Scientists have created the largest map of dark matter yet, part of a slew of new measurements that help pin down the universe’s dark contents. Covering about a thirtieth of the sky, the map (above) charts the density of both normal matter — the stuff that’s visible — and dark matter, an unidentified but far more abundant substance that pervades the cosmos.
Matter of both types is gravitationally attracted to other matter. That coupling organizes the universe into more empty regions of space (No. 1 below and blue in the map above) surrounded by dense cosmic neighborhoods (No. 2 below and red in the map above). Researchers from the Dark Energy Survey used the Victor Blanco telescope in Chile to survey 26 million galaxies in a section of the southern sky for subtle distortions caused by the gravitational heft of both dark and normal matter. Scientists unveiled the new results August 3 at Fermilab in Batavia, Ill., during a meeting of the American Physical Society.
Dark matter is also accompanied by a stealthy companion, dark energy, an unseen force that is driving the universe to expand at an increasing clip. According to the new inventory, the universe is about 21 percent dark matter and 5 percent ordinary matter. The remainder, 74 percent, is dark energy.
The new measurements differ slightly from previous estimates based on the cosmic microwave background, light that dates back to 380,000 years after the Big Bang (SN: 3/21/15, p. 7). But the figures are consistent when measurement errors are taken into account, the researchers say. “The fact that it’s really close, we think is pretty remarkable,” says cosmologist Josh Frieman of Fermilab, who directs the Dark Energy Survey. But if the estimates don’t continue to align as the survey collects more data, something might be missing in cosmologists’ theories of the universe.
A new genetics study adds fuel to the debate about muscle aches that have been reported by many people taking popular cholesterol-lowering drugs called statins.
About 60 percent of people of European descent carry a genetic variant that may make them more susceptible to muscle aches in general. But counterintuitively, these people had a lower risk of muscle pain when they took statins compared with placebos, researchers report August 29 in the European Heart Journal. Millions of people take statins to lower cholesterol and fend off the hardening of arteries. But up to 78 percent of patients stop taking the medicine. One common reason for ceasing the drugs’ use is side effects, especially muscle pain, says John Guyton, a clinical lipidologist at Duke University School of Medicine.
It has been unclear, however, whether statins are to blame for the pain. In one study, 43 percent of patients who had muscle aches while taking at least one type of statin were also pained by other types of statin (SN: 5/13/17, p. 22). But 37 percent of muscle-ache sufferers in that study had pain not related to statin use. Other clinical trials have found no difference in muscle aches between people taking statins and those not taking the drugs.
The new study hints that genetic factors, especially ones involved in the immune system’s maintenance and repair of muscles, may affect people’s reactions to statins. “This is a major advance in our understanding about myalgia,” or muscle pain, says Guyton, who was not involved in the study.
People with two copies of the common form of the gene LILRB5 tend to have higher-than-usual blood levels of two proteins released by injured muscles, creatine phosphokinase and lactate dehydrogenase. Higher levels of those proteins may predispose people to more aches and pains. In an examination of data from several studies involving white Europeans, people with dual copies of the common variant were nearly twice as likely to have achy muscles while taking statins as people with a less common variant, Moneeza Siddiqui of the University of Dundee School of Medicine in Scotland and colleagues discovered.
But when researchers examined who had pain when taking statins versus placebos, those with two copies of the common variant seemed to be protected from getting statin-associated muscle pain. Why is not clear. People with double copies of the common form of the gene who experience muscle pain may stop taking statins because they erroneously think the drugs are causing the pain, study coauthor Colin Palmer of the University of Dundee said in a news release.
The less common version of the gene is linked to reduced levels of the muscle-damage proteins, and should protect against myalgia. Yet people with this version of the gene were the ones more likely to develop muscle pain specifically linked to taking statins during the trials.
The finding suggests that when people with the less common variant develop muscle pain while taking statins, the effect really is from the drugs, the researchers say.
But researchers still don’t know the nitty-gritty details of how the genetic variants promote or protect against myalgia while on statins. Neither version of the gene guarantees that a patient will develop side effects — or that they won’t. The team proposes further clinical trials to unravel interactions between the gene and the drugs.
More study is needed before doctors can add the gene to the list of tests patients get, Guyton says. “I don’t think we’re ready to put this genetic screen into clinical practice at all,” he says. For now, “it’s much easier just to give the patient the statin” and see what happens.
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.
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 (SN: 11/12/16, p. 14). But those particles have yet to be spotted.
