Quake risk in parts of central U.S. as high as in fault-filled California

Northern Oklahoma is just as susceptible to a damaging earthquake within the next year as the most quake-prone areas of California. That’s because earthquakes are no longer just a natural hazard, the U.S. Geological Survey says. In its new quake hazards forecast released March 28, the agency for the first time has included artificially triggered seismicity.

An increased risk in the central United States largely stems from sites where fluids, such as wastewater from fracking, are injected underground (SN: 8/9/14, p. 13). Rising fluid pressure underground can unclamp faults and unleash earthquakes (SN: 7/11/15, p. 10). From 1973 to 2008, an average of 24 potentially damaging quakes rattled the central United States each year. From 2009 to 2015, an uptick in fracking activity helped skyrocket that number to 318 annual quakes on average, with a record-setting 1,010 tremors in 2015 alone. Around 7 million people currently live and work in central and eastern U.S. areas vulnerable to shakes stemming from earthquakes roughly above magnitude 2.7, USGS scientists estimate.

Human-caused quakes aren’t as powerful as their natural counterparts (the strongest induced quake in the United States clocked in at magnitude 5.6 in 2011 compared with the magnitude 7.8 San Francisco temblor in 1906, for instance). But the potential for more powerful shakes exists, the scientists warn. The new hazard assessment should help regulators revise building codes to better prepare for the rising risk.

EPA underestimates methane emissions

The U.S. Environmental Protection Agency has a methane problem — and that could misinform the country’s carbon-cutting plans. Recent studies suggest that the agency’s reports fail to capture the full scope of U.S. methane emissions, including “super emitters” that contribute a disproportionate share of methane release. Those EPA reports influence the country’s actions to combat climate change and the regulation of methane-producing industries such as agriculture and natural gas production.

With EPA’s next annual methane report due to be published by April 15, early signs suggest that the agency is taking steps to fix the methane mismatch. A preliminary draft of the report revises the agency’s methane calculations for 2013 — the most recent year reported — upward by about 27 percent for the natural gas and petroleum sectors, a difference of about 2 million metric tons.
Yet it’s unclear how that and other revisions will factor into final methane emission totals in the upcoming report. The draft estimates that U.S. methane emissions from all sources in 2014 were about 28 million metric tons, up slightly from the revised estimate for 2013 and well above the original 2013 estimate of 25.453 million metric tons. But the totals in the draft don’t include updates to emission estimates from the oil and gas industry.
“EPA is reviewing the substantial body of new studies that have become available in the past year on the natural gas and petroleum sector,” says EPA spokesperson Enesta Jones. The agency is also gathering feedback from scientists and industry experts to further improve their reporting.

Methane, which makes up the bulk of natural gas, originates from natural sources, such as wetlands, as well as from human activities such as landfills, cattle ranches (SN: 11/28/15, p. 22) and the oil and gas industry. Globally, human activities release about 60 percent of the 600 million metric tons of methane emitted into the atmosphere each year. Once in the air, methane prevents some of Earth’s heat from escaping into space, causing a warming effect. Methane emissions currently account for about a quarter of human-caused global warming.

The EPA’s underestimation of U.S. methane emissions comes down to accounting. EPA samples emissions from known methane sources, such as cows or natural gas pipelines, and works out an average. That average is then multiplied by the nation’s number of cows, lengths of pipe and other methane sources. Results from this method disagree with satellite and land-based observations that measure changes in the total amount of methane in the air. A 2013 report in the Proceedings of the National Academy of Sciences found that U.S. methane emissions based on atmospheric measurements are about 50 percent larger than EPA estimates (SN Online: 11/25/13).
EPA’s reports don’t just misjudge the scale of emissions, they also miss the long-term trend, recent work suggests. EPA reported that U.S. methane emissions remained largely unchanged from 2002 to 2014. But researchers report online March 2 in Geophysical Research Letters that emissions of the greenhouse gas rose more than 30 percent over that period. The United States could be responsible for as much as 30 to 60 percent of the global increase in methane emissions over the last decade, the study’s authors conclude. “We’re definitely not a small piece of that pie,” says Harvard University atmospheric scientist Alex Turner, who coauthored the study.
Correctly tracking methane is important, Turner says, because over a 100-year period, the warming impact of methane is more than 25 times that of the same amount of CO2. Methane levels have also risen faster: Since the start of the industrial revolution, methane concentrations have more than doubled while CO2 has risen more than 40 percent.

