In July of 1972, NASA launched the first Landsat satellite into orbit around Earth. Since then, the spacecraft and its successors have transformed our understanding of Antarctica (and the rest of the planet, too). In the first year following the launch, Landsat’s images of the faraway continent showed “uncharted mountain ranges, vast ice movements and errors in maps as little as two years old,” according to an article published in Science News. William MacDonald of the U.S. Geological Survey, who had spent eight years mapping a part of West Antarctica, was “shocked” to learn of previously unknown peaks just 100 miles from McMurdo Station.
Landsat’s images weren’t the first overhead shots of Antarctica, but to this day the program provides researchers a reliable and repeating view of hard-to-reach corners of the planet. It was Landsat images that in November of 2014 first alerted scientists to a growing crack in the Larsen C ice shelf that, after lengthening by about 20 kilometers in less than nine months, threatened to break off a Delaware-sized chunk of the shelf. With thermal imagery from Landsat 8 along with data from the European Space Agency’s Sentinel-1 satellites, scientists sitting half a world away tracked the Larsen C crack to its final break, as described by Ashley Yeager. While satellites are scientists’ eyes in the skies, seismic sensors serve as ears to the ground. Alexandra Witze describes the work of scientists who are using seismic sensors to monitor nuclear weapons activity in a part of the planet where access to information is limited: North Korea. Five nuclear weapons tests have been confirmed in the country since 2006, all at an underground test site in Mount Mantap. By tracking seismic waves produced by such explosions, and comparing these rumbles with each other and with those produced by natural earthquakes and in experimental tests, researchers around the world gain valuable clues to where the hidden explosions are happening and, importantly, how powerful they are. A North Korea weapons test last year was detected as far away as Bolivia.
The art of eavesdropping certainly has its rewards. There are plenty more examples. Rachel Ehrenberg writes about how snooping scientists might listen in on kelp to predict ecosystem health. And Emily Conover reports on a newly discovered, relatively itty-bitty star some 600 light-years away. Astronomers spied on the star by watching it pass in front of a larger star, dimming the larger star’s light.
Sometimes astronomers get lucky and distant phenomena are much more straightforward to study. That will be the case later this month when a total solar eclipse passes across North America from Oregon to South Carolina. People will be monitoring the August 21 eclipse in all sorts of ways, including via a livestream from balloons at the edge of the atmosphere, as Lisa Grossman describes in “Watch the moon’s shadow race across the Earth from balloons.” Grossman will be reporting on the eclipse on the ground with scientists in Wyoming. You’ll find her stories — along with many others about the ways scientists watch, listen and learn — at www.lssfzb.com
Thanks, Holly Gaff. Soon, anyone straining to tweeze off a mid-back tick can find answers to the obvious question: What if humankind just went after the little bloodsuckers with killer robots?
Gaff, who calls herself a mathematical ecoepidemiologist, at Old Dominion University in Norfolk, Va., is one of the few people collecting real field data on the efficacy of tick-slaying robots. This summer, she’s been supervising a field test of a terminator named TickBot deployed to try making mowed grass safe for children. Researchers will start analyzing results in early fall.
Ticks make formidable enemies. “Almost every control measure that has been tried has failed, and has failed miserably,” Gaff says. “We are slowly coming to embrace the fact that you cannot eradicate ticks.” What human ingenuity might do, however, is manage the risks and — dream big! — make ticks irrelevant. That’s an urgent hope. Data from the Cary Institute of Ecosystem Studies in Millbrook, N.Y., have for two years suggested 2017 will be a high risk one for Lyme disease in the Northeastern United States. Of the various illnesses that North America’s ticks pass along, Lyme is the most common, caused by a squiggle of a parasite called Borrelia burgdorferi. The disease can bring on an eerie red bull’s-eye rash, flulike misery and risks of long-term neurological and joint troubles if not treated early. In 2015, the U.S. Centers for Disease Control and Prevention tallied about 30,000 confirmed cases. Considering gaps in case reporting, some estimates put the number closer to several hundred thousand.
So bring on the robots and other science revenge fantasies. It’s time to rethink humankind’s defenses against ticks. Pesticides and tick checks just aren’t doing the trick. There may be ways to attack ticks without touching a single molecule of their die-hard little bodies. Ecologists have made progress in tracing what ticks need from the woods and lawns where they lurk. For instance, researchers believe that it was a bumper crop of acorns in 2015 that, through a Rube Goldberg series of consequences, created conditions for a perfect tick storm two years later. Breaking key ecological connections could knock back the tick menace in the future.
Molecular biologists are focusing on tick survival tricks. Researchers are looking for weak spots inside tick guts and trying to take advantage of ticks’ reckless abandon in mating. Biology is proving as important as electronics in the robot line of defense.
Though, Gaff warns, the top design is not the laser-blazing Armageddon that a recently tick-bitten human might crave. Ticks attack First, a quick intro to ticks.