Recent results, posted at arXiv.org, 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 hints of WIMPs, 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 continuing to expand the search beyond WIMPs.
Every day, it seems like there’s a new natural disaster in the headlines. Hurricane Harvey inundates Texas. Hurricane Irma plows through the Caribbean and the U.S. south, and Jose is hot on its heels. A deadly 8.1-magnitude earthquake rocks Mexico. Wildfires blanket the western United States in choking smoke.
While gripping tales of loss and heroism rightly fill the news, another story quietly unfolds. Hurricanes, droughts, oil spills, wildfires and other disasters are natural labs. Data quickly gathered in the midst of such chaos, as well as for years afterward, can lead to discoveries that ultimately make rescue, recovery and resilience to future crises possible.
So when disaster strikes, science surges, says human ecologist Gary Machlis of Clemson University in South Carolina. He has studied and written about the science done during crises and was part of the U.S. Department of the Interior’s Strategic Sciences Group, which helps government officials respond to disasters.
The science done during Hurricane Harvey is an example. Not long after the heavy rains stopped, crews of researchers from the U.S. Geological Survey fanned across Texas, dropping sensors into streams. The instruments measure how swiftly the water is flowing and determine the severity of the flooding in different regions affected by the hurricane. Knowing where the flooding is the worst can help the Federal Emergency Management Agency and other government groups direct funds to areas with the most extreme damage. In the days leading up to Irma’s U.S. landfall, scientists from the same agency also went to the Florida, Georgia and South Carolina coasts to fasten storm-tide sensors to pier pylons and other structures. The sensors measure the depth and duration of the surge in seawater generated by the change in pressure and winds from the storm. This data will help determine damage from the surge and improve models of flooding in the future, which could help provide a better picture of where future storm waters will go and who needs to be evacuated ahead of hurricanes.
Even as Irma struck Florida, civil engineer Forrest Masters of the University of Florida in Gainesville, his students and collaborators traveled to the southern part of the state to study the intensity and variation in the hurricane’s winds. As winds blew and rain pelted, the team raised minitowers decked with instruments designed to measure ground-level gusts and turbulence. With this data, the researchers will compare winds in coastal areas, near buildings and around other structures, data that can help government agencies assess storm-related damage to buildings and other structures. The team will also take the data back to the Natural Hazards Engineering Research Infrastructure labs at the University of Florida to study building materials and identify those most resistant to extreme winds. “Scientists want to use their expertise to help society in whatever way they can during a disaster,” says biologist Teresa Stoepler, who was a member of the Strategic Sciences Group when she worked at USGS.
As a former science & technology policy fellow with the American Association for the Advancement of Science, Stoepler studied the science that resulted from the 2010 Deepwater Horizon oil spill. This devastating explosion of an oil rig spewed 210 million gallons of petroleum into the Gulf of Mexico. It also opened the door for scientific research. Biologists, chemists, psychologists and a range of other scientists wanted to study the environmental, economic and mental health consequences of the disaster; local scientists wanted to study the effects of the spill on their communities; and leaders at the local and federal government needed guidance on how to respond. There was a need to coordinate all of that effort.
That’s where the Strategic Sciences Group came in. The group, officially organized in 2012, brought together researchers from federal, academic and nongovernmental organizations. The goal was to use data collected from the spill to map out possible long-term environmental and economic consequences of the disaster, determine where research still needed to be done and determine how to allocate money for response and recovery efforts.
Not long after its formation, the group had another disaster to respond to: Superstorm Sandy devastated the U.S. East Coast, even pushing floodwaters into the heart of New York City. Scientific collaborations allowed researchers and policy makers to get a better sense of whether wetlands, sea walls or other types of infrastructure would be best to invest in to prevent future devastation. The work also gave clues as to what types of measurements, such as the height of floodwaters, should be made in the future — say, during storms like Harvey and Irma — to speed recovery efforts afterward.
Moving forward, we’re likely to see this kind of collaboration coming into play time and again. No doubt, more natural disasters loom. And other groups are getting into crisis science. For instance, Stanford University, with its Science Action Network, aims to drive interdisciplinary research during disasters and encourage communication across the many groups responding to those disasters. And the Disaster Research Response program at the National Institutes of Health provides a framework for coordinating research on the medical and public health aspects of disasters and public health emergencies.
Surges in science will stretch from plunging into the chaos of a crisis to get in-the-moment data to monitoring years of aftermath. Retrospective studies of the data collected a year, three years or even five years after a disaster could reveal where there are gaps in the science and how those can be filled in during future events.