While methane is more potent than CO2, there is about 200 times less methane in the atmosphere than CO2. Furthermore, methane stays in the atmosphere for only around 12 years before being absorbed by soil or breaking apart in chemical reactions. “If we reduce methane emissions, the climate responds very quickly and global warming would slow down almost immediately,” says Cornell University earth systems scientist Robert Howarth. “CO2, on the other hand, has an influence that will go hundreds to even thousands of years into the future.”

Turner and colleagues tracked methane across the continental United States using land stations that measure methane in the air and satellite observations that record dips in the infrared radiation frequencies absorbed and reemitted by methane. The researchers compared these methane measurements with those taken over Bermuda and the North Pacific Ocean — places upwind of the United States and far from major methane sources.

From 2002 through 2014, methane concentrations over the continental United States grew faster than those over the oceans, the researchers found. The difference was most pronounced over the central United States, where methane concentrations rose nearly twice as fast as in the rest of the country. Natural gas drilling and production boomed in in the central United States during the period studied, though the researchers could not precisely trace the source of the additional methane.

Turner and colleagues say they’re now working with EPA to reconcile the methane estimates. EPA will provide small-scale estimates of methane emissions down to a 10-kilometer-wide grid. By combining that grid with space and land observations, scientists should be able to isolate where methane mismatches are the most pronounced.

While Turner’s research can’t pinpoint the exact origins of the additional methane, other studies point to the oil and gas industry. The numbers that the EPA uses to tabulate methane emissions assume that equipment is functioning as intended, says Stanford University sustainability engineer Adam Brandt. Malfunctioning equipment can spew huge amounts of methane. That became abundantly – and visibly – clear last October when the largest U.S. methane leak in history began in an underground storage facility near Los Angeles. The leak released 97,100 metric tons of methane, equivalent to the annual greenhouse gas emissions of 572,000 cars, before being permanently sealed in February, researchers estimated in the March 18 Science.

Super methane emitters are a big problem elsewhere, too, albeit typically much smaller than the California leak, researchers report in the June 2016 Environmental Pollution. Surveying emissions from 100 natural gas leaks around Boston, the researchers found that 7 percent of leaks contributed half of the total methane released. In 2014, a different research team reported in Environmental Science & Technology that 19 percent of pneumatic controllers used at natural gas production sites accounted for 95 percent of all controller emissions.

Monitoring and quick repairs can stamp out rogue methane sources quickly, Brandt says. “This is a problem that’s easier to fix than it is to understand,” he says.

‘A Most Improbable Journey’ offers scientific take on human history

Most people do not marvel much at sand. We may enjoy how it feels under our bare feet, or get annoyed when someone tracks it into the house. But few of us see those quartz grains the way geologist Walter Alvarez does — as the product of 4.5 billion years of improbable cosmic and geologic events that defined the course of human history.

Sandy beaches exist because silicon — a relatively rare element in the solar system — happened to become concentrated on Earth during the solar system’s early days, Alvarez, of the University of California, Berkeley, writes in A Most Improbable Journey. While powerful solar particles swept lighter, gaseous elements toward the outer planets, more massive, mineral-forming elements such as silicon, magnesium and iron were left behind for Earth. Later on, in the molten crucibles between Earth’s colliding tectonic plates, these elements formed the raw materials for pivotal human inventions, including stone tools, glass and computer chips.
The 4.5 billion years of history that led to a computer chip is just one of many stories of scientific happenstance that Alvarez presents. Best known for proposing that an asteroid impact killed off the dinosaurs, Alvarez argues that rare, unpredictable cosmic, geologic and biological events — what he calls “contingencies” — are key to understanding the human condition.

