An intergalactic race between light and a bizarre subatomic particle called a neutrino has ended in a draw.
The tie suggests that high-energy neutrinos, which are so lightweight they behave as if they’re massless, adhere to a basic rule of physics: Massless particles travel at the speed of light.
Comparing the arrival times of a neutrino and an associated blaze of high-energy light emitted from a bright, flaring galaxy (SN Online: 7/12/18) showed that the neutrino and light differed in speed by less than a billionth of a percent, physicists report in a paper posted July 13 at arXiv.org. Massless particles — including the particles of light known as photons — consistently move about 300,000 kilometers per second, while massive particles move more slowly. Although neutrinos have mass, their heft is so infinitesimal that high-energy neutrinos travel at a rate effectively indistinguishable from that of light.
Some theories propose that a “spacetime foam” might slow particles of very high energies. The idea is that spacetime on extremely small scales is not smooth, but foamy. As a result, high-energy particles could get bogged down, as if moving through molasses. That effect could cause a significant difference between the speeds of the neutrino and the associated light, which would build up into a delay over the 4-billion-light-year trip from the neutrino’s home galaxy to Earth. But since the flare of light was spotted around the same time as the neutrino, there’s no evidence for such a discrepancy.
The result once again refutes a 2011 claim that neutrinos might travel faster than light. That measurement, made by a particle detector known as OPERA, was eventually determined to have been distorted by a loose cable (SN: 4/7/12, p. 9).
In the final frenzy of reproduction and death, social amoebas secrete proteins that help preserve a starter kit of food for its offspring.
Dictyostelium discoideum, a type of slime mold in soil, eats bacteria. Some wild forms of this species essentially farm the microbes, passing them along in spore cases that give the next generation of amoebas the beginnings of a fine local patch of prey. Tests find that the trick to keeping the parental immune system from killing this starter crop of bacteria is a surge of proteins called lectins, researchers say in the July 27 Science. Lectins create a different way for the amoebas to treat bacteria: as actual symbionts inside cells, instead of as prey or infections, says study coauthor Adam Kuspa, a molecular cell biologist at Baylor College of Medicine in Houston. In a lab test of this ability, coating other bacteria with lectin derived from a plant allowed bacteria to slip inside cells from mice and survive as symbiotic residents.
The findings mark another chapter in a story that has been upending decades of what people thought they knew about social amoebas eating bacteria. The basic, almost alien, scenario is still true: D. discoideum amoebas, nicknamed Dicty, start life as single cells. When food dwindles, cells come together into a much bigger, multicellular slug-shaped creature with eight to 10 types of cells and the power to crawl. It then develops into something more like a fungus with a stalk holding up a case of spores, which start the next generation of amoebas. Those casings, scientists once believed, held only spores. “For 70 years, we all thought that Dictyostelium development was sterile,” meaning no bacteria survived among spores, Kuspa says. “If you were not a very good microbiologist and contaminated your amoeba sample, one way to cure them of bacteria was to put them through a cycle of development.” Then in 2011, researchers discovered that some Dicty strains are “farmers,” routinely packing live bacteria into spore cases, and jump-starting new bacterial livestock with each generation (SN: 2/12/11, p. 11). “That was a shock,” Kuspa says.
Researchers also discovered that the Dicty animal-like slug phase forms an immune system that kills bacteria, even as evidence grew that some bacteria had uses beyond food, such as providing defense chemistry. But how the slug avoided killing its own helpful bacteria was a mystery.
Comparing secretions of Dicty strains carrying bacteria versus strains that don’t showed a “dead-obvious” difference, Kuspa says: more lectins called discoidin A and discoidin C in the carrier forms. A series of tests supplying and withholding the proteins showed big effects on the fates of bacteria. The researchers found that the lectins raise the chances that bacteria can slip inside an amoeba cell and live hidden from immune-system sentinels that purge free-living intruders. That gives the bacteria a chance to end up in the spore case.
Lectins’ powers help make sense of how the startling discovery of bacterial farming fits with the revelation of social amoebas’ bacteria-killing immune systems. “Outstanding” work, says Debra Brock of Washington University in St. Louis, who studies both phenomena. “I love mechanisms.”