The more data collected, the more discoveries made and lessons learned, the more likely we’ll be ready to face the next disaster.
For the first time, researchers have disabled a gene in human embryos to learn about its function.
Using molecular scissors called CRISPR/Cas9, researchers made crippling cuts in the OCT4 gene, Kathy Niakan and colleagues report September 20 in Nature. The edits revealed a surprising role for the gene in the development of the placenta.
Researchers commonly delete and disable genes in mice, fruit flies, yeast and other laboratory critters to investigate the genes’ normal roles, but have never done this before in human embryos. Last year, government regulators in the United Kingdom gave permission for Niakan, a developmental biologist at the Francis Crick Institute in London, and colleagues to perform gene editing on human embryos left over from in vitro fertilization treatments (SN Online: 2/1/16). The researchers spent nearly a year optimizing techniques in mouse embryos and human stem cells before conducting human embryo experiments, Niakan says. This groundbreaking research allows researchers to directly study human development genes, says developmental biologist Dieter Egli of Columbia University. “This is unheard of. It’s not something that has been possible,” he says. “What we know about human development is largely inferred from studies of mice, frogs and other model organisms.”
Other researchers have used CRISPR/Cas9 to repair mutated genes in human embryos (SN: 4/15/17, p. 16; SN: 9/2/17, p. 6). The eventual aim of that research is to prevent genetic diseases, but it has led to concerns that the technology could be abused to produce “designer babies” who are better looking, smarter and more athletic than they otherwise would be.
“There’s nothing irresponsible about the research in this case,” says stem cell researcher Paul Knoepfler of the University of California, Davis, School of Medicine. The researchers focused on basic questions about how one gene affects human embryo development. Such studies may one day lead to better fertility treatments, but the more immediate goal is to gain better insights into human biology.
Niakan’s group focused on a gene called OCT4 (also known as POU5F1), a master regulator of gene activity, which is important in mouse embryo development. This gene is also known to help human embryonic stem cells stay flexible enough to become any type of body cell, a property known as pluripotency. Scientists use OCT4 protein to reprogram adult cells into embryonic-like cells, an indication that it is involved in early development (SN: 11/24/07, p. 323). But researchers didn’t know precisely how the OCT4 gene operates during human development. Niakan already had clues that it works at slightly different times in human embryos than it does in mice (SN: 10/3/15, p. 13).
In the experiment, human embryos lacking OCT4 had difficulty reaching the blastocyst stage: Only 19 percent of edited embryos formed blastocysts, while 47 percent of unedited embryos did. Blastocysts are balls of about 200 cells that form about five or six days after fertilization. The ball’s outer layer of cells gives rise to the placenta. Inside the blastocyst, one type of embryonic stem cells will become the yolk sac. Another kind, about 20 cells known as epiblast progenitor cells, will give rise to all the cells in the body. Niakan and colleagues predicted from earlier work with mice and human embryonic stem cells that the protein OCT4 would be necessary for the epiblast cells to develop correctly. As predicted, “knocking out” the OCT4 gene disrupted epiblasts’ development. What the researchers didn’t expect is that OCT4 also affects the development of the placenta precursor cells on the outside of the blastocyst.
“That’s not predicted anywhere in the literature,” Niakan says. “We’ll be spending quite a lot of time on this in the future to uncover exactly what this role might be.”
A single genetic mutation made the Zika virus far more dangerous by enhancing its ability to kill nerve cells in developing brains, a new study suggests.
The small change — which tweaks just one amino acid in a protein that helps Zika exit cells — may cause microcephaly, researchers report September 28 in Science. The mutation arose around May 2013, shortly before a Zika outbreak in French Polynesia, the researchers calculate.
Zika virus was discovered decades ago but wasn’t associated with microcephaly — a birth defect characterized by a small head and brain — until the 2015–2016 outbreak in Brazil. Women who had contracted the virus while pregnant started giving birth to babies with the condition at higher-than-usual rates (SN: 4/2/16, p. 26). Researchers weren’t sure why microcephaly suddenly became a complication of Zika infections, says Pei-Yong Shi, a virologist at the University of Texas Medical Branch at Galveston. Maybe the virus did cause microcephaly before, scientists suggested, but at such low rates that no one noticed. Or people in South America might be more vulnerable to the virus. Perhaps their immune systems don’t know how to fight it, they have a genetic susceptibility or prior infections with dengue made Zika worse (SN: 4/29/17, p. 14). But Shi and colleagues in China thought the problem might be linked to changes in the virus itself. The researchers compared a strain of Zika isolated from a patient in Cambodia in 2010 with three Zika strains collected from patients who contracted the virus in Venezuela, Samoa and Martinique during the epidemic of 2015–2016. The team found seven differences between the Cambodian virus and the three epidemic strains.