Fans of Bill Bryson’s A Short History of Nearly Everything will appreciate Alvarez’s enthusiastic, clearly written tour of contingencies that have shaped our world, starting with the origins of life on Earth. No matter how distant the event, Alvarez quickly zeroes in on its eventual impact on people: For instance, the formation of oceanic crust helped expose rich deposits of copper ore on Cyprus, later an epicenter of the Bronze Age. A catastrophic Ice Age flood formed the English Channel in which the Spanish Armada would later sink. And ancient rivers in North America smoothed the terrain of the westward trail for American pioneers in covered wagons.

Not all of Alvarez’s arguments are convincing — his claim in the final chapter that every individual is a “contingency” in his or her own right, given how many other people could have been born instead, feels more flattering than important. Still, it’s hard to argue with his observation that impulsive human actions can transform the planet just as much as earthquakes, asteroids and other difficult-to-predict, occasionally world-changing phenomena.

Critics of this macro view, described in academia as “Big History,” say that the approach sacrifices important nuance and detail. At roughly 200 pages of text, however, A Most Improbable Journey does not claim to be a comprehensive account of history or a replacement for more detailed, focused examinations of the past. Instead, it makes a compelling case for Big History as a fun, perspective-stretching exercise — a way to dust off familiar topics and make them sparkle.

Ricin poisoning may one day be treatable with new antidote

WASHINGTON — It has been used by an assassin wielding a poisoned umbrella and sent in a suspicious letter to a president.

Ricin, the potent toxin and bioterrorism agent, has no antidote and can cause death within days. But a cocktail of antibodies could one day offer victims at least a slim window for treatment.

A new study presented February 7 at the American Society for Microbiology’s Biothreats meeting reveals a ricin antidote that, in mice, works even days after exposure to the toxin. Another presented study offers a potential explanation for how such an antidote might work.
Doctors need some way to deal with ricin poisoning, said Patrick Cherubin, a cell biologist at the University of Central Florida in Orlando. Immunologist Nicholas Mantis agreed: “There is no specific treatment or therapy whatsoever.”

Though ricin has an innocuous origin (it’s found in castor beans), the poison is anything but harmless. It’s dangerous and relatively easy to spread — rated by the U.S. Centers for Disease Control and Prevention as a category B bioterrorism agent, just behind the highest-risk category A agents such as anthrax, plague and Ebola.

Ricin poisoning is rare but has featured in some high-profile cases. In 1978, Bulgarian writer Georgi Markov was hit in the thigh with a ricin-poisoned pellet shot from an umbrella gun. A few days later, he was dead. In 2013, a letter addressed to President Barack Obama tested positive for granules of the deadly toxin. A Texas woman had ordered castor bean seeds and lye online, for a do-it-yourself approach to making ricin. No one was injured.

Symptoms of ricin poisoning depend on how the toxin enters the body, and how much gets in. Inhaling ricin can make breathing so difficult the skin turns blue. Ingesting ricin can cause diarrhea, vomiting and seizures. Death can come as soon as 36 hours after exposure.

Ricin is known as an RIP — a scary-sounding acronym that stands for ribosome-inactivating protein, said Mantis, of the New York State Department of Health in Albany. In the cell, ribosomes serve as tiny protein factories. After ricin exposure, “the whole machinery comes to a screeching halt,” Mantis said. For cells, shutting down protein factories for too long is a death sentence.
Scientists have developed two vaccines for ricin, though neither is available yet for use in humans. A vaccine may be “good for soldiers going into the field,” said biochemist Ohad Mazor of the Israel Institute for Biological Research in Ness Ziona. But unvaccinated people are out of luck.
Mazor and colleagues developed a new treatment that could potentially help. The treatment is a mixture of three proteins called neutralizing antibodies; they grab onto ricin and don’t easily let go. With antibodies hanging onto its back, ricin has trouble slipping into cells and wreaking its usual havoc.
Even 48 hours after inhaling ricin, roughly 73 percent of mice, 22 out of 30, treated with the antibodies survived, the team reported at the meeting and in a paper published in the March 1 Toxicon. Untreated mice died within a week.