Unlike mosquitoes, ticks are pure vampires, consuming nothing but blood. Mosquitoes get colloquially called vampires, but blood is just their version of a pregnancy craving, a female-only nutrient gorge to aid reproduction in an adult life of sipping flower nectar. For most of the troublesome tick species in North America, including the black-legged ticks that spread Lyme, blood is the elixir that lets them transition to the next life stage — from larva to nymph to adult. And after a single meal, an adult female can lay 1,000 or even 15,000 eggs without anything else to eat for the rest of her life. Hard ticks, the Ixodidae family, which includes the black-legged variety, typically have only two or three meals of any kind during the entire two or three years they live.
Soft ticks are gluttons, relatively speaking. Many move into mammal dens for a bedbug lifestyle. These ticks hide and, whenever they get hungry, just crawl over to the resident dinner.
For ticks without live-in prey, many “quest,” as the ambush is called. Ticks climb to some promising spot like the top of a grass blade, raise their front legs and just wait until something brushes by. But there are also ticks that hunt vigorously, even pursuing human prey.
A visit to Dennis Bente at the University of Texas Medical Branch in Galveston is unforgettable, in part because of a video of a Hyalomma tick chasing down one of Bente’s collaborators. The tiny brown creature scurries like a frantic ant in an almost-straight line over bare dirt, onto a boot and finally into a hand reaching down to grab it. This hunter doesn’t live in North America.
Ticks can spread a wide variety of diseases. Despite its name, Rocky Mountain spotted fever, which brings a higher risk of fatality than Lyme, is more common in the central United States and the South than in the Rockies. Other tickborne diseases are lately getting attention: A tick-bitten baby in Connecticut in April became the state’s first reported victim of the rare, but potentially fatal Powassan virus, thought to enter the bloodstream in just 15 minutes after a tick starts feeding. And medical journals are publishing discussions of whether a tick bite might lead to a sudden, deadly allergy to red meat. With a possible threat even to our beloved hamburger, new approaches to fending off ticks can’t come soon enough. Super reactors The most dramatic way of rendering a disease irrelevant is a vaccine. One company raised hopes for this approach in April in Washington, D.C., at the World Vaccine Congress by announcing the start of human safety tests of a new Lyme disease formulation. The only Lyme vaccine for humans in the United States was withdrawn voluntarily in 2002 when controversy stalled sales. (Dogs can still get a Lyme vaccination.)
The strategy for the new Lyme vaccine isn’t like the familiar flu or tetanus vaccines because the pathogens get killed outside the human body. The company, Valneva, based in Lyon, France, has redesigned a protein, OspA, used in previous Lyme vaccines. The vaccine trains the human immune system to fight OspA, found on the surface of B. burgdorferi. When a black-legged tick starts sucking human blood, human immune cells get slurped in too and kill the Lyme-causing pathogens before they leave the tick’s gut. “The idea of this vaccine … is vaccinating the tick,” says CEO Thomas Lingelbach. Even if the new vaccine proves to be safe and effective, its first shot in a doctor’s office, in the most optimistic view, is five to 10 years away.
There may be a bigger-picture way to imagine vaccines, however, than targeting each disease with its own shot. Ecologist Richard Ostfeld of the Cary Institute is one of the people hoping for a vaccine that stops the tick itself, and thus all the diseases it may pass along. By the luck of the great lottery of genetics, Ostfeld has a hyperactive immune response to tick saliva. Think of it as a natural version of what a tick vaccine might achieve.
Despite “many, many dozens of tick bites” over his career monitoring Lyme disease risk, Ostfeld has not gotten sick. He often wakes in the middle of the night with a “burning sensation” somewhere on his body. “I … put on my glasses and, sure enough, there’s a little dark spot surrounded by what’s already turned kind of red.” Warned by his vigilant immune system, he pulls off the dark bit of tick, which is usually dead or dying.
Maybe it’s a thing among tick scientists. Sam Telford of Tufts University’s veterinary school in North Grafton, Mass., who also studies the ecology of Lyme disease, has a similar reaction. Bites, he says, “itch like crazy.” A vaccine that makes people itch doesn’t sound very marketable, but blood that somehow poisons ticks sounds good.
A vaccine to protect cattle against debilitating blood loss from bites already targets the tick itself. Newer ways of targeting ticks are being developed for livestock, and for humans, though protecting our species poses extra challenges. Ticks east and west Of the nine or so tick species that spread diseases in North America, the three highlighted below cause the most trouble. Maps show each tick’s U.S. habitat. Fix the landscape “It would be lovely if we could get a vaccine,” says biochemist Kevin Esvelt of MIT. “But there’s a certain elegance to tackling the heart of the problem, which is ecological.” In several papers posted online at bioRxiv.org in 2016 and this year, Esvelt and colleagues laid out an approach that could slash Lyme risks by causing genetic changes in one of the mammals that ticks feed on, changes that could spread across whole landscapes.