Researchers engineered seven versions of the Cambodian virus, each with one of the epidemic strains’ mutations, and injected the viruses into fetal mouse brains. Viruses with one of these mutations, dubbed S139N, killed brain cells in fetal mice and destroyed human brain cells grown in lab dishes more aggressively than the Cambodian strain from 2010 did, the researchers found. “That’s pretty convincing evidence that it at least plays some role in what we’re seeing now,” says Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases.
The mutation changes an amino acid in a Zika protein called prM. That protein helps the virus mature within infected cells and get out of the cells to infect others. Shi and colleagues don’t yet know why tweaking the protein makes the virus kill brain cells more readily.
The alteration in that protein probably isn’t the entire reason epidemic strains cause microcephaly, Shi says. The Cambodian strain also led to the death of a few brain cells, but perhaps not enough to cause microcephaly. “We believe there are other changes in the virus that collectively enhance its virulence,” he says. In May in Nature, Shi and colleagues described a different mutation that allows the virus to infect mosquitoes more effectively.
Brain cells from different people vary in their susceptibility to Zika infections, says infectious disease researcher Scott Weaver, also at the University of Texas Medical Branch but not involved in the study. He says more work on human cells and in nonhuman primates is needed to confirm whether this mutation is really the culprit in microcephaly.
Physicists often ponder small things, but probably not the ones on Kerwyn Casey “KC” Huang’s mind. He wants to know what it’s like to be a bacterium.
“My motivating questions are about understanding the physical challenges bacterial cells face,” he says. Bacteria are the dominant life-forms on Earth. They affect the health of plants and animals, including humans, for good and bad. Yet scientists know very little about the rules the microbes live by. Even questions as basic as how bacteria determine their shape are still up in the air, says Huang, of Stanford University.
Huang, 38, is out to change that. He and colleagues have determined what gives cholera bacteria their curved shape and whether it matters (a polymer protein, and it does matter; the curve makes it easier for cholera to cause disease), how different wavelengths of light affect movement of photosynthetic bacteria (red and green wavelengths encourage movement; blue light stops the microbes in their tracks), how bacteria coordinate cell division machinery and how photosynthetic bacteria’s growth changes in light and dark.
All four of these findings and more were published in just the first three months of this year. Huang also looks for ways to use tools and techniques his team develops to solve problems unrelated to bacteria. Computer programs that measure changes in bacterial cell shape can also track cells in plant roots and in developing zebrafish embryos. He’s even helped determine how a protein’s activity and stability contribute to a human genetic disease.
A physicist by training, Huang delves into biology, biochemistry, microbial ecology, genetics, engineering, computer science and more, partnering with a variety of scientists from across those fields. He’s even teamed up with his statistician sister. He’s an “all-in-one scientist,” says longtime collaborator Ned Wingreen, a biophysicist at Princeton University.
When Huang started his lab at Stanford in 2008, after getting his Ph.D. at MIT and spending time at Princeton as a postdoctoral fellow, his background was purely theoretical. He designed and ran the computer simulations and then his collaborators carried out the experiments. But soon, he wanted to do hands-on research too, to learn why cells are the way they are. Such a leap “is not trivial,” says Christine Jacobs-Wagner, a microbiologist at Yale University who also studies bacterial cell shape. But Huang is “a really, really good experimentalist,” she says.
Jacobs-Wagner was particularly impressed with a “brilliant microfluidics experiment” Huang did to test a well-established truism about how bacteria grow. Researchers used to think that turgor pressure — water pressure inside a cell that pushes the outer membrane against the cell wall — controlled bacterial growth, just like it does in plants. But abolishing turgor pressure didn’t change E. coli’s growth rate, Huang and colleagues reported in 2014 in Proceedings of the National Academy of Sciences. “This result blew my mind away,” Jacobs-Wagner says. The finding “crumbled the foundation” of what scientists thought about bacterial growth.
“He uses clever experiments to challenge old paradigms,” Jacobs-Wagner says. “More than once he has come up with a new trick to address a tough question.” Sometimes Huang’s tricks require breaking things. Zemer Gitai, a microbiologist at Princeton, remembers talking with Huang and Wingreen about a question that microbiologists were stuck on: How are molecules oriented in bacterial cell walls? Researchers knew that the walls are made of rigid sugar strands connected by flexible proteins, like a chain link fence held together by rubber bands. What they didn’t know was whether the rubber bands circled the bacteria like the hoops on a wine barrel, ran in stripes down the length of the cell or stuck out like hairs.
