What builds up can also tear down, a new study of bacteria suggests.
Bacteria build biofilms, communities of the microorganisms encased in a protective goo that shields the microbes from antibiotics and immune system attacks. But the very enzymes bacteria use to construct that shield can also destroy some of its molecules and strip away the protection, researchers report May 20 in Science Advances.
“We’re weaponizing the bacteria against themselves,” says P. Lynne Howell, a structural microbiologist at the Hospital for Sick Children in Toronto. Howell and colleagues studied Pseudomonas aeruginosa bacteria, which can cause pneumonia and other infections and is particularly problematic for people with the lung disease cystic fibrosis. The researchers discovered that two enzymes, PelAh and PslGh, which the bacteria use to build two different sugar polymers, can degrade those same polymers. That delete function, supplied by parts of the enzymes known as glycoside hydrolase domains, normally helps correct mistakes or prevents buildup of the sugar chains inside bacterial cells, Howell says.
In laboratory tests, synthetic versions of the glycoside hydrolase domains applied to P. aeruginosa cultures stopped the bacteria from forming new biofilms and melted existing ones. Stripping away sugar polymers did not kill the bacteria but did make them more vulnerable to antibiotics and immune cells. Human lung cells grown in dishes containing the enzymes suffered no harm, suggesting the enzymes wouldn’t damage human tissues.
Animal tests are needed to determine whether the enzymes are safe and can fight biofilm infections in the body, Howell says. Similar enzymes from other bacteria and fungi may also fight biofilm infections caused by those organisms, she says.
Giant pandas have better ears than people — and polar bears. Pandas can hear surprisingly high frequencies, conservation biologist Megan Owen of the San Diego Zoo and colleagues report in the April Global Ecology and Conservation.
The scientists played a range of tones for five zoo pandas trained to nose a target in response to sound. Training, which took three to six months for each animal, demanded serious focus and patience, says Owen, who called the effort “a lot to ask of a bear.”
Both males and females heard into the range of a “silent” ultrasonic dog whistle. Polar bears, the only other bears scientists have tested, are less sensitive to sounds at or above 14 kilohertz. Researchers still don’t know why pandas have ultrasonic hearing. The bears are a vocal bunch, but their chirps and other calls have never been recorded at ultrasonic levels, Owen says. Great hearing may be a holdover from the bears’ ancient past.
Two newly discovered Triceratops relatives sported some peculiar headgear.
Researchers uncovered skull fragments of Machairoceratops cronusi in 77-million-year-old mudstone from the Wahweap Formation in southern Utah. Unlike other horned dinosaurs, the roughly 8-meter-long M. cronusi had two grooved horns with spatula-like tips bowed forward from the back of its neck shield. The grooves’ function baffles researchers.
A different research team found a younger cousin of M. cronusi in Montana’s Judith River Formation. Spiclypeus shipporum lived about 76 million years ago and had distinct brow horns that protruded sideways from its skull along with unusual spikes on its neck shield — some pointing outward, others bent forward. S. shipporum’s distinct horns and spikes may have allowed individuals of the species to recognize one another, says Jordan Mallon, a paleobiologist involved in the research at the Canadian Museum of Nature in Ottawa.
The new finds add to the diversity among the herbivorous horned dinosaurs that roamed North America during the Late Cretaceous period. “We thought we knew most things [about horned dinosaurs],” says Eric Lund, a paleontologist at Ohio University in Athens who analyzed M. cronusi. “But we’ve just scratched the surface.”
Papers detailing the new species were published May 18 in PLOS ONE.
Armor-plated marine microbes surprised scientists a few years ago by recovering their shell-building prowess in levels of ocean acidification expected under future climate change. But those gains were short-lived, new research shows.
For four years, marine ecologist Lothar Schlüter and colleagues steeped Emiliania huxleyi phytoplankton in seawater acidified by carbon dioxide. After an initial drop in shell calcification — a process that helps sequester CO2 from the atmosphere — the microbes mostly restored their calcification activities within a year, the researchers had reported. But as the experiment continued, the phytoplankton began making less and less shell material. By the end of the experiment, the phytoplankton in the acidified water were calcifying less than a population that hadn’t been exposed to such harsh conditions, the researchers report July 8 in Science Advances.