Previous antibody treatments for ricin work well only if mice are treated within hours after exposure, Mazor said. For poisoned humans, that may not be long enough to diagnose the problem. Mazor doesn’t know how his antibodies might work in people, but he’d like to follow up his mouse work with studies in monkeys or pigs.

Scientists haven’t figured out exactly how antibodies help animals recover, but another study presented at the meeting offers a clue. Cherubin and colleagues added ricin to monkey cells in a dish, and then tracked how much protein was manufactured by the cells.

At high enough levels, ricin exposure shuttered the factories as expected. But when researchers stopped exposing cells to the toxin, protein synthesis started up again and cells recovered. “You need ongoing toxin delivery to eventually kill the cell,” Cherubin said. It’s possible that antibody treatments could cut off ricin delivery to cells, letting them bounce back from poisoning, said study coauthor Ken Teter, also a cell biologist at the University of Central Florida.

Selfish genes hide for decades in plain sight of worm geneticists

A strain of wild Hawaiian worms has helped unmask long-studied genes as just plain selfish. The scammers beat the usual odds of inheritance and spread extra fast by making mother worms poison some of their offspring.

Biologists have for decades discussed how two genes in the familiar lab nematode Caenorhabditis elegans might help embryos build their organs. Working with a little-studied wild strain, however, caused a rethink of the genes’ supposedly beneficial role “that flipped it on its head,” says UCLA geneticist Leonid Kruglyak.
Instead of doing some body sculpting, the gene sup-35 doses the eggs with a toxin that will kill them after fertilization, two postdocs in the Kruglyak lab discovered. The toxin gene doesn’t poison itself out of the gene pool because it’s linked to a partner, pha-1, that lets embryos manufacture an antidote. Embryos die unless they inherit a copy of the antidote gene in either egg or sperm, and so the poison-antidote duo can spread unusually fast through populations.

Making a mom on occasion poison some of her offspring doesn’t benefit her but certainly helps the genes. Thus the long-known sup-35 and pha-1 form what’s called a selfish genetic element, Kruglyak’s team proposes May 11 in Science.

That analysis is “very clearly accurate,” says evolutionary geneticist Jack Werren of the University of Rochester in New York. The idea that a gene could behave selfishly, promoting its own spread regardless of its host’s interests, was once controversial (SN: 3/19/16, p. 12). But as molecular biology techniques have improved, researchers have found more and more examples. Many of the most dramatic forms of selfishness, the murderous cheats, come from bacteria, so Werren welcomes the C. elegans scam as a rare case discovered in animals.
Kruglyak’s lab has described an earlier example in C. elegans: a gene that doses sperm with a toxin that kills embryos unless an antidote gene rescues them. Finding a second selfish element in the nematode, he says, suggests that these may not be as rare in animals as people have thought.
The big community of researchers regularly studying C. elegans had missed discovering the selfish role for a simple reason: The main lab strain of nematodes carries the selfish element, explains study coauthor Eyal Ben-David. Whenever the standard strain mates or self-fertilizes (the species has both males and hermaphrodites), all the offspring inherit sup-35 and pha-1. Researchers see no weird die-offs.

In the Kruglyak lab, however, Ben-David and fellow postdoc Alejandro Burga were doing a project that required crossing the usual lab nematodes with the DL238 strain from Hawaii. In its natural state, this strain has somehow escaped invasion by the selfish sup-35/pha-1 pair.