If bacteria were put under pressure, the cells would crack along the weak rubber band–like links, Huang and Wingreen reasoned. If the cells split like hot dogs on a grill, it would mean the links ran the length of the cells. If they opened like a Slinky, it would suggest a wine-barrel configuration. The researchers reported the results — opened like a Slinky — in 2008. Another group, using improved microscope techniques, got the same result.
Huang teamed up with other researchers to do microfluidics experiments, growing bacteria in tiny chambers and tracking individual cells to learn how photosynthetic bacteria grow in light and dark.
But in nature, bacteria don’t live alone. So Huang has also worked with Stanford colleague Justin Sonnenburg to answer a basic question: “Where and when are bacteria in the gut growing? No one knows,” Huang says. “How can we not know that? It’s totally fundamental.” Without that information, it’s impossible to know, for example, how antibiotics affect the microbial community in the intestines, he says.
Stripping fiber from a mouse’s diet not only changes the mix of microbes in the gut, it alters where in the intestines the microbes grow, the researchers discovered. Bacteria deprived of fiber’s complex sugars began to munch on the protective mucus lining the intestines, bumping against the intestinal lining and sparking inflammation, Huang, Sonnenburg and colleagues reported in Cell Host & Microbe in 2015.
Huang’s breadth of research — from deciphering the nanoscale twists of proteins to mapping whole microbial communities — is sure to lead to many more discoveries. “He’s capable of making contributions to any field,” Jacobs-Wagner says, “or any research question that he’s interested in.”
Over the last 40 years, the number of kids and teens with obesity has skyrocketed worldwide. In 1975, an estimated 5 million girls and 6 million boys were obese. By 2016, those numbers had risen to an estimated 50 million girls and 74 million boys, according to a report published online October 10 in the Lancet. While the increase in childhood obesity has slowed or leveled off in many high-income countries, it continues to grow in other parts of the world, especially in Asia.
Using the body mass index, a ratio of weight to height, of more than 30 million 5- to 19-year-olds, researchers tracked trends from 1975 to 2016 in five weight categories: moderate to severe underweight, mild underweight, healthy weight, overweight and obesity. The researchers defined obesity as having a BMI around 19 or higher for a 5-year-old up to around 30 or higher for a 19-year-old.
Globally, more kids and teens — an estimated 117 million boys and 75 million girls — were moderately or severely underweight in 2016 than were obese. But the total number of obese children is expected to overtake the moderately or severely underweight total by 2022, the researchers say.
The globalization of poor diet and inactivity is part of the problem, says William Dietz, a pediatrician at George Washington University in Washington D.C., who wrote a commentary that accompanies the study. Processed foods and sugary drinks have become widely available around the world. And urbanization, which also increased in the last four decades, tends to reduce physical activity, Dietz says.
While obesity rates for kids and teens have largely leveled off in most wealthy countries, those numbers continue to increase for adults. The findings in children are consistent with evidence showing a drop in the consumption of fast food among children and adults in the United States over the last decade, Dietz says. “Children are going to be much more susceptible to changes in caloric intake than adults.”
Discovering an itchy welt is often a sign you have been duped by one of Earth’s sneakiest creatures — the mosquito.
Scientists have puzzled over how the insects, often laden with two or three times their weight in blood, manage to flee undetected. At least one species of mosquito — Anopheles coluzzii — does so by relying more on lift from its wings than push from its legs to generate the force needed to take off from a host’s skin, researchers report October 18 in the Journal of Experimental Biology. The mosquitoes’ undetectable departure, which lets them avoid being smacked by an annoyed host, may be part of the reason A. coluzzii so effectively spreads malaria, a parasitic disease that kills hundreds of thousands of people each year.
Researchers knew that mosquito flight is unlike that of other flies (SN Online: 3/29/17). The new study provides “fascinating insight into life immediately after the bite, as the bloodsuckers make their escape,” says Richard Bomphrey, a biomechanist at the Royal Veterinary College of the University of London, who was not involved in the research.
To capture mosquito departures, Sofia Chang of the Animal Flight Laboratory at the University of California, Berkeley and her colleagues set up a flight arena for mosquitoes. Using three high-speed video cameras, the researchers created computer reconstructions of the mosquitoes’ takeoff mechanisms to compare with those of fruit flies.