A new species of Ebola virus has been discovered in bats in Sierra Leone, the country’s government announced July 26. Researchers looking to identify new viruses before the pathogens spill over into human populations found the new Ebola strain while sampling bats in the northern Bombali district. This is the sixth known species of the virus.
RNA analysis of the virus revealed that it is “definitely related to other Ebola viruses,” says Tracey Goldstein, a pathologist at University of California, Davis, who is with the virus-hunting PREDICT project. “But [it] was quite different.” Goldstein and her colleagues confirmed that the Bombali virus can infect human cells, but they still don’t know whether or not it can cause disease in people. “It has the machinery” to enter a human cell, she says, but that doesn’t mean that it can make people sick.
Some species of Ebola, such as the Reston virus, can cause disease in nonhuman primates but do not sicken humans. Other species of the virus however, like the Zaire virus, have been responsible for widespread epidemics, including a recent outbreak in the Democratic Republic of Congo that killed 33 people (SN Online: 5/18/18) and an earlier one responsible for more than 11,000 deaths across West Africa (SN: 1/24/15, p.12).
“We don’t really know where on the spectrum [the Bombali virus] stands,” Goldstein says. PREDICT and its partners are continuing to study the virus, and are educating people in the Bombali region to stay away from bats. At this point, Goldstein says, “I don’t think people should be alarmed.”
For nearly 60 years, scientists in Siberia have bred silver foxes in an attempt to replay how domestication occurred thousands of years ago. Now, in a first, researchers have compiled the genetic instruction book, or genome, of Vulpes vulpes, the red fox species that includes the silver-coated variant. This long-awaited study of the foxes’ DNA may reveal genetic changes that drove domestication of animals such as cats and dogs, the team reports online August 6 in Nature Ecology & Evolution.
At the Institute of Cytology and Genetics of the Russian Academy of Sciences in Novosibirsk, Russia, researchers bred one group of foxes for ever-tamer behavior, while another group was bred for increasing aggressiveness toward humans (SN: 5/13/17, p. 29). Rif, the male silver fox whose DNA serves as the example, or reference, genome for all members of the species, was the son of an aggressive vixen and a tame male. Geneticist Anna Kukekova of the University of Illinois at Urbana-Champaign and colleagues also conducted less-detailed examinations of 30 foxes’ DNA: 10 foxes each from the tame and aggressive groups and 10 animals from a “conventional” group that hadn’t been bred for either friendliness or aggression. Those genomes are an invaluable resource for researchers studying domestication, behavioral and population genetics and even human disorders such as autism and mental illness, says Ben Sacks, a canid evolutionary geneticist at the University of California, Davis, School of Veterinary Medicine. “It makes all kinds of research possible that weren’t before,” he says. Domestication researchers want to pinpoint the genes that set tame foxes apart from conventionally bred and aggressive foxes because those genes may be the same ones that were altered in dogs and other domesticated animals. Kukekova and colleagues haven’t yet identified the precise genetic changes that led to the foxes’ tameness. But the team did find 103 regions of the genome where tame foxes tend to have one pattern of genetic variants and aggressive foxes are more likely to have a different pattern. Some of the regions contain multiple genes and DNA tweaks. Narrowing the search to precise DNA changes will take more work, but the research is an important first step, says geneticist Elaine Ostrander, chief of the Cancer Genetics and Comparative Genomics Branch at the National Human Genome Research Institute in Bethesda, Md. She likens it to zooming in on a map.
“Before you get to the right house, you have to get to the right street. Before you can get to the right street, you have to get to the right city, state and so on,” she says. “It’s exciting that they’re to the right city at this point. Now they have to find the right addresses.” The list of 103 regions gives researchers clues about where to focus future studies, she says.
Many of the genes in the 103 regions are involved in brain development or function. In particular, the researchers found that a gene called SorCS1 is involved in making friendlier foxes. In people, some versions of the gene have been associated with autism or schizophrenia. Versions of that gene, which encodes a protein involved in transmitting chemical information between brain cells, determined whether foxes wanted to interact with humans “or never wanted to come close or see you again,” Kukekova says. One version of SorCS1 was found in 61 percent of tame foxes, but none of the aggressive foxes. Other genes that differed between tame and aggressive foxes included ones involved in brain-cell signaling with the chemical messenger glutamate (SN Online: 5/15/13). Changes in these genes have also been associated with domestication in dogs, cats and rabbits.