A series of oddities in interbreeding the disparate strains pushed the researchers to reconsider the two genes. For instance, much higher percentages of offspring died in mixed-parent crosses than the routine few percent in same-strain pairings. And when Ben-David and Burga looked at the genes in the Hawaiian strain isolated from the wild, sup-35 and pha-1 just weren’t there.

That was a shock. Earlier experiments in the lab strain had shown that disabling pha-1 caused death in offspring — which it certainly does. The feeding tube of the dying embryos was not forming properly, so researchers at first speculated that the gene controlled tube development. Later work suggested a more nuanced role for it, Ben-David says, but the overall hypothesis remained that the genes helped regulate embryo development. The Hawaiian strain changed that thinking: “How is this wild isolate alive and happy without a gene that’s supposed to be essential for development?” Kruglyak wanted to know.

A better way of interpreting the old experiments, he and his colleagues suggest, is that the embryos died because pha-1 wasn’t providing the antidote to the sup-35 toxin. “No one had previously considered the possibility,” says David S. Fay of the University of Wyoming in Laramie, who has done much of the work exploring the role of these genes. “All the data, including a lot of our previous published and unpublished findings, seem to fit the [selfish gene] model perfectly,” he says. And perhaps the highest praise: “I wish we had somehow come up with the solution ourselves.”

A baby ichthyosaur’s last meal revealed

As far as last meals go, squid isn’t a bad choice. Cephalopod remains appear to dominate the stomach contents of a newly analyzed ichthyosaur fossil from nearly 200 million years ago.

The ancient marine reptiles once roamed Jurassic seas and commonly pop up in England’s fossil-rich coast near Lyme Regis. But a lot of ichthyosaur museum specimens lack records of where they came from, making their age difficult to place.

Dean Lomax of the University of Manchester and his colleagues reexamined one such fossil. Based on its skull, they identified the creature as a newborn Ichthyosaurus communis. Microfossils of shrimp and amoeba species around the ichthyosaur put the specimen at 199 million to 196 million years old, the researchers estimate.

Tiny hook structures stand out in the newborn’s ribs — most likely the remnants of prehistoric black squid arms. Another baby ichthyosaur fossil that lived more recently had a stomach full of fish scales. So the new find suggests a shift in the menu for young ichthyosaurs at some point in their evolutionary history, the researchers write October 3 in Historical Biology.

A bacteria-virus arms race could lead to a new way to treat shigellosis

When some bacteria manage to escape being killed by a virus, the microbes end up hamstringing themselves. And that could be useful in the fight to treat infections.

The bacterium Shigella flexneri — one cause of the infectious disease shigellosis — can spread within cells that line the gut by propelling itself through the cells’ barriers. That causes tissue damage that can lead to symptoms like bloody diarrhea. But when S. flexneri in lab dishes evolved to elude a type of bacteria-killing virus, the bacteria couldn’t spread cell to cell anymore, making it less virulent, researchers report November 17 in Applied and Environmental Microbiology.

The research is a hopeful sign for what’s known as phage therapy (SN: 11/20/02). With antibiotic-resistant microbes on the rise, some researchers see viruses that infect and kill only bacteria, known as bacteriophages or just phages, as a potential option to treat antibiotic-resistant infections (SN: 11/13/19). With phage therapy, infected people are given doses of a particular phage, which kill off the problematic bacteria. The problem, though, is that over time those bacteria can evolve to be resistant against the phage, too.

“We’re kind of expecting phage therapy to fail, in a sense,” says Paul Turner, an evolutionary biologist and virologist at Yale University. “Bacteria are very good at evolving resistance to phages.”
But that doesn’t mean the bacteria emerge unscathed. Some phages attack and enter bacteria by latching onto bacterial proteins crucial for a microbe’s function. If phage therapy treatments relied on such a virus, that could push the bacteria to evolve in such a way that not only helps them escape the virus but also impairs their abilities and makes them less deadly. People infected with these altered bacteria might have less severe symptoms or may not show symptoms at all.