The view of Lyme as an ecological disease blames much of the rise in cases on the suburbanization and fragmentation of once-wild countryside in North America. The shifts have fueled population booms in mammals such as white-footed mice that easily become great scurrying reservoirs of Lyme parasites. Ticks gorge on the mouse blood and a high percentage ingest the parasites.
Deer pick up a lot of the Lyme-spreading black-legged ticks. Yet deer aren’t biologically friendly to B. burgdorferi. The mice make a much better parasite paradise than deer do and are more likely to transmit those parasites.
The common name, “deer tick,” was a fluke of early misidentification, Ostfeld says. The tick was easy to collect on deer. But taxonomists realized the hard tick is just a northern form of the long-known black-legged tick, which dines on many mammals. In fact, just how deer abundance affects tick abundance was the No. 1 outstanding uncertainty about Lyme listed in a 12-person consensus published in the June 5 Philosophical Transactions of the Royal Society B. Fighting Lyme disease appeals to Esvelt, who, like his pediatrician wife, grew up in the low-tick landscapes of the West Coast where Lyme is rare. In Massachusetts now, he says, “to both of us, it’s just horrific that a) there are that many ticks out there, and b) that they give you horrific diseases.” He especially regrets that neither of his two kids, nor anyone else’s, can tromp around outdoors, like he used to, carefree.
Esvelt calls the work of his lab, which plans to engineer a Lyme-resistant mouse, “sculpting evolution.” He and colleagues aim to tackle big biological problems like Lyme spread by using the insights of evolutionary biology plus the powerful gene-editing tool known as CRISPR/Cas9 (SN: 9/3/16, p. 22). But Esvelt wants to use that power with a startling openness and extreme public oversight.
“Right now, people don’t trust scientists to ensure that technologies are well understood before throwing them out there,” he says. “We have to fix that somehow.”
Before he even started to create a Lyme-resistant mouse in the lab, he asked for public meetings on the two Massachusetts islands where he hopes to test mice: Martha’s Vineyard and Nantucket. He got the green light to begin from citizen steering committees on both islands. But they still have the power to shut down the tests at milestones in the project. If the citizens nix the idea, he will walk away.
Originally Esvelt planned to sculpt Lyme disease into insignificance by acting on the ticks directly, driving down their numbers or changing them to be less dangerous. “But I talked to a lot of tick biologists who said, ‘Look, it’s not gonna happen.’ ” The black-legged ticks take so long to reproduce that the plan would only succeed “if you’re willing to wait about 50 years,” he says.
It’s actually faster to work with a mammal, the white-footed mouse. For the first tests, on islands, he plans great caution. He won’t even use a gene drive, the powerful way of deploying CRISPR/Cas9 so it overrides chancy natural inheritance and passes the desired genes to all offspring (SN: 12/12/15, p. 16). Instead he’ll just release mice genetically tweaked to be bad transmitters of Lyme and let natural mouse powers spread the genes.
Those mice won’t even be transgenic: They won’t carry genes from any other species. He’ll vaccinate island-captured mice in the lab, with an anti-Lyme vaccine or one that should confer an active immune response to tick bites. Then he’ll identify genes that produce the most protective reaction and put a large selection of them into what should be a safer animal that’s still “100 percent mouse,” he says.
While he’s tailoring safer mice for the island, however, he’s imagining new gene drives for a larger, mainland campaign. The way forward may require making gene drives less powerful, so they sputter out after a certain number of generations — “daisy chains,” he calls them, with loosely linked elements that fall apart easily. Going for the gut Ticks themselves probably have weaknesses that people haven’t yet exploited. The study of microbes in human guts has revolutionized ideas about human health and physiology. So Yale University’s Sukanya Narasimhan and Erol Fikrig are looking deep into the microbiome of the tick gut. Narasimhan describes the gut as a many-branched thing, “like a glove.” Ticks do have consistent bacterial residents, which could perhaps be exploited, but interactions look complex.
Along with Lyme, black-legged ticks can deliver other unpleasantries, such as human granulocytic anaplasmosis. When Anaplasma pathogens first tumble into a tick gut, invasion isn’t easy because some resident microbes form a biofilm along the gut lining that may be hard to breach. The pathogen, however, makes the tick secrete what’s essentially antifreeze, Fikrig, Narasimhan and colleagues reported in the Jan. 31 Proceedings of the National Academy of Sciences. The secretions can prevent biofilms from forming and ease the way for pathogen infection.
The sex lives of ticks could offer opportunities for completely different kinds of defenses, says longtime tick specialist Daniel Sonenshine of Old Dominion, author of Biology of Ticks.
He imagines, for instance, protecting livestock or dogs with decoys, “little bits of plastic” treated with a chemical cocktail that includes 2,6-dichlorophenol. That’s the come-hither substance female lone star and some other ticks release when they grab a mammal for a blood-feed. Like drinking venues for our species, mammals provide ticks with hot spots for finding mates. “These little plastic devices mimic a female tick,” Sonenshine says. And believe it or not, plastic fooled males long enough for a pesticide on the decoy to kill the ticks. (Tick sex on humans is possible but not likely, Gaff says. Humans rarely carry enough ticks at once to generate much of a scene.)