In the future, the shell-making phytoplankton “may calcify even less than we assume today based on short-term experiments,” says study coauthor Thorsten Reusch, a marine ecologist who works with Schlüter at the GEOMAR Helmholtz Center for Ocean Research in Kiel, Germany. “One year just isn’t long enough to tell us something about how evolutionary adaptation will play out.” While phytoplankton in the ocean may ultimately follow a different evolutionary path than those under lab conditions, the work shows that the evolutionary response to climate change is more complex than previously thought, Reusch says. There is a silver lining, though: When returned to present-day seawater conditions, the phytoplankton bounced back to their original calcification rates. So even if ocean acidification continues, the phytoplankton could quickly restart calcifying if conditions ever improved. “This isn’t a case of ‘use it or lose it,’” Reusch says. Photosynthetic plankton produce about half of Earth’s oxygen and their sinking carcasses transport carbon from the ocean surface to the seafloor — both key steps in the temperature-regulating carbon cycle. The weight of E. huxleyi’s circular, shieldlike shells serves as ballast during the descent, accelerating the carbon drawdown.
The shell-making process requires E. huxleyi to lower its own acidity by pushing protons out through its cell wall. But as the ocean becomes more acidic, that proton pushing will require more energy to overcome an increasing acidity difference between the inside and outside of the cell. Many scientists worry that that energy cost could cause calcifying phytoplankton such as E. huxleyi to ultimately give up their shells. That would slow the CO2 drawdown and worsen climate change, the scientists fear.
Schlüter, Reusch and colleagues started their tests with a single cell of E. huxleyi collected off the coast of Norway in 2009. Populations grown from this cell lived in containers of acidified seawater about the size of soda cans. Around 2,100 generations later, at the end of the study, the acidity-acclimated phytoplankton population calcified about four-fifths as much shell material as a population that had been kept in regular seawater before being plopped into acidified water.
That calcification decline could be an evolutionary trade-off, Reusch says. The shells probably protect E. huxleyi from predators and pathogens. But in more acidic waters, the energy costs of building shells may outweigh their benefits. The researchers plan to conduct the same experiment again, this time introducing predators to see if the added hazard makes the phytoplankton hold on to their shells.
“There are a lot of surprises in store for us in terms of the kinds of evolutionary responses these organisms can have,” says Tatiana Rynearson, an oceanographer at the University of Rhode Island’s Narragansett campus who was not involved in the study. “Evolution continues.”
ORLANDO, Fla. — Weight gain may depend on how an individual’s genes react to certain diets, a new study in mice suggests.
Four strains of mice fared differently on four different diets, William Barrington of North Carolina State University in Raleigh reported July 15 at the Allied Genetics Conference.
One strain, the A/J mouse, was nearly impervious to dietary changes. Those mice didn’t gain much weight or have changes in insulin or cholesterol no matter what they ate: a fat-and-carbohydrate-laden Western diet, traditional Mediterranean or Japanese diet (usually considered healthy) or very low-carbohydrate, fat-rich fare known as the ketogenic diet. In contrast, NOD/ShiLtJ mice gained weight on all but the Japanese diet. Those mice’s blood sugar shot up — a hallmark of diabetes — on a Mediterranean diet, but decreased on the Japanese diet.
FVB/NJ mice didn’t get fat on the Western diet, but became obese and developed high cholesterol and other health problems on the ketogenic diet. The opposite was true for C57BL/6J mice. They became obese and developed cholesterol and other problems linked to heart disease and diabetes in people on the Western diet, but not on the ketogenic diet. They also fattened up on the Mediterranean diet.
The results indicate that “there’s no universally healthy diet,” Barrington said. The findings echo results of a human study in which blood sugar rose in some people after eating some foods, even when the same food had no effect on other people (SN: 1/9/16, p. 8). Such individual reactions to food suggest that diets should be personalized.
Barrington and colleagues are working to find the genes that control the mouse strains’ varying responses to what they eat. There is still no way to predict how people will fare on a given diet, he said.
MANCHESTER, England — The human nose harbors not only a deadly enemy — Staphylococcus aureus — but also its natural foe. Scientists have now isolated a compound from that foe that might combat MRSA, the methicillin-resistant strain of S. aureus.