Previous studies with the bacteria Pseudomonas aeruginosa, for instance, have found that phage and bacteria can engage in evolutionary battles that drive the bacteria to be more sensitive to antibiotics. The new study hints that researchers could leverage the arms race between S. flexneri and the newly identified phage, which was dubbed A1-1 after being found in Mexican wastewater, to treat shigellosis.

S. flexneri in contaminated water is a huge problem in parts of the world where clean water isn’t always available, such as sub-Saharan Africa and southern Asia, says Kaitlyn Kortright, a microbiologist also at Yale University. Every year, approximately 1.3 million people die from shigellosis, which is caused by four Shigella species. More than half of those deaths are in children younger than 5 years old. What’s more, antibiotics to treat shigellosis can be expensive and hard to access in those places. And S. flexneri is becoming resistant to many antibiotics. Phage therapy could be a cheaper, more accessible option to treat the infection.

The blow to S. flexneri’s cellular spread comes because to enter cells, A1-1 targets a protein called OmpA, which is crucial for the bacteria to rupture host cell membranes. The researchers found two types of mutations that made S. flexneri resistant to A1-1. Some bacteria had mutations in the gene that produces OmpA, damaging the protein’s ability to help the microbes spread from cell to cell. Others had changes to a structural component of bacterial cells called lipopolysaccharide.

The mutations in lipopolysaccharide were surprising, Kortright says, because the relationship between that structural component and OmpA isn’t fully worked out. One possibility is that those mutations distort OmpA’s structure in a way that the phage no longer recognizes it and can’t enter bacterial cells.

One lingering question is whether S. flexneri evolves in the same way outside a lab dish, says Saima Aslam, an infectious diseases physician at the University of California, San Diego who was not involved in the work. Still, the findings show that it’s “not always a bad thing” when bacteria become phage-resistant, she says.

How sleep may boost creativity

The twilight time between fully awake and sound asleep may be packed with creative potential.

People who recently drifted off into a light sleep later had problem-solving power, scientists report December 8 in Science Advances. The results help demystify the fleeting early moments of sleep and may even point out ways to boost creativity.

Prolific inventor and catnapper Thomas Edison was rumored to chase those twilight moments. He was said to fall asleep in a chair holding two steel ball bearings over metal pans. As he drifted off, the balls would fall. The ensuing clatter would wake him, and he could rescue his inventive ideas before they were lost to the depths of sleep.

Delphine Oudiette, a cognitive neuroscientist at the Paris Brain Institute, and colleagues took inspiration from Edison’s method of cultivating creativity. She and her colleagues brought 103 healthy people to their lab to solve a tricky number problem. The volunteers were asked to convert a string of numbers into a shorter sequence, following two simple rules. What the volunteers weren’t told was that there was an easy trick: The second number in the sequence would always be the correct final number, too. Once discovered, this cheat code dramatically cut the solving time.
After doing 60 of these trials on a computer, the volunteers earned a 20-minute break in a quiet, dark room. Reclined and holding an equivalent of Edison’s “alarm clock” (a light drinking bottle in one dangling hand), participants were asked to close their eyes and rest or sleep if they desired. All the while, electrodes monitored their brain waves.

About half of the participants stayed awake. Twenty-four fell asleep and stayed in the shallow, fleeting stage of sleep called N1. Fourteen people progressed to a deeper stage of sleep called N2.

After their rest, participants returned to their number problem. The researchers saw a stark difference between the groups: People who had fallen into a shallow, early sleep were 2.7 times as likely to spot the hidden trick as people who didn’t fall asleep, and 5.8 times as likely to spot it as people who had reached the deeper N2 stage.

Such drastic differences in these types of experiments are rare, Oudiette says. “We were quite astonished by the extent of the results.” The researchers also identified a “creative cocktail of brain waves,” as Oudiette puts it, that seemed to accompany this twilight stage — a mixture of alpha brain waves that usually mark relaxation mingled with the delta waves of deeper sleep.

