Hunter-gatherers who built and worshiped at one of the oldest known ritual centers in the world carved up human skulls in a style all their own.
At Turkey’s Göbekli Tepe site — where human activity dates to between around 11,600 and 10,000 years ago — people cut deep grooves in three human skulls and drilled a hole in at least one of them, say archaeologist Julia Gresky of the German Archaeological Institute in Berlin and colleagues. Ancient hunter-gatherers there practiced a previously unknown version of a “skull cult,” in which human skulls were ritually modified after death and then deposited together, Gresky’s team reports online June 28 in Science Advances.
Collections of human skulls modified in other ways have been found at several sites from around the same time. For instance, deliberately broken faces on skulls were unearthed at a Syrian settlement and may represent a form of punishment after death.
Seven excavated skull fragments enabled Gresky’s group to reconstruct the Göbekli Tepe skulls. These skulls of the recently deceased were carved for use in ceremonies to worship them as ancestors, the researchers propose. It’s also possible that the skull incisions marked deceased individuals who had been especially revered or reviled while alive.
A cord inserted through the hole drilled in one skull may have suspended that skull for display. Grooves probably ran from front to back on the skulls and possibly stabilized cords that held decorations of some kind.
Microscopic study of skull pieces from Göbekli Tepe indicates that grooves were cut with stone tools. A lack of healed bone on the edges of incisions suggests skull carving occurred shortly after death.
PORTLAND, Ore. — Petals of wildflowers called starry campions may be a pretty little battleground for a sexual skirmish between the plant’s male and female parts.
As is common in flowers, each Silene stellata bloom forms both male and female sex organs. After measuring petal variation between plants and tracking parenthood of seeds, Juannan Zhou suspected a sexual tug-of-war.
Flowers with greater male success in spreading pollen and siring seeds across a flower patch tended toward longer and narrower petals, Zhou reported June 26 at the Evolution 2017 meeting. Yet flowers that did especially well by their female organs, maturing abundant seeds in their own ovaries, tended toward wider and shorter petals. Zhou, of the University of Maryland in College Park, pieced together the story while working in a fenced-in plot of wild campions at Mountain Lake Biological Station in southwestern Virginia. During two summers, he tracked floral details and collected seeds. He sprouted almost 2,400 seedlings and for each genetically worked out which of 227 fenced-in adults had been the father.
If a conflict smolders between what’s best for male versus female functions, parental blossom trends that went along with greater fatherhood should tilt in the opposite direction from blossom trends linked with greater motherhood. Some traits such as number of fringe tassels showed no signs of conflict, but petal dimensions did.
Zhou suggests that the contrary trends might arise from the sexes’ opposite interests in visits from one of its pollinating moths, the mottled gray-brown Hadena ectypa. These moths do much of the pollen carrying early in midsummer. One mothload of pollen typically fertilizes all the eggs a female has, so from the motherhood perspective, once is enough. More than once means more risk for little benefit, because female moths leave an unwanted gift behind.
Besides sucking nectar, a H. ectypa often sticks her rear into the cup of a flower and with a wiggle, lays an egg or two. When eggs hatch, the tiny caterpillars chew their way into the flower ovary and start feeding on the plant’s own seeds. Caterpillars eventually grow too long and fat to fit inside blooms. Certain petal shapes, Zhou speculates, might be more attractive to moths, or perhaps more discouraging for the fattest, most destructive caterpillars to invade.
From the male point of view, the loss of the home flower’s seeds could be more than recouped by repeated moth visits to pick up more pollen to spread to other flowers. More moths could mean many more offspring. Sexual conflicts show up elsewhere in nature, such as in the compounds that fruit flies use to dope their sperm. After a jolt of these extras, females tend to put more resources into eggs and offspring. Never mind that it shortens a female’s life. Data on sexual conflicts from plants are much rarer, says evolutionary ecologist Locke Rowe of the University of Toronto. He welcomes the starry campion work also because the plants are hermaphrodites, a lifestyle uncommon in conflict studies.
People and pooches may have struck up a lasting friendship after just one try, a new genetic study suggests.
New data from ancient dogs indicates that dogs became distinct from wolves between 20,000 and 40,000 years ago, researchers report July 18 in Nature Communications. Dogs then formed genetically distinct eastern and western groups 17,000 to 24,000 years ago, the researchers calculate. That timing and other genetic data point to dogs being domesticated just once.