“We didn’t expect to find this. We were just trying to understand the ecology of the nose to understand how S. aureus causes problems,” bacteriologist Andreas Peschel of the University of Tübingen in Germany said at a news briefing July 26 during the EuroScience Open Forum. Investigating the intense interspecies competition in the nose — where microbes fight for space and access to scant sugars and amino acids — might offer a fertile alternative to searching for new drug candidates in soil microbes. Antibiotic researcher Kim Lewis of Northeastern University in Boston agrees in general that the approach might produce new drug discovery leads. But so far the human microbiome has produced only a handful of potential new antibiotics (including lactocillin). If “the compound they found is membrane-acting, [it] will be useful for topical applications, but not as a systemic antibiotic,” he wrote in an e-mail. And new systemic antibiotics are needed most, he says. Despite being a relatively nutrient-poor environment, the human nose is home to more than 50 species of bacteria. One of these is S. aureus, a dominant cause of hospital-acquired infections such as MRSA, as well as infections of the blood and heart. But there’s a huge variability in the nasal microbe scene between individuals: while S. aureus is present in the nasal passages of roughly 30 percent of people, the other 70 percent don’t have any sign of it.
Trying to explain this difference led Peschel and colleagues to study “the ecology of the nose.” They suspected that other nasal inhabitants, well-tuned to compete in that harsh niche, might be blocking S. aureus from colonizing the nose in those who don’t carry it.
From nasal secretion samples, the team isolated 90 strains of different Staphylococcus species. Of these, one bacterium, S. lugdunensis, killed S. aureus when the two were grown together in a dish. Introducing a variety of mutations into S. lugdunensis produced a strain that didn’t kill. The missing gene, the team showed, normally produced an antibiotic, which the researchers named lugdunin; it represents the first example of a new class of antibiotic.
Lugdunin was able to fend off MRSA as well as a strain of Enterococcus resistant to the antibiotic vancomycin. Neither bacteria developed resistance. The team also pitted S. lugdunensis against S. aureus in test tube and mouse studies, with S. lugdunensis besting S. aureus. Only 5.9 percent of 187 hospital patients had S. aureus in their noses if they also carried S. lugdunensis, the team found, while S. aureus was present in 34.7 percent of those without S. lugdunensis. Peschel and colleagues also reported the results July 28 in Nature. Lugdunin cleared up a staph skin infection in mice, but it’s unclear how the compound works. Researchers could not rule out that it damages the cell membrane, which could limit its use in humans to a topical antibiotic. Peschel and coauthor Bernhard Krismer also suggest that the bacterium itself might be a good probiotic, applied nasally, to fend off staph infections in vulnerable hospital patients.
For the first time in the United States, free-flying genetically modified mosquitoes have federal approval to take wing in Florida. But when, and if, that will happen is still up in the air. Local officials will make the final decision — possibly not until after the November elections.
The World Health Organization has recognized these mosquitoes as possible tools for fighting the spread of mosquito-borne Zika virus. But the U.S. Food and Drug Administration’s decision, announced August 5, covers only a specific, preliminary test release of GM mosquitoes on Key Haven in the Florida Keys, where no locally transmitted Zika cases have been reported. This trial of OX513A mosquitoes, genetically engineered by the British company Oxitec, “would be unlikely to result in adverse effects on the environment or human health,” the FDA ruled. If Key West commissioners approve it, the trial would release abundant GM male Aedes aegypti species carrying a gene that will cause their offspring to die. In tests in Brazil, Panama and the Cayman Islands, months of releasing these mosquitoes has reduced the wild populations of Ae. aegypti mosquitoes by 90 percent or more. As a result, a Brazil neighborhood has seen mosquito-borne dengue cases plummet (SNOnline: 7/15/16).
To see whether OX513A could work in the United States, too, the test release would now need approval from the Florida Keys Mosquito Control District Board of Commissioners. Opponents of GM organisms have protested the idea, so the five commissioners have arranged for a nonbinding referendum question to appear on the November ballot. Commissioners plan to wait until the community has weighed in before making their final decision, says mosquito control district spokeswoman Beth Ranson.
If the mosquito plan gets a thumbs up, Oxitec could release mosquitoes in December, said Hadyn Parry, the company’s chief executive officer. Monitoring and testing could take six months and results would go back to the FDA with an application to allow the mosquitoes to be released commercially — and more broadly — in the United States for mosquito control.
As Zika rages in Puerto Rico, and with Miami reporting the first locally mosquito-transmitted cases on the U.S. mainland, debate over the controversial mosquito has taken on new urgency. Tom Frieden, director of the U.S. Centers for Disease Control and Prevention, has noted that efforts to eradicate mosquitoes in an area in Miami have fallen short (SNOnline: 8/1/16).
