining the inner walls of blood vessels sealed less tightly in the presence of Aedes saliva. The researchers also found that mice inoculated with virus alone could be rescued if the skin around the injection site was removed four hours later. The same procedure did not rescue mice dosed with virus and saliva.

These results should be interpreted with caution, says Duane Gubler, an infectious disease researcher at Duke University who was not involved in the study. Various environmental and genetic factors also play a role in the severity of the disease. “It’s not clear-cut,” he says.

The first, tiny root that emerges from a baby plant can make it or break it.

Anchor to a good patch of ground, and the plant can thrive for decades. Set up someplace else, without enough water or sunshine, and all may be lost.

The odds of a single rootlet mooring itself to just the right spot of soil are more than a million to one, writes geobiologist Hope Jahren. “The gamble is everything, and losing means death.”
Jahren touches only briefly on the plight of the newborn root, just a page or so near the beginning of her new book, Lab Girl, but it’s enough to bring drama to a topic not usually considered all that thrilling. Jahren’s great skill, here and throughout the book, is making readers care — to root for the root, in this case.

In Lab Girl — which is part memoir, part plant love story — each cactus, tree and leaf gets the same empathetic treatment. Jahren doesn’t so much spice up plant life as she does reveal it — histories, triumphs, tragedies and all — to those who might not have been paying close enough attention.

But this isn’t just a book for botanists. Or science geeks. Or lovers of nonfiction. This is a book for anyone who has stayed up late with a flashlight beneath the covers, vowing to finish just one last chapter.

Interspersed between snippets about plants, Jahren puts her own life under the microscope, baring gritty details about her struggles with bipolar disorder (she had to go off her medications during pregnancy) and as a woman desperately scrambling to eke out a career in science. She’s made it now, and is currently at the University of Hawaii at Manoa in Honolulu, studying, among other things, how carbon in fossilized plants can reveal information about ancient climates.

But the book’s lifeblood, or xylem and phloem, if you will, are Jahren’s stories from her early days as a scientist. For Jahren, and her long-term scientific partner in crime, an otherworldly character named Bill Hagopian (he once lived in a hole he dug in his parents’ yard), life is a series of adventures. The duo crisscross the country for scientific meetings, take students on madcap road trips and regularly pull all-nighters in the lab.
Though Jahren and Hagopian often end up in exotic places (an island in the Arctic Ocean or Miami’s Monkey Jungle, among other places), Jahren somehow makes the everyday tasks of lab work thrilling, too. And through it all, she pauses to tell the untold stories of plants — to consider life’s wonders from a plant’s point of view.

Vines, for instance, “do not play by the rules of the forest,” she writes. They steal light and water, and will climb over anything in their paths to do so. And trees, scientists have discovered, can actually “remember” their childhood.

In the epilog, Jahren eases the reader back to the reality we know. “Plants are not like us,” she writes. “They are beings we can never truly understand.”

But anyone who reads Lab Girl will know that can’t be true. Because for nearly 300 pages, Jahren has made us feel like we can.

Buy Lab Girl from Amazon.com. Sales generated through the links to Amazon.com contribute to Society for Science & the Public’s programs.

Genetically modified mosquitoes can put a dent in dengue cases. The first evidence of the health effects of releasing the insects into the real world comes from a year’s worth of disease data from Brazil, says biotech company Oxitec, the mosquitoes’ engineer.

Over much of the city of Piracicaba, where conventional methods of mosquito control were used, cases of the debilitating virus dropped 52 percent from mid-2015 to mid-2016. But in neighborhoods where Oxitec released GM Aedes aegypti mosquitoes as an extra control, the results were even better. Dengue cases there dropped 91 percent, from 133 to 12, according to a press statement from Oxitec, based in Abingdon, England.
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Oxitec’s genetically modified line of Ae. aegypti mosquitoes attack a wild population by romantic deception. The GM males sire offspring with built-in self-destruct DNA that kills the new generation off in the wild before they begin to bite. This is the modern biotech twist on a decades-old strategy for controlling insects by releasing sterile males in such numbers that many females waste their reproductive effort, and a population eventually breeds itself out of existence.

In tests around the world before this, Oxitec has published or released evidence that mosquito numbers go down when the GM decoys swarm through a neighborhood. But this is the first claim that reducing those mosquitoes indeed means less disease.
That information — though not the result of a full epidemiological study — could address a gap in the debate in the Florida Keys over a proposed test release there. Opponents of introducing GM organisms, even ones pretty reliably programmed to die, have objected that there has been no evidence the measure brings any health benefit.

Brazil, where dengue and now Zika have wreaked havoc, has been much more open to the use of GM mosquitoes. In this case, Oxitec looked at the numbers of dengue cases reported mid-year to mid-year from Piracicaba’s epidemiologic surveillance program. The GM mosquito test focused on an area, called CECAP/Eldorado, of about 5,000 residents where the dengue rates were higher than in the rest of the city in 2014‒2015 — 2.66 percent incidence rate versus 0.902 percent. After a year of control measures including releasing the GM mosquitoes, the 2015‒2016 numbers show the test area now fares better than the rest of the city. Its dengue incident rate dropped to 0.24 percent compared with the municipality incidence rate of 0.437 percent.