That idea contrasts with a hypothesis put forward last year that dogs were domesticated separately in Europe and East Asia, with the Asian dogs eventually replacing the European mutts (SN: 7/9/16, p. 15). Scientists agree that dogs stem from wolves, but where, when and how many times dogs were domesticated — passing down tameness and other traits over generations — has been rethought many times in the last few years (SN: 7/8/17, p. 20).
The new study “puts dog origins into one time and place again. That’s really important,” says Peter Savolainen, an evolutionary geneticist at KTH Royal Institute of Technology in Stockholm who was not involved in either study. These new data indicate “there’s a single origin, and it wasn’t in Europe,” says Savolainen, a proponent of an East Asian origin of dogs.
The new study examined the complete genetic blueprints, or genome, from a 7,000-year-old dog from Herxheim in Germany, and a 4,700-year-old dog from Cherry Tree Cave (also known as Kirshbaumhöle) in Germany. The scientists also analyzed DNA data from a 4,800-year-old dog from Newgrange, Ireland, that had been described in the previous study positing two domestication events. A claim of multiple domestications for dogs requires extraordinary evidence, says study coauthor Krishna Veeramah, an evolutionary geneticist at Stony Brook University in New York. But complete genomes of the ancient dogs suggest a simpler story. “We can explain all of our data just using one domestication event,” Veeramah says. Although Veeramah and colleagues see a split between eastern and western dogs, that split probably happened after domestication took place. Modern European dogs still share heritage with Stone Age canines on the continent, hinting that all the pups came from a common source rather than separately domesticated Asian dogs replacing their European counterparts.
These new data don’t completely rule out multiple domestications (the single event is just the simpler explanation), nor do they indicate where humans and canines became BFFs, Veeramah says. A family tree constructed from the DNA data puts today’s Southeast Asian breeds on the earliest branch, implying an origin in Asia. But a dog breed’s present-day location may not reflect where dogs were actually domesticated more than 20,000 years ago, Veeramah says.
The team that proposed double domestication is not convinced of a single origin. The new study is based on genetic data alone and doesn’t take archaeological evidence into account, says Greger Larson, an evolutionary geneticist at the University of Oxford.
“There’s no smoking gun here, and there’s no direct contradiction,” says Larson. “Our hypothesis of a dual origin remains a possibility, as does a single origin.” Researchers won’t know for sure until they’ve analyzed older dogs from multiple places.
The ancient doggy data also challenge a recently proposed idea that dogs were domesticated when early mongrels developed the ability to digest starch better than wolves could (SN Online: 1/23/13), allowing them to eat grains in early farmers’ trash heaps. A previous study found that today’s dogs have many copies of the AMY2B gene, which produces an enzyme that helps break down starch, while wolves have only two copies.
The new study finds that both ancient German dogs had two copies of AMY2B, while the Newgrange dog had three. Since those dogs lived thousands of years after domestication, the findings suggest the first domesticated dogs were no better equipped to digest starch than wolves were. But the ancient dogs do have other genetic variants that made it possible for the amylase gene to be copied later, Veeramah says. Exactly when that happened isn’t clear.
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.
It’s not every day that a spacecraft gets vaporized by the very planet it sought to explore.
After 13 years studying Saturn and its moons, NASA’s Cassini spacecraft will plunge into the ringed gas giant’s atmosphere. The mission will come to a close at about 7:55 a.m. EDT (4:55 a.m. PDT) Friday, when Saturn’s atmosphere pushes Cassini’s antenna away from Earth, terminating the signal. Shortly thereafter, the spacecraft will disintegrate.
If you want to keep tabs on the action, you’ve got a few options. Science News astronomy writer Lisa Grossman is at the Jet Propulsion Laboratory in Pasadena, Calif. — home of mission control for the Cassini probe. She’ll be popping on to the Science News Facebook page throughout the day Thursday with live updates, and she (@astrolisa) and Science News (@ScienceNews) will have details for you on Twitter as well.
Cassini’s death won’t be captured on film. But thanks to the internet, you can watch NASA scientists react to the probe’s impending doom live. In the early hours of Friday morning (7-8:30 a.m. EDT/4-5:30 a.m. PDT), NASA plans to stream a live video feed from the control room, which you can watch here: And, you can also watch on NASA JPL’s YouTube channel and NASA’s Facebook page.
For more on Cassini’s exploits, check out all of our past coverage of the mission.
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.