Mosquitoes are as fast as fruit flies while flying away but use only about a quarter of the leg force that fruit flies typically use to push off, Chang and her colleagues found. And 61 percent of a mosquito’s takeoff power comes from its wings. As a result, the mosquitoes do not generate enough force on a mammal’s skin to be detected.
Unlike fruit flies’ short legs, mosquitoes’ long legs extend the insects’ push-off time. That lets mosquitoes spread out already-minimal leg force over a longer time frame to reach similar takeoff speeds as fruit flies, the researchers found. This slow and steady mechanism is the same regardless of whether the bloodsuckers sense danger or are leaving of their own accord, and whether they are full of blood or have yet to get a meal. While in flight, though, a belly full of blood slowed the mosquitoes down by about 18 percent.
Chang next wants to determine whether mosquitoes land as gently as they depart. “If they are so stealthy when they leave, they must be stealthy as they land, too.”
Saplings grown in soil microbes that have experienced drought, cold or heat are more likely to survive when faced with those same conditions, researchers report in the May 26 Science. And follow-up tests suggest that the microbes’ protective relationship with trees may linger beyond initial planting.
The team’s findings could aid massive tree planting efforts by giving new saplings the best chance of survival over the long run, says Ian Sanders, a plant and fungal ecologist at the University of Lausanne in Switzerland. “If you can control which microbes are put onto tree saplings in a nursery, you can probably help to determine whether they’re going to survive or not when they’re transplanted to the field.” As climate change pushes global temperatures ever higher, many species must either adapt to new conditions or follow their ideal climate to new places (SN: 1/25/23). While forests’ ranges have changed as Earth’s climate has warmed and cooled over hundreds of millions of years, the pace of current climate change is too fast for trees to keep up (SN: 4/1/20).
Trees live a long time, and they don’t move or evolve very quickly, says Richard Lankau, a forest ecologist at the University of Wisconsin–Madison. They do have close relationships with fast-adapting soil microbes, including fungi, which can help plants survive stressful conditions.
But it was unclear whether microbes that had previously survived various climates and stresses might give inexperienced baby trees encountering a changing climate a leg up. With friends in the soil, “trees might have more tools in their toolkit than we give them credit for” to survive tough conditions, Lankau says.
For the study, Lankau and fellow ecologists Cassandra Allsup and Isabelle George — both also at UW–Madison — collected soil from 12 spots in Wisconsin and Illinois that varied in temperature and amount of rain. The team then used the soils to plant an abundance of 12 native tree species, including white oak (Quercus alba) and silver maple (Acer saccharinum). Overall, “we had thousands of plants we were monitoring,” Allsup says.
Those saplings grew in the soils in a greenhouse for two months before being transplanted in one of two field sites — one warm and one cold. To simulate drought, some trees in each spot were placed under transparent plastic sheets that blocked direct rainfall.
One site in northern Wisconsin was at the northern edge of the trees’ range and represented how trees might take root in a new area that’s getting warm enough for them to grow. There, trees planted in soil containing cold-adapted microbes better survived Wisconsin’s frigid winter temperatures. Plants that faced drought in addition to the cold, on the other hand, didn’t have the same benefit.
The other location, set up in central Illinois, was designed to represent a region where the climate is getting too hot or dry for the tree species to tolerate. Saplings grown in soil with microbes from arid spots were more likely to survive a lack of rain. But those grown in soils with heat-tolerant microbes were only slightly more likely to survive when they received normal rainfall. Resident species already living in the area didn’t outcompete all of the transplanted microbes. Newly introduced fungi persisted in the soil for three years, a sign that any protective effects might last at least that long, the team found.
It’s still unclear which microbes best aid the trees. Analyses of microbes living in the soil hinted that fungi that live inside plant roots may better help trees survive drought. Cold-adapted soils seem to have fewer fungal species. But soils also contain bacteria, archaea and protists, Sanders says. “We don’t know what it is yet that seems to affect the plant survival in these changing climates.” Determining which microbes are the important ones and whether there are specific conditions that best suit the soil is next up on the list, Allsup says. For example, can dry-adapted soil from Iowa help when planting trees in Illinois? “We need to think more about soils and combinations and [transplant] success… to actually save the forest.”
One caution, Sanders says, is that transporting microbes from one place to another en masse could bring the bad along with the good. Some microbes might be pathogens in the new place where they’re transplanted. “That’s also a big danger.”