Finding the same tweaked genes in studies of many different domesticated animals gives researchers confidence that they are closing in on the right answer, says evolutionary geneticist Krishna Veeramah of Stony Brook University in New York. But because of its long history and wealth of data, the fox study is the true test, he says. Having the same genes pop up in silver foxes “is incredibly encouraging that they are the real ones involved in domestication.”
Some lizards shed their still-wriggling tails to distract predators, but sea cucumbers take this sort of strategy to the next level. Some startled sea cucumbers shoot a silky — and sticky — substance out of their rear ends that is actually an entire organ.
The tangle of tubules looks like intestines, but it evolved from the invertebrates’ respiratory system, and, like lizard tails, it regenerates after use. In a new study in the April 10 Proceedings of the National Academy of Sciences, researchers delved into the black sea cucumber’s genome to see how the stringlike tubules, called the Cuvierian organ, work at the molecular level. The black sea cucumber (Holothuria leucospilota) is “the most dominant sea cucumber species in the South China Sea,” says Ting Chen, a biologist at the South China Sea Institute of Oceanology in Guangzhou. “We would like to know what evolutionary advantage this sea cucumber has gained … so that its population can expand so widely and predominantly.” So the team analyzed the sea cucumber’s entire genome, or genetic instruction book, and focused on genes from the Cuvierian organ because it’s such an odd structure. Then the team predicted what proteins would be made from Cuvierian organ genes using a program called AlphaFold (SN: 9/23/22). Some unexpected predicted proteins were new types of receptors on cells’ surfaces that may play a role in expelling the organ.
The team also found that the “silk” proteins of sea cucumbers’ tubules don’t contain the same sequences of amino acids seen in spider silk, but are similarly made up of long repeated chains of amino acids. This finding hints that these long repeats might be a shared structure across silklike proteins, even when those proteins evolved independently.
What’s more, Chen says, is that the organ’s stickiness — which stops sea cucumber predators like fish, crabs and starfish in their tracks — comes from proteins that have features similar to amyloids. Amyloids are associated with many diseases in humans, including neurodegenerative conditions like Alzheimer’s (SN: 9/9/15).
This paper not only highlights unexpected proteins that are specific to the Cuvierian tubules, says Patrick Flammang, a biologist at the University of Mons in Belgium who was not involved with the study. It also provides a lot of data that can be used to answer other questions about how the enigmatic organ evolved, he says.
And the usefulness of a high-quality genome doesn’t stop there. “We need genomic data for our studies on the reproductive, endocrine, immune and digestive systems of H. leucospilota,” Chen says. The team, he says, is now investigating the genetics behind how the sea cucumbers detect light and digest food.
A good genome, Flammang says, is “a cornerstone to be able to do this work.”
To understand the human brain, take note of the rare, the strange and the downright spooky. That’s the premise of two new books, Unthinkable by science writer Helen Thomson and The Disordered Mind by neuroscientist Eric R. Kandel.
Both books describe people with minds that don’t work the same way as everyone else’s. These are people who are convinced that they are dead, for instance; people whose mental illnesses lead to incredible art; people whose memories have been stolen by dementia; people who don’t forget anything. By scrutinizing these cases, the stories offer extreme examples of how the brain creates our realities. In the tradition of the late neurologist Oliver Sacks (SN: 10/14/17, p. 28), Thomson explores the experiences of nine people with unusual minds. She travels around the world to interview her subjects with compassion and curiosity. In England, she meets a man who, following a bathtub electrocution, became convinced that he was dead. (Every so often, he still feels “a little bit dead,” he tells Thomson.) In Los Angeles, she spends time with a 64-year-old man who can remember almost every day of his life in extreme detail. And in a frightening encounter in a hospital in the United Arab Emirates, she interviews a man with schizophrenia who transmogrifies into a growling tiger. By visiting them in their element, Thomson presents these people not as parlor tricks, but as fully rendered human beings. Kandel chooses the brain disorders themselves as his subjects. He explains the current neuroscientific understanding of autism, depression and schizophrenia, for example, by weaving together the history of the research and human examples. His chapter on dementia and memory is particularly compelling, given his own Nobel Prize–winning role in revealing how brains form memories (SN: 10/14/00, p. 247).