Robot vs. tick Tick biology is also important in designing a robot army. The concept behind TickBot came out of a collision of two very different visions of pest-fighter robotics.
As Gaff tells the story, engineers at the Virginia Military Institute in Lexington, “were under this mistaken idea … that ticks live in trees and they fall on your head.” The engineers’ solution: Use lasers to shoot ticks out of trees.
When they called to enlist Sonenshine in the project, he had to break the bad news: no blasting into shrubbery; ticks are on the ground. His advice: Don’t build a robot to attack ticks at all. Get the ticks to attack the robot. Instead of a laser-shooting, macho terminator, the concept morphed into a panting raccoon-sized machine that kills with dragged strips of pesticide-carrying cloth. The engineers’ four-wheeled buggy chugs slowly along following a looped guideline set up along a trail or in an open area.
As the bot works its way along, its motion, in some cases the passing shadow, will trick a tick into jumping at the cloth as it would the fur of a mouse or the sock of a hiker. But the big pull is carbon dioxide. Pest ticks “act like very lazy teenagers who don’t move unless they’re prodded,” says James Squire, one of the Military Institute engineer designers. Adding CO2 gets ticks’ attention and strengthens the illusion of a breathing, warm-blooded something.
The engineers — Squire, David Livingston and Gerald Sullivan — “came up with this amazing system of tubing and carbon dioxide canisters” for releasing CO2 from the bot, Gaff says. However, a student last year put a bit of dry ice in a cup with holes to mimic mammal breath. It worked and made the bot far easier to lug around.
Gaff remembers when she was first pulled in to do the field testing. “I was a huge skeptic coming in,” she says. To test TickBot outdoors, she chose as the first site a path through a wooded park with what she calls “infinite ticks.” There weren’t many Lyme ticks there to test, but the creeping cart tricked so many of the abundant lone star ticks that — high praise from a tick scientist in summer — she sat on the ground and had lunch.
Within a day, however, more ticks moved onto the cleared path from the nearby woods, she and colleagues reported in 2015 in Ticks and Tick-borne Diseases. Still, the notion of robotic tick catchers may be catching on. Gregory Gray, who teaches at Duke University’s Global Health Institute, worked with students from the local robotics club to design their own creeping, cloth-dragging cart.
And the TickBot team is now planning a bigger and faster robot that might ease the uncomfortable business of monitoring for cattle ticks on grazing land. Usually, people “dress up in woolly pajamas” as Squire puts it, and move through brush with an eye out for rattlesnakes in the Texas summer heat. The ticks grab the suit and are later counted. There’s got to be a better way.
For the TickBot itself, summer 2017 brought testing on grass around a playground. Like a little Roomba vacuum cleaner (but with guide wires), it set out twice a week to carve a safe zone by whisking away ticks, Gaff says.
“I’m giving them their space, and I’m asking them to respect my space,” she says. It’s all part of the mind-set of surrendering to the notion that there will always be ticks. But someday maybe we won’t care as much.
Add a new ingredient to the sugar, spice and everything nice needed to make girls.
A protein called COUP-TFII is necessary to eliminate male reproductive tissue from female mouse embryos, researchers report in the Aug. 18 Science. For decades, females have been considered the “default” sex in mammals. The new research overturns that idea, showing that making female reproductive organs is an active process that involves dismantling a primitive male tissue called the Wolffian duct. In males, the Wolffian duct develops into the parts needed to ejaculate sperm, including the epididymis, vas deferens and seminal vesicles. In females, a similar embryonic tissue called the Müllerian duct develops into the fallopian tubes, uterus and vagina. Both duct tissues are present in early embryos.
A study by French endocrinologist Alfred Jost 70 years ago indicated that the testes make testosterone and an anti-Müllerian hormone to maintain the Wolffian duct and suppress female tissue development. If those hormones are missing, the Wolffian duct degrades and an embryo by default develops as female, Jost proposed.
That’s the story written in textbooks, says Amanda Swain, a developmental biologist at the Institute of Cancer Research in London. But the new study “demonstrates that females also have a pathway to make sure you don’t get the wrong ducts,” says Swain, who wrote a commentary in the same issue of Science.
Testing Jost’s hypothesis wasn’t what reproductive and developmental biologist Humphrey Yao and colleagues set out to do. Instead, the researchers wanted to learn how tissues on the outside of the early ducts communicate with the tubes’ lining, says Yao, of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C.
The COUP-TFII protein is produced in that outer layer, and Yao suspected it was involved in talking with the lining. The researchers blocked the communication in early female mouse embryos’ reproductive tissue by removing the gene that produces COUP-TFII. To the team’s surprise, the Wolffian duct remained in the female mice along with the female Müllerian duct. That shouldn’t happen, according to the textbooks. “We were just scratching our heads,” Yao says.