Ae. aegypti mosquitoes resist many pesticides, bite during the day, love human houses, and can breed in plant saucers and other small pools of water. Virtually a domestic animal, this species bites people almost exclusively. It’s suspected to be the main spreader of Zika virus, and also does a fine job of infecting people with dengue, chikungunya and yellow fever viruses. Oxitec GM mosquitoes, developed in 2002, would target Floridian pests via a new twist in the decades-old strategy of male sterilization. Mid-20th century entomologists sterilized screwworms by irradiating them and releasing the decoy males in overwhelming clouds. So many wild females mated with these sterile males that eventually the gruesome screwworm pests of livestock disappeared from the United States.
OX513A, with their mix of old-fashioned strategy and newfangled genetic tinkering, has kicked up anti-GMO feeling, even though it’s not the first U.S. approval of testing a GM insect in pest control. That honor goes to pink bollworms in the Southwest in 2009, though their release passed largely unnoticed outside the pest-control community. But when the FDA released a favorable draft opinion in March, saying the GM-mosquito test would probably have “no significant impact” on people or the environment, more than 2,000 people typed comments on the public FDA site. Many were vehemently opposed to the plan, peppering their comments with multiple exclamation points and the occasional “OMG!!!”
Some commenters worried about blood contact from the bite of a GM organism, possible allergies should someone accidentally swallow one and unknown consequences to the environment.
Oxitec posted explanations responding to those fears: Almost all mosquitoes released would be males, which don’t bite; males will die three or four days after release; their offspring are engineered to die without unnatural amounts of tetracycline — a lab-provided supplement — in their diets. Angry public comments, however, largely dismissed these reassurances as corporate-funded research.
Another commenter wondered whether a successful test, driving down the Ae. aegypti population on the Keys, could make room for some other insect menace. That’s a reasonable question, says Phil Lounibos of the University of Florida in Vero Beach. He has studied competition between Ae. aegypti and the relentlessly biting Asian tiger mosquito, Aedes albopictus. These tiger mosquitoes were once rare on the Keys, but he has found that they can take over from Ae. aegypti, in part by sexual deception. Tigers that mate with Ae. aegypti females render the females sterile and have thus conquered other parts of Florida. Even though Ae. aegypti is recognized as a more potent vector for human disease, the tigers can carry many of the same viruses (including Zika), Lounibos warns (SNOnline: 5/16/16).
As far as ecological concerns go, entomologist Bruce Tabashnik of the University of Arizona in Tucson, has no problem with eradicating Ae. aegypti from the Florida Keys or anywhere else in the Americas. “It’s an invasive species,” he says. “There are no ecological ethics violated.”
Tabashnik was part of the research team monitoring the first GM insect release in the United States: sterile male pink bollworms. Males of this invasive pest species that prey on cotton in the Southwest were sterilized by radiation. However, Oxitec had inserted a gene that made them fluoresce red so monitors could tell the friendlies from the wild targets. Tabashnik recalls no particular public outcry over the experiment. It took place in a sparsely populated area and, instead of mosquitoes, involved a kind of moth only a cotton farmer could hate.
So far outrage, or even interest, in other tweaked pest-control animals seems minimal compared with GM-mosquito fever. A proposed test of Oxitec’s GM diamondback moth in New York has inspired fewer comments. Tests of a non-GM but still tinkered-with mosquito — Ae. albopictus developed to carry Wolbachia bacteria that interfere with mating — were first approved in 2012 for release in American Samoa. Later tests have released these bacteria-carrying mosquitoes in California and other sites in the mainland United States.
WASHINGTON — When bacteria lose genes needed to make enzymes for important chemical reactions, defeat isn’t inevitable. Sometimes other enzymes will take on new roles to patch together a work-around chain of reactions that does the job, biologist Shelley Copley reported August 4 at the 2nd American Society for Microbiology Conference on Experimental Microbial Evolution.
Bacteria that can adapt in this way are more likely to survive when living conditions change, passing along these new tricks to their descendants. So studying these biochemical gymnastics is helping scientists to understand how evolution works on a molecular level. Working with different strains of Escherichia coli bacteria, Copley and colleagues deleted genes responsible for making crucial enzymes. The team then watched the microbes replicate for many generations to see how they worked around those limitations.