With diagrams of key brain regions, Alzheimer’s plaques and even chromosomes, Kandel’s book reads in some ways as a primer on the basic tenets of biology and neuroscience. Also included are stories of people, such as a woman who describes her bipolar illness in stark terms: “Feelings of ease, intensity, power, well-being, financial omnipotence and euphoria pervade one’s marrow.” But then, she says, everything changes. “You are irritable, angry, frightened, uncontrollable and enmeshed totally in the blackest caves of the mind. You never knew those caves were there. It will never end, for madness carves its own reality.”
Though these cases seem extreme, Thomson and Kandel relate unusual brains to more common forms of thinking. Observing huge emotional swings that come with bipolar disorder can help inform scientists about more mundane changes in our happiness or sorrow. Figuring out why a person thinks he’s dead could reveal how we more generally create our sense of self. Understanding why someone might remember everything, or nothing, could help us understand how memories physically change the brain (SN: 2/3/18, p. 22).
By connecting these strange brains to everyday mental processes, both books make clear how much we all have in common, and more than that, how all our brains are a little bit unusual.
A microRNA called miR-30c-5p contributes to nerve pain in rats and people, a new study finds. A different microRNA, miR-711, interacts with a well-known itch-inducing protein to cause itching, a second study concludes. Together, the research highlights the important role that the small pieces of genetic material can play in nerve cell function, and may help researchers understand the causes of chronic nerve pain and itch. MicroRNAs help regulate gene activity and protein production. The small molecules play a big role in controlling cancer (SN: 8/28/10, p. 18) and other aspects of health and disease (SN: 2/20/16, p. 18). Usually, microRNAs work by pairing up with bigger pieces of RNA called messenger RNAs, or mRNA. Messenger RNAs contain copies of genetic instructions that are read by cellular machinery to build proteins. When microRNAs glom onto the messengers, the mRNA can be degraded or the microRNAs can prevent the protein-building machinery from reading the instructions. Either way, the result is typically to dial down production of certain proteins.
In the case of nerve pain, miR-30c-5p limits production of an important protein called TGF-beta that’s involved in controlling pain, María Hurlé, a pharmacologist at the University of Cantabria in Santander, Spain, and colleagues report August 8 in Science Translational Medicine. The researchers discovered the link in experiments with mice, rats and people.
In the rat experiments, researchers cut the sciatic nerve in the thigh, making the rodents more sensitive to pain caused by heat or cold. These rats had more miR-30c-5p in their blood and cerebral spinal fluid than uninjured rats did, Hurlé and colleagues found. And the amount of the microRNA in the rats’ blood correlated with their pain sensitivity. People with nerve pain caused by a lack of blood flow to a limb also had elevated levels of the microRNA in their blood and spinal fluid. Hurlé’s group confirmed that the microRNA was causing pain by injecting uninjured rats with miR-30c-5p or an imposter microRNA. Those rats that got the imposter injected into their brains had normal pain sensitivity, but rodents shot up with miR-30c-5p became sensitive to cold pain. Researchers also blocked miR-30c-5p by using another piece of RNA that would latch onto it and prevent it from interacting with the mRNA for TGF-beta. Pain-sensitive rats that got the blocker RNA recovered normal pain responses. “This was a spectacular result,” Hurlé says. But the finding doesn’t mean that doctors can treat nerve pain by blocking the microRNA in people, she says. Both the microRNA and TGF-beta do too many other important jobs throughout the body to mess with them. The research, however, does suggest that the level of miR-30c-5p in people’s blood and spinal fluid might be a good indicator of nerve pain.
Having a nerve pain indicator would be useful, says Marzia Malcangio, a neuropharmacologist at King’s College London who was not involved in either study. Pain doctors don’t know of any biological molecules that can distinguish nerve pain from pain caused by inflammation or other causes, Malcangio says. Making that distinction is important because different types of pain are treated differently.
A different microRNA, miR-711, seems to be the culprit causing chronic itching in people with lymphoma, neurobiologist and pain researcher Ru-Rong Ji and colleagues report in the Aug. 8 Neuron.