Searching for an explanation, Yao and colleagues first tested whether removing COUP-TFII changed the ovaries to produce testosterone like testes do. Testosterone could feed the male tissue and allow it to persist, the researchers thought.
“No, the ovary is just like an ovary. There’s nothing wrong with it,” Yao says. “We were just shocked. This can’t be happening.” Further experiments demonstrated that no stray testosterone was responsible for the male tissue sticking around.
Instead, COUP-TFII appears to be the foreman of a biochemical wrecking crew that demolishes the Wolffian duct in females. Without the protein barking orders, the demolition crew is idle and the male duct isn’t torn down. Signals that trigger COUP-TFII production and activity aren’t yet understood.
“This study fills a void in our understanding of the mechanism of regression of the Wolffian duct,” reproductive biologists Patricia Donahoe and David Pepin of Harvard Medical School said in an e-mail. More research is needed to understand how the protein interacts with male hormones to regulate reproductive tract development, they say.
While the study used mice, COUP-TFII probably works the same way in other mammals, including humans, Donahoe says. Females rarely still carry Wolffian duct remnants, sometimes leading to tumors. The opposite sometimes happens, too, resulting in males with female reproductive organs. Those men may be infertile and have other problems, such as cysts. Researchers should look for defects in COUP-TFII in patients with reproductive problems, Donahoe says.
Craft brewers are going wild. Some of the trendiest beers on the market are intentionally brewed to be sour and funky. One of the hottest new ingredients in the beverages: Yeast scavenged from nature.
Unlike today’s usual brewing, which typically relies on carefully cultivated ale or lager yeast and rejects outsider microbes, some brewers are returning to beer’s roots. Those beginnings go back thousands of years and for most of that time, the microbes fermenting grain into alcohol were probably wild yeast and bacteria that fell into the brew. Now local microbes — in some cases with the help of scientists — are being welcomed back into breweries.
Wild and sour beers are a niche, but growing segment of the craft brewing market, says Bart Watson, chief economist of the Brewers Association. Last year, more than 245,000 cases of wild and sour beers were sold and sales are up 9 percent so far this year.
For geneticist Maitreya Dunham, wild, funky and sour beers aren’t just a market trend; they are ecological microcosms. Dunham’s lab group at the University of Washington in Seattle uses yeast to study genetic variation and evolution. She got interested in beer when her husband took up home brewing. In the bottom of his five-gallon fermentation bucket, the yeast formed a thick mat that bubbled rapidly. “That’s not how we grow yeast in the lab,” Dunham said. She wanted to test a new technique her lab had developed to identify wild yeast in their natural habitat. And what better habitat to explore than a barrel of beer? Dunham teamed up with a brewer who made a wild beer with microbes from a warehouse. “Whatever is living in the old warehouse ended up in the beer,” she says. On a lab outing to the brewery, Dunham and her team took samples from beer barrels, marveling at the thriving mass of microbes gurgling inside. “You could see it being alive in there.” DNA tests revealed that four kinds of bacteria and four kinds of yeast, including a newly identified hybrid yeast, lived in the wild brew, Dunham and colleagues reported June 15 on bioRxiv.org. The hybrid doesn’t have a name yet, because Dunham is still trying to identify its parents. One is Pichia membranifaciens, but the other is an unknown fungus P. membranifaciens is a food spoiler, and no lightweight: It can handle up to 11 percent alcohol. The other parent’s identity and attributes aren’t known, and that ID can take time. People have known for a long time that lager yeast Saccharomyces pastorianus is a hybrid, but scientists didn’t identify both of its parents until 2011.
As excited as Dunham is to find a hybrid yeast, she’s not sure that it will take beer brewing by storm. Her lab brewed a small batch of “science beer” with the hybrid yeast. The yeast didn’t make much ethanol or other flavor compounds. “It didn’t do much on its own,” she laments. But she hasn’t given up hope. Sometimes a yeast needs bacteria or other fungi to really shine. Maybe, she says, “when it’s mixed in with all its friends, it may bring something interesting to the party.”
A Facebook group of home brewers called Milk the Funk is about to help her find out. People from the group saw Dunham’s study on bioRxiv.org and volunteered to ferment beers with and without the hybrid. “I’m about to have a couple dozen people doing experiments for me,” Dunham says. “In fact, they’re going to send me free beer, although it may be weird beer.” (“Funk is one of the flavors they go for in these weirdo beers,” Dunham explains. Descriptions of funk encompass barnyard tastes and smells such as goat, horse blanket, urine, sweat, cheese and manure, as well as spicy notes and complex flavors of clove, smoke, Band-Aid, bacon and bitter, says fellow scientist and yeast hunter Matthew Bochman. “Funk basically covers anything ‘weird’ in beer that might be interesting or pleasant in small amounts but off-putting at higher concentrations.”) Bochman, a biochemist at Indiana University Bloomington and a self-professed yeast whisperer, is also bagging new kinds of wild yeast. Bochman, who studies how cells keep their DNA intact, was a home brewer for years before moving to Indiana. He soon made friends with many local craft brewers there. In 2014, he met brewer Robert Caputo, who wanted to make an all-Indiana beer. There were farmers in the state growing hops and malt grains. Indiana water was plentiful. “The missing ingredient was the Indiana yeast,” Bochman says. Caputo asked Bochman to help him find the missing microbe. “So we went yeast hunting.”