The study doesn’t show that the time spent in N1 actually triggered the later realization, cautions John Kounios, a cognitive neuroscientist at Drexel University in Philadelphia who cowrote the 2015 book The Eureka Factor: Aha Moments, Creative Insight, and the Brain. “It could have been possible that grappling with the problem and initiating an incubation process caused both N1 and the subsequent insight,” he says, making N1 a “by-product of the processes that caused insight rather than the cause.”

More work is needed to untangle the connection between N1 and creativity, Oudiette says. But the results raise a tantalizing possibility, one that harkens to Edison’s self-optimizations: People might be able to learn to reach that twilight stage of sleep, or to produce the cocktail of brain waves associated with creativity on demand.

It seems Edison was onto something about the creative powers of nodding off. But don’t put too much stock in his habits. He is also said to have considered sleep “a criminal waste of time.”

Brainless sponges contain early echoes of a nervous system

Brains are like sponges, slurping up new information. But sponges may also be a little bit like brains.

Sponges, which are humans’ very distant evolutionary relatives, don’t have nervous systems. But a detailed analysis of sponge cells turns up what might just be an echo of our own brains: cells called neuroids that crawl around the animal’s digestive chambers and send out messages, researchers report in the Nov. 5 Science.

The finding not only gives clues about the early evolution of more complicated nervous systems, but also raises many questions, says evolutionary biologist Thibaut Brunet of the Pasteur Institute in Paris, who wasn’t involved in the study. “This is just the beginning,” he says. “There’s a lot more to explore.”

The cells were lurking in Spongilla lacustris, a freshwater sponge that grows in lakes in the Northern Hemisphere. “We jokingly call it the Godzilla of sponges” because of the rhyme with Spongilla, say Jacob Musser, an evolutionary biologist in Detlev Arendt’s group at the European Molecular Biology Laboratory in Heidelberg, Germany.

Simple as they are, these sponges have a surprising amount of complexity, says Musser, who helped pry the sponges off a metal ferry dock using paint scrapers. “They’re such fascinating creatures.”
With sponges procured, Arendt, Musser and colleagues looked for genes active in individual sponge cells, ultimately arriving at a list of 18 distinct kinds of cells, some known and some unknown. Some of these cells used genes that are essential to more evolutionarily sophisticated nerve cells in other organisms for sending or receiving messages in the form of small blobs of cellular material called vesicles.

One such cell, called a neuroid, caught the scientists’ attention. After seeing that this cell was using those genes involved in nerve cell signaling, the researchers took a closer look. A view through a confocal microscope turned up an unexpected locale for the cells, Musser says. “We realized, ‘My God, they’re in the digestive chambers.’”

Large, circular digestive structures called choanocyte chambers help move water and nutrients through sponges’ canals, in part by the beating of hairlike cilia appendages (SN: 3/9/15). Neuroids were hovering around some of these cilia, the researchers found, and some of the cilia near neuroids were bent at angles that suggested that they were no longer moving.
The team suspects that these neuroids were sending signals to the cells charged with keeping the sponge fed, perhaps using vesicles to stop the movement of usually undulating cilia. If so, that would be a sophisticated level of control for an animal without a nervous system.

The finding suggests that sponges are using bits and bobs of communications systems that ultimately came together to work as brains of other animals. Understanding the details might provide clues to how nervous systems evolved. “What did animals have, before they had a nervous system?” Musser asks. “There aren’t many organisms that can tell us that. Sponges are one of them.”

Some songbirds now migrate east to west. Climate change may play a role

As the chill of autumn encroaches on Siberia’s grasslands, Richard’s pipits usually begin their southward trek to warmer latitudes. But a growing number of the slender, larklike songbirds seem to be heading west instead, possibly establishing a new migratory route for the species.

This would be the first new route known to emerge on an east-west axis in a long-distance migratory bird, researchers report October 22 in Current Biology. The finding could have implications for how scientists understand the evolution of bird migration routes over time and how the animals adapt to a shifting climate.