Cancerous immune cells called T-cells secrete miR-711, the team showed in experiments with mice. And giving mice the microRNA by itself made the rodents scratch. Surprisingly, the researchers found, the microRNA gloms onto a well-known pain and itch sensing protein called TRPA1 outside of a cell, instead of binding to an mRNA inside a cell like other microRNAs.
That finding may be a big advance in understanding how itch works, Malcangio says. Chemicals that trigger TRPA1 from inside a nerve cell open a floodgate that allows calcium to pour in and launch a pain signal. Tickling TRPA1 with the microRNA on the outside of the cell causes just a trickle of calcium into the nerve, producing itch instead of pain, Ji, of Duke University School of Medicine, and colleagues propose.
The team designed a peptide (a small protein or portion of a protein) that could block miR-711 from binding to TRPA1. Itchy mice that got the blocking peptide scratched about half as often as mice that got miR-711 injections alone.
Ji thinks the blocking peptide may be able to reduce itch in lymphoma patients, but the team needs to do more research before giving it to people. About a third of Hodgkin’s lymphoma patients and 15 percent of people with non-Hodgkin’s lymphoma have severe itching. The researchers are also investigating whether the microRNA is involved in other types of itchy conditions, such as eczema.
Landing sites on the asteroid Ryugu for the Hayabusa2 spacecraft and its hitchhiking landers have been picked out, scientists with Japan’s Aerospace Exploration Agency announced in a news conference on August 23.
Hayabusa2 arrived at the 1,000-meter-wide asteroid on June 27, and has been scanning the surface since. More than 100 mission team members met on August 17 to choose the first spots for the spacecraft to land.
The team decided that the two landers, called MINERVA-II and MASCOT, will touch down on the diamond-shaped asteroid’s surface first. MINERVA-II, which carries small hopping rovers equipped with cameras and other instruments, will land at a spot near Ryugu’s north pole on September 21. MASCOT, a tumbling rover, will land closer to the south pole on October 4. The craft will roam the landscape making measurements of the asteroid’s composition, temperature and magnetic properties. The main body of Hayabusa2 will join them in late October, touching down at a point near the asteroid’s equator and gathering a sample of dust there.
The mission team looked for regions 100 meters in diameter that were relatively flat, with slopes less than 30 degrees and with few boulders. Ryugu turned out to be strewn with more boulders than expected based on the first Hayabusa mission, which brought back bits of a smoother asteroid called Itokawa.
But the observations from orbit suggest Ryugu’s surface is well-mixed, meaning that no matter where Hayabusa2 lands, it has a good chance of picking up something interesting. The spacecraft will collect samples from two other, still unknown sites over the next 15 months before returning the samples to Earth in 2020.
A firefly’s blinking behind is more than just a pretty summer sight.
It’s known that fireflies flash to attract mates (SN Online: 8/12/15) — but the twinkles may serve another purpose as well. Jesse Barber, a biologist at Boise State University, had a hunch that the lights also warn off potential nighttime predators. He wasn’t the first person with this hypothesis. As far back as 1882, entomologist G.H. Bowles wrote of fireflies: “May not the light then serve … as a warning of their offensiveness to creatures that would devour them?” But the theory hadn’t been tested, until now. “We always assumed that bats don’t use vision for much,” Barber says. Many species of fireflies are “chemically protected,” meaning they taste awful to predators, Barber says. Yet if an insect doesn’t offer a warning of its bad taste, it may get sampled anyway. Barber noticed that, unlike moths, which signal their toxicity to bats with noises, fireflies don’t make a peep (SN Online: 7/3/13). He wondered if lightning bugs were warning bats of their disgusting taste with their blinking lights. Barber and colleagues wanted to see if it took bats longer to learn to avoid fireflies when the flashings were masked. The team began by introducing fireflies to three bats that had never encountered the bugs before. The bats learned to avoid the bright creatures “after just a few interactions,” Barber says. Those early exchanges went something like: catch, taste, drop. Soon, the bats avoided the fireflies completely. Next came the tricky part: The team needed flying fireflies that wouldn’t blink. Painstakingly, the researchers secured each firefly with a minuscule paper belt under a microscope, and, with a tiny brush, applied two coats of black paint to the flashing back end. Each bug rump — they painted dozens — took about 45 minutes to cover. That’s one of the reasons the experiment took three years, Barber jokes. But the work paid off: When the researchers exposed a new set of bats to the darkened fireflies, the bats took about twice as long to learn that the bugs had an awful taste.