That spring and summer, Bochman collected about 100 strains of yeast. “Whenever I was out and about I would grab something — a piece of a bark, a berry — bring it back to the lab and get yeast from it.” The microbes are everywhere, he says. “It’s hard not to find yeast.”
But not just any yeast will do. For beer brewing, he needed to find yeast that eat the sugar maltose in the wort — the liquid extracted from grain mash that will be fermented into beer. Yeasts used for brewing also have to be tolerant of hops, which make weak acids that might slow yeast growth. The yeast must be able to live in 4 to 5 percent alcohol. In addition, the microbes have “to smell and taste at least neutral, if not good,” Bochman said.
Not all yeast can pass the sniff test. For instance, eight strains of Saccharomyces paradoxus “all smelled and tasted heavily of adhesive bandages,” Bochman and colleagues reported August 7 on bioRxiv.org.
But in 2015, a batch of wild beer brewed in an open vat in a vacant lot in Indianapolis by Bochman’s friends at Black Acre Brewing Co., yielded a winner. Among the four species and six strains of yeast in the beer was a Saccharomyces cerevisiae strain called YH166. S. cerevisiae is the species of yeast used to brew ales and wine and to make bread. YH166 lends beer an aroma that is “an amazing pineapple, guava something. Like an umbrella drink,” says Bochman.
He doesn’t yet know what chemicals the yeast makes to produce the tropical fruit scent. He puts his money on one of the sweet-smelling esters yeast use to attract the fruit flies that can give the fungi a lift — sort of a microbial version of a ride-hailing app. Sour beer brewers may also benefit from Bochman’s bio-prospecting. Sour beers generally contain lactic acid bacteria in addition to yeast. Brewers need separate equipment for brewing sour beers, because it’s difficult to get rid of all the bacteria in order to brew a nonsour beer. Among 54 species of yeasts Bochman and colleagues investigated, he found five strains that can make both alcohol and lactic acid to brew sour beers without troublesome bacteria. The researchers described the five sourpusses — Hanseniaspora vineae, Lachancea fermentati, Lachancea thermotolerans, Schizosaccharomyces japonicus and Wickerhamomyces anomalus — July 28 on bioRxiv.org. Bochman and Caputo formed Wild Pitch Yeast, a company to sell the strains, in part, to fund his yeast research. The company supplied yeasts isolated from cobwebs, trees and other spots to brewers for making all-Indiana beers, dubbed “Bicentenni-ales” in honor of the state’s 200th anniversary.
Both Bochman and Dunham are relying on brewers to tell them how their newfound yeast perform in the real world. “The proof is in the brewing,” Bochman says. “You can do as many lab tests as you want, but you’re never going to know how something will act until you throw it into some wort and let it bubble away for a couple of weeks.”
Patience is a virtue in the hunt for dark matter. Experiment after experiment has come up empty in the search — and the newest crop is no exception.
Astronomical observations hint at the presence of an unknown kind of matter sprinkled throughout the cosmos. Several experiments are focused on the search for one likely dark matter candidate: weakly interacting massive particles, or WIMPs. But those particles are yet to be spotted.
New results, posted online at arXiv.org in recent months, continue the trend. The PandaX-II experiment, based in China, found no hint of the particles, scientists reported August 23. The XENON1T experiment in Italy also came up WIMPless according to a May 18 paper. Scientists with the DEAP-3600 experiment in Sudbury, Canada, reported their first results on July 25. Signs of dark matter? Nada. And the SuperCDMS experiment in the Soudan mine in Minnesota likewise found no WIMP hints, scientists reported August 29.
Another experiment, PICO-60, also located in Sudbury, reported its contribution to the smorgasbord of negative results June 23 in Physical Review Letters.
Scientists haven’t given up hope. Researchers are building ever-larger detectors, retooling their experiments and expanding the search beyond WIMPs, in hopes of glimpsing a dark matter particle.
For some poison dart frogs, gaining resistance to one of their own toxins came with a price.
The genetic change that gives one group of frogs immunity to a particularly lethal toxin also disrupts a key chemical messenger in the brain. But the frogs have managed to sidestep the potentially damaging side effect through other genetic tweaks, researchers report in the Sept. 22 Science.