Most enzymes are highly specialized: They only work well to speed up one type of reaction, the way a key fits only one lock. But some enzymes are more like master keys — they can boost multiple reactions, though they tend to specialize in one. These so-called “promiscuous” enzymes can switch away from their specialty if conditions change.
Copley’s team found that new enzymes would sub in to replace the missing ones. For instance, E. coli missing an enzyme needed to make vitamin B6 synthesized the vitamin using a different set of enzymes. But surprisingly, the promiscuous enzymes didn’t end up directly triggering the same reaction as the enzymes they replaced. Instead, the replacement enzymes cobbled together a different (often longer) work-around series of reactions that ultimately achieved the same function.
“We were rerouting metabolism,” said Copley, of the University of Colorado Boulder.
By modifying the bacteria’s genes and forcing the microbes to survive with a more limited chemical toolkit, Copley’s work gives a more detailed look at the biochemistry underlying evolution, says biologist Gavin Sherlock of Stanford University, who was not involved in the research. Betul Kacar, a synthetic biologist at Harvard University, says promiscuity could also be a window into the past, giving hints about enzymes’ previous roles earlier in evolutionary history. The role that an enzyme jumps in to play in a pinch could have once been its main job. “Trying to understand how novel pathways arise, what kind of mechanistic underlying forces shape those trajectories, is quite essential,” she says.
Bacteria can piece together all sorts of alternative routes in response to missing enzymes, depending on specific environmental conditions, Copley said. The ones that are most successful are more efficient —they have fewer steps, or they yield more of the desired reaction product.
Climate change flaunted its deadly side during the 2003 European heat wave, which killed over 70,000 people across the continent. In London and Paris alone, global warming led to 570 more heat-related deaths than would be expected without human-caused warming, researchers estimate in the July Environmental Research Letters.
Daniel Mitchell of the University of Oxford and colleagues ran thousands of climate simulations with and without the influence of greenhouse gases emitted by humans. The simulations showed that 70 percent of heat-related deaths in central Paris during the heat wave and 20 percent in Greater London could be attributed to climate change. The study is the first to quantify climate change’s role in the event and will inform policy makers on the risks climate change poses, the researchers say.
Even if you’ve never lived in rattlesnake territory, you know what the sound of a snake’s rattle means: Beware! A shake of its rattle is an effective way for a snake to communicate to a potential predator that an attack could result in a venomous bite.
For more than a century, scientists have posited how that rattle might have evolved. The rattle is composed of segments of keratin (the same stuff that makes up human hair), and specialized muscles in a snake’s tail vibrate those segments rapidly to create the rattling sound. The rattlesnake’s rattle is a trait that evolved only once in the past and is now found in only two closely related genera of snakes that live in North and South America. But plenty of other species of snakes also vibrate their tails as a warning to potential predators.
Bradley Allf and colleagues at the University of North Carolina in Chapel Hill think that the tail vibration and the evolution of the rattle might be connected. They gathered 155 snakes of 56 species — 38 species from the Viperidae family, which includes rattlesnakes, and 18 species from the largest snake family, Colubridae — from museums, zoos and private collectors. Working with captive snakes let them control conditions, such as temperature, that can affect tail vibration. With each snake, one of the researchers tried to get it to behave defensively by waving a stuffed animal in front of it. The team videotaped the snakes as they vibrated their tails, or not.
The researchers plotted the snakes’ tail vibration duration and rate against how closely related a species was to rattlesnakes. One group of snakes that lives in the Americas was taken out of the analysis because its tail vibrations were so similar to those of rattlesnakes; it appears that these species are mimicking the dangerous snakes that live near them (not a bad strategy for survival). Among the rest of the snakes analyzed, those that were more closely related had tail behavior that was more similar to that of rattlesnakes.
“Our results suggest that tail vibration by rattleless ancestors of rattlesnakes may have served as the signal precursor to rattlesnake rattling behavior,” the researchers write in the October issue of the American Naturalist. “If ancestral tail vibration was a reliable cue to predators that a bite was imminent, then this behavior could have become elaborated as a defensive signal.”
Allf and his colleagues propose a couple of ways that this could have happened. Perhaps snakes that made noise with their tails were better at startling predators, and this may have prompted such noise-making tail features to spread and eventually become refined into what is now a rattle. Or maybe snakes that shook their tails longer and faster developed calluses of keratin. If these calluses provided better warning, that may have somehow evolved into a rattle.
“Thus, the rattlesnake rattle might have evolved via elaboration of a simple behavior,” they conclude.