Data on mosquito populations and diseases are rare and important, says Grayson Brown, who directs the Public Health Entomology lab at the University of Kentucky in Lexington. He wonders how far down the GM mosquitoes drove the wild population before dengue rates started dropping. (Oxitec reports that mosquito numbers dropped 82 percent, but, Brown asks, 82 percent of what?) Such a useful number turns out to be virtually unknown for most mosquito-borne diseases and their countermeasures, except for malaria, he says. Plenty of programs monitor disease outbreaks as they treat mosquitoes, but ethically and politically, “you can’t just leave a section of the city untreated.” Adding the extra measure of the GM treatments offers a way to fill that data gap.

Alcoholism may stem from using genes incorrectly, a study of hard-drinking rats suggests.

Rats bred either to drink heavily or to shun alcohol have revealed 930 genes linked to a preference for drinking alcohol, researchers in Indiana report August 4 in PLOS Genetics.

Human genetic studies have not found most of the genetic variants that put people at risk for alcoholism, says Michael Miles, a neurogenomicist at Virginia Commonwealth University in Richmond. The new study takes a “significant and somewhat novel approach” to find the genetic differences that separate those who will become addicted to alcohol from those who drink in moderation.
It took decades to craft the experiment, says study coauthor William Muir, a population geneticist at Purdue University in West Lafayette, Ind. Starting in the 1980s, rats bred at Indiana University School of Medicine in Indianapolis were given a choice to drink pure water or water mixed with 10 percent ethanol, about the same amount of alcohol as in a weak wine. For more than 40 generations, researchers selected rats from each generation that voluntarily drank the most alcohol and bred them to create a line of rats that consume the rat equivalent of 25 cans of beer a day. Simultaneously, the researchers also selected rats that drank the least alcohol and bred them to make a line of low-drinking rats. A concurrent breeding program produced another line of high-drinking and teetotaling rats.

For the new study, Muir and colleagues collected DNA from 10 rats from each of the high- and low-drinking lines. Comparing complete sets of genetic instructions from all the rats identified 930 genes that differ between the two lines.

Such a large number of genes, “shows how complex the genetic underpinnings of the drive to consume alcohol might be,” says Miles.

Often, human genetic studies known as genome-wide association studies, or GWAS, can’t determine which of many genes in a particular region of DNA is involved in a disease or addiction. But the Indiana researchers’ DNA data allowed them to pinpoint the exact genetic tweaks implicated in the rats’ drinking. “With GWAS, they’re just trying to get down to the gene — we’ve got it down to the parts of the genes,” Muir says.

That precision “is clearly an advance,” says John Crabbe, a neuroscientist at the Portland VA Medical Center in Oregon. “No one has gone into this much detail before in any alcohol-related trait.”
Most of the time, the genetic variant associated with drinking behavior wasn’t located within the part of the gene containing blueprints for a protein, the researchers discovered. Only four genes contained variants in their protein-producing parts. The majority of the differences were in surrounding DNA that regulates gene activity. Those changes could alter how much protein is produced from the genes, says study coauthor Feng Zhou, a neurobiologist at Indiana University School of Medicine. In turn, altering amounts of proteins could shift biochemical reactions important for determining behavior.

Until recently, scientists thought alcoholism and other problems stemmed from inheriting altered forms of genes that would produce faulty proteins. “Well, that game’s over,” says Crabbe. Now researchers realize that regulating gene activity is often just as important as changing the genes themselves.

The researchers don’t yet know whether the genes identified in the rats are the same ones that lead to drinking problems in people.

Understanding sea anemones’ exceptional healing abilities may help scientists figure out how to restore hearing.

Proteins that the marine invertebrates use to repair damaged cells can also repair mice’s sound-sensing cells, a new study shows. The findings provide insights into the mechanics of hearing and could lead to future treatments for traumatic hearing loss, researchers report in the Aug. 1 Journal of Experimental Biology.

“This is a preliminary step, but it’s a very useful step in looking at restoring the structure and function of these damaged cells,” says Lavinia Sheets, a hearing researcher at Harvard Medical School who was not involved in the study.
Tentacles of starlet sea anemones (Nematostella vectensis) are covered in tiny hairlike cells that sense vibrations in the water from prey swimming nearby. The cells are similar to sound-sensing cells found in the ears of humans and other mammals. When loud noises damage or kill these hair cells, the result can range from temporary to permanent hearing loss.

Anemones’ repair proteins restore their damaged hairlike cells, but landlubbing creatures aren’t as lucky. Glen Watson, a biologist at the University of Louisiana at Lafayette, wondered if anemones’ proteins — which have previously been shown to mend similar cells in blind cave fish — might also work in mammals.

Watson and colleagues mimicked traumatic hearing loss in mice hair cells by depriving them of calcium ions, which are crucial for maintaining cell structure and transmitting sounds. Within a few hours, the normally stiff, hairlike structures that detect sound “looked like spaghetti,” he says.
Researchers bathed the damaged hair cells in a cocktail of anemone repair proteins. After an hour, the cells showed remarkable improvement compared with untreated cells. Proteins rebuilt molecular tethers that bundle hair cells and act as gatekeepers for calcium ions. As a result, the cells absorbed more fluorescent dye — an indication of how well calcium flows into the cells.

What’s more, researchers identified a bevy of mice proteins that are analogs of anemones’ repair proteins. But mammalian versions work less effectively than anemone proteins, if at all. More research could point the way to one day harnessing human repair proteins, Sheets says.

Moving forward, Watson plans to investigate the ability of the anemones’ proteins to repair damaged cells in the ears of living mice. “If we could get to those hair cells before they commit to die and treat them, there’s a possibility we could reduce hearing loss,” he says.