Those bats that eventually learned to avoid the dark fireflies may have sensed the insects’ distinctive straight-line flight pattern via echolocation, the researchers hypothesize. Bats may avoid fireflies through a combination of senses, echolocation to sense the insects’ flight patterns and vision to glimpse those double-duty flashers.
The sleepy sun turns out to be a factory of extremely energetic light.
Scientists have discovered that the sun puts out more of this light, called high-energy gamma rays, overall than predicted. But what’s really weird is that the rays with the highest energies appear when the star is supposed to be at its most sluggish, researchers report in an upcoming study in Physical Review Letters. The research is the first to examine these gamma rays over most of the solar cycle, a roughly 11-year period of waxing and waning solar activity. That newfound oddity is probably connected to the activity of the sun’s magnetic fields, the researchers say, and could lead to new insights about the mysterious environment.
“The almost certain thing that’s going on here is the magnetic fields are much more powerful, much more variable, and much more weirdly shaped than we expect,” says astrophysicist John Beacom of the Ohio State University in Columbus. The sun’s high-energy gamma rays aren’t produced directly by the star. Instead, the light is triggered by cosmic rays — protons that zip through space with some of the highest energies known in nature — that smack into solar protons and produce high-energy gamma rays in the process ( SN: 10/14/27, p. 7 ) . All of those gamma rays would get lost inside the sun, if not for magnetic fields. Magnetic fields are known to take charged particles like cosmic rays and spin them around like a house in a tornado. Theorists have predicted that cosmic rays whose paths have been scrambled by the tangled mass of magnetic fields at the solar surface should send high-energy gamma rays shooting back out of the sun, where astronomers can see them.
Beacom and colleagues, led by astrophysicist Tim Linden of Ohio State, sifted through data from NASA’s Fermi Gamma-ray Space Telescope from August 2008 to November 2017. The observations spanned a period of low solar activity in 2008 and 2009, a period of higher activity in 2013 and a decline in activity to the minimum of the next cycle, which started in 2018 (SN: 11/2/13, p. 22). The team tracked the number of solar gamma rays emitted per second, as well as their energies and where on the sun they came from.
There were more high-energy gamma rays, above 50 billion electron volts, or GeV, than anyone predicted, the team reports. Weirder still, rays with energies above 100 GeV appeared only during the solar minimum, when the sun’s activity level was low. One photon emitted during the solar minimum had an energy as high as 467.7 GeV.
Strangest of all, the sun seems to emit gamma rays from different parts of its surface at different times in its cycle. Because cosmic rays that hit the sun come in from all directions, you would expect the entire sun to light up in gamma rays uniformly. But Beacom’s team found that during the solar minimum, gamma rays came mainly from near the equator, and during the solar maximum, when the sun’s activity level was high, they clustered near the poles.
“All of these things are way more weird than anyone had predicted,” Beacom says. “And that means the magnetic fields must be way more weird than anyone had thought.” Beacom and colleagues tried to connect the excess gamma rays to other solar behaviors that change with magnetic activity, like solar flares or sunspots (SN: 9/30/17, p. 6). “So far nothing has really held up to any sort of scrutiny,” says astrophysicist Annika Peter, also at Ohio State.
High-energy gamma rays may offer a new way to probe the magnetic fields in the uppermost layer of the solar surface, called the photosphere. “You can’t see [the fields] with a telescope,” Beacom says. “But these [cosmic rays] are journeying there, and the gamma rays they send back are messengers of the terrible conditions there.”
More observations are coming soon. NASA’s Parker Solar Probe, which launched on August 12, will take the first direct measurements of the magnetic field in the sun’s outer atmosphere, or corona (SN: 7/21/18, p. 12). And as the sun enters the next solar minimum, the highest-energy gamma rays are starting to return. In February, Fermi caught its first gamma ray with an energy above 100 GeV since 2009.
“There really is something strange afoot,” says solar physicist Craig DeForest of the Southwest Research Institute, who is based in Boulder, Colo., and was not involved in the work. “When there’s some new discovery, scientists don’t shout ‘Eureka!’ They go, ‘Hm, that’s funny. That can’t be right.’ This is a classic case of that.”