Richard’s pipits (Anthus richardi) typically breed in Siberia during the summer and travel south for the winter to southern Asia. Occasionally, “vagrant” birds get lost and show up far from this range, including in Europe. But as a Ph.D. student at the Université Grenoble Alpes in France, evolutionary biologist Paul Dufour noticed, along with colleagues, that described sightings and photo records of the pipits wintering in southern France had increased from a handful of birds annually in the 1980s and 1990s to many dozens in recent years.

So, Dufour, now at the University of Gothenburg in Sweden, and his team started monitoring the pipits in France and Spain to see where the birds were coming from, and if the birds were visiting Europe on purpose or just getting lost.

The researchers captured seven pipits in France during the winter of 2019–2020, tagging them with a sensor that estimates the birds’ geographic positions based on light levels and length of day. The team then released the birds. The next winter, the team successfully recaptured three of them. Those sensors showed that the birds had all flown back to the same part of southwestern Siberia for the summer before returning to France.

The researchers also examined images in citizen-science databases of 331 Richard’s pipits that were photographed in Europe and North Africa, categorizing the birds by apparent age. Among songbirds, Dufour says, vagrants are always young birds. Songbirds tend to follow a route based on instincts written into their DNA, replicating the trip their ancestors took. But storms or mutations that create faulty wayfinding abilities can send young songbirds off target.
Wherever it arrives, the songbird’s first migration creates a mental map for every migration after, so any adult birds in Europe have made the trip more than once. Since more than half of the birds in southern Europe and nearby northwestern Africa documented in the winter were adults, Dufour and his colleagues think that many of these pipits are seasonal migrants.

Contemporary shifts in migration routes are more common in species that travel via the cues of a traveling group, like geese or cranes. Songbirds usually migrate alone, following their instinctual route when young, Dufour says, so changes to migration patterns are rarer.

What’s more, east-west migration is unusual in birds. Most species that travel this way are ones that migrate short distances within the tropics, says Jessie Williamson, an ornithologist at the University of New Mexico in Albuquerque who was not involved with the research. “It’s exciting that an understudied migratory behavior like east-west migration is in the spotlight,” she says.

If the pipits’ European trek is in fact now an established route, it’s possible that the detour was facilitated by climate change, which may also be meddling with birds’ migrations in other ways (SN: 12/17/19). Dufour and his team used computer models that estimate climate suitability for the pipits in Europe based on variables like temperature and precipitation. The researchers compared two periods — 1961 to 1990 and 1990 to 2018 — and found that warmer temperatures in the latter period have made most parts of southern Europe a better wintering location for the birds than they were before.
The selection of European wintering grounds may also involve the deterioration of ancestral, southern Asian sites, but the researchers haven’t investigated that yet. Climate change could be affecting that too, Dufour says. But “we suspect that habitat modification in Southeast Asia — increasing urbanization, less open areas — may also be part of the equation.”

Ginny Chan, an ecologist at the Swiss Ornithological Institute in Sempach who was not involved with the research, says that the types of environmental changes that could be hurting bird populations “are happening very quickly in the traditional wintering range [for Richard’s pipits] in South and East Asia.” In India, the Richard’s pipit population has declined by more than 90 percent over the last couple of decades, Chan says.

Other Siberian bird species that typically migrate south but have recently shown up in Europe in growing numbers, like the yellow-browed warbler and Siberian chiffchaff, may also be making their own westward routes, Dufour suspects.

If other Siberian songbird species are also establishing new western migration routes, this could mean that migratory songbirds are more flexible travelers than scientists previously thought, Dufour says.

That could have hopeful implications for some birds as species worldwide deal with a changing climate. But the new research, he adds, shouldn’t overshadow other studies of migratory birds — like barnacle geese and the European pied flycatcher — which show that some of these species are not as able to cope with climate change.