While other studies have identified genetic changes that give frogs resistance to particular toxins, this study “lets you look under the hood” to see the full effects of those changes and how the frogs are compensating, says Butch Brodie, an evolutionary biologist at the University of Virginia in Charlottesville who wasn’t involved in the research. Many poison dart frogs carry cocktails of toxic alkaloid molecules in their skin as a defense against predators (SN Online: 3/24/14). These toxins, picked up through the frogs’ diets, vary by species. Here, researchers studied frogs that carry epibatidine, a substance so poisonous that just a few millionths of a gram can kill a mouse.
Previous studies have shown that poisonous frogs have become resistant to the toxins the amphibians carry by messing with the proteins that these toxins bind to in the body. Switching out certain protein building blocks, or amino acids, changes the shape of the protein, which can prevent toxins from latching on. But making that change could have unintended side effects, too, says study coauthor Rebecca Tarvin, an evolutionary biologist at the University of Texas at Austin.
For example, the toxin epibatidine binds to proteins that are usually targeted by acetylcholine, a chemical messenger that’s necessary for normal brain function. So Tarvin and her colleagues looked at how this acetylcholine receptor protein differed between poison frog species that are resistant to epibatidine and some of their close relatives that aren’t. Identifying differences between the frogs in the receptor protein’s amino acids allowed researchers to systematically test the effects of each change. To do so, the scientists put the genetic instructions for the same protein in humans, who aren’t resistant to epibatidine, into frog eggs. The researchers then replaced select amino acids in the human code with different poison frog substitutions to find an amino acid “switch” that would make the resulting receptor protein resistant to epibatidine.
But epibatidine resistance wasn’t a straightforward deal, it turned out. “We noticed that replacing one of those amino acids in the human [protein] made it resistant to epibatidine, but also affected its interaction with acetylcholine,” says study coauthor Cecilia Borghese, a neuropharmacologist also at the University of Texas at Austin. “Both are binding in the exact same region of the protein. It’s a very delicate situation.” That is, the amino acid change that made the receptor protein resistant to epibatidine also made it harder for acetylcholine to attach, potentially impeding the chemical messenger’s ability to do its job.
But the frogs themselves don’t seem impaired. That’s because other amino acid replacements elsewhere in the receptor protein appear to have compensated, Borghese and Tarvin found, creating a protein that won’t let the toxin latch on, but that still responds normally to acetylcholine.
The resistance-giving amino acid change appears to have evolved three separate times in poison frogs, Tarvin says. Three different lineages of the frogs have resistance to the poison, and all of them got that immunity by flipping the same switch. But the amino acid changes that bring back a normal acetylcholine response aren’t the same across those three groups.
“It’s a cool convergence that these other switches weren’t identical, but they all seem to recover that function,” Brodie says.
A skull and other fossils from northeastern Australia belong to a new species in the extinct family of marsupial lions.
This newly named species, Wakaleo schouteni, was a predator about the size of a border collie, says vertebrate paleontologist Anna Gillespie of the University of New South Wales in Sydney. At least 18 million years ago (and perhaps as early as 23 million years ago), it roamed what were then hot, humid forests. Its sturdy forelimbs suggest it could chase possums, lizards and other small prey up into trees. Gillespie expects W. shouteni — the 10th species named in its family — carried its young in a pouch as kangaroos, koalas and other marsupials do. Actual lions evolved on a different fork in the mammal genealogical tree, but Australia’s marsupial lions got their feline nickname from the size and slicing teeth of the first species named, in 1859. Thylacoleo carnifex was about as big as a lion. And its formidable teeth could cut flesh. But unlike other pointy-toothed predators, marsupial lions evolved a horizontal cutting edge. A bottom tooth stretched back along the jawline on each side, its slicer edge as long as four regular teeth. An upper tooth extended too, giving this marsupial lion a bite like a “bolt cutter,” Gillespie says.
The newly identified species lived some 17 million years before its big bolt-cutter relative. Though the new species’ tooth number matched those of typical early marsupials, W. schouteni already had a somewhat elongated tooth just in front of the molars, Gillespie and colleagues report December 7 in the Journal of Systematic Paleontology. W. schouteni is “pushing the history of marsupial lions deeper into time,” she says.
Old blood can prematurely age the brains of young mice, and scientists may now be closer to understanding how. A protein located in the cells that form a barrier between the brain and blood could be partly to blame, experiments on mice suggest.
If something similar happens in humans, scientists say, methods for countering the protein may hold promise for treating age-related brain decline.
The preliminary study, published online January 3 at bioRxiv.org, focused on a form of the protein known as VCAM1, which interacts with immune cells in response to inflammation. As mice and humans age, levels of that protein circulating in the blood rise, Alzheimer researcher Tony Wyss-Coray at Stanford University and colleagues found. After injecting young mice behind an eye with plasma from old mice, the team discovered that VCAM1 levels also rose in certain parts of the blood-brain barrier, a mesh of tightly woven cells that protect the brain from harmful factors in the blood. The young mice showed signs of brain deterioration as well, including inflammation and decreased birthrates of new nerve cells. Plasma from young mice had no such effects.
Interfering with VCAM1 may help prevent the premature aging of brains. Plasma from old mice didn’t have a strong effect when injected into young mice genetically engineered to lack VCAM1 in certain blood-brain barrier cells. Nor did it affect mice treated with antibodies that blocked the activity of VCAM1. Those antibodies also seemed to help the brains of older mice that had aged naturally, the team found.
The results suggest that anti-aging treatments targeting specific aspects of the blood-brain barrier may hold promise.
These fins were made for walking, and that’s just what these fish do — thanks to wiring that evolved long before vertebrates set foot on land.
Little skates use two footlike fins on their undersides to move along the ocean floor. With an alternating left-right stride powered by muscles flexing and extending, the movement of these fish looks a lot like that of many land-based animals.
Now, genetic tests show why: Little skates and land vertebrates share the same genetic blueprint for development of the nerve cells needed for limb movement, researchers report online February 8 in Cell. This work is the first to look at the origins of the neural circuitry needed for walking, the authors say. “This is fantastically interesting natural history,” says Ted Daeschler, a vertebrate paleontologist at the Academy of Natural Sciences in Philadelphia.
“Neurons essential for us to walk originated in ancient fish species,” says Jeremy Dasen, a neuroscientist at New York University. Based on fossil records, Dasen’s team estimates that the common ancestor of all land vertebrates and skates lived around 420 million years ago — perhaps tens of millions of years before vertebrates moved onto land (SN: 1/14/12, p. 12). Little skates (Leucoraja erinacea) belong to an evolutionarily primitive group. Skates haven’t changed much since their ancestors split from the fish that evolved into land-rovers, so finding the same neural circuitry in skates and land vertebrates was surprising.
The path to discovery started when Dasen and coauthor Heekyung Jung, now at Stanford University, saw YouTube videos of the little skates walking.
“I was completely flabbergasted,” Dasen says. “I knew some species of fish could walk, but I didn’t know about these.”
Most fish swim by undulating their bodies and tails, but little skates have a spine that remains relatively straight. Instead, little skates move by flapping pancake-shaped pectoral fins and walking on “feet,” two fins tucked along the pelvis.
Measurements of the little skates’ movements found that they were “strikingly similar” to bipedal walking, says Jung, who did the work while at NYU. To investigate how that similarity arose, the researchers looked to motor nerve cells, which are responsible for controlling muscles. Each kind of movement requires different kinds of motor nerve cells, Dasen says.
The building of that neural circuitry is controlled in part by Hox genes, which help set the body plan, where limbs and muscles and nerves should go. For instance, snakes and other animals that have lost some Hox genes have bodies that move in the slinky, slithery undulations that many fish use to swim underwater.
By comparing Hox genes in L. erinacea and mice, researchers discovered that both have Hox6/7 and Hox10 genes and that these genes have similar roles in both. Hox6/7 is important for the development of the neural circuitry used to move the skates’ pectoral fins and the mice’s front legs; Hox10 plays the same role for the footlike fins in little skates and hind limbs in mice. Other genes and neural circuitry for motor control were also conserved, or unchanged, between little skates and mice. The findings suggest that both skates and mice share a common ancestor with similar genetics for locomotion.
The takeaway is that “vertebrates are all very similar to each other,” says Daeschler. “Evolution works by tinkering. We’re all using what we inherited — a tinkered version of circuitry that began 400-plus million years ago.”
Orangutan numbers on the Southeast Asian island of Borneo plummeted from 1999 to 2015, more as a result of human hunting than habitat loss, an international research team finds.
Over those 16 years, Borneo’s orangutan population declined by about 148,500 individuals. A majority of those losses occurred in the intact or selectively logged forests where most orangutans live, primatologist Maria Voigt of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and colleagues report February 15 in Current Biology. “Orangutan killing is likely the number one threat to orangutans,” says study coauthor Serge Wich, a biologist and ecologist at Liverpool John Moores University in England. Humans hunt the forest-dwelling apes for food, or to prevent them from raiding crops, the investigators say. People also kill adult orangutans to steal their babies for the international pet trade.
Between 70,000 and roughly 100,000 orangutans currently live on Borneo, Wich says. That’s substantially higher than previous population estimates. The new figures are based on the most extensive survey to date, using ground and air monitoring of orangutans’ tree nests. Orangutans live only on Borneo and the island of Sumatra and are endangered in both places.
Still, smaller orangutan populations in deforested areas of Borneo — due to logging or conversion to farm land — experienced the severest rates of decline, up to a 75 percent drop in one region.
Satellite data indicate that Borneo’s forest area has already declined by about 30 percent from 1973 to 2010. In the next 35 years, Voigt’s team calculates that further habitat destruction alone will lead to the loss of around 45,000 more of these apes. “Add hunting to that and it’s a lethal mix,” Wich says. But small groups of Bornean orangutans living in protected zones and selectively logged areas will likely avoid extinction, the researchers say.
