Genetic switch offers clue to why grasses are survival masters

Grasses have top-notch border control to conserve water in their leaves. Now, scientists have identified the genetic switch that makes them such masters at taking in carbon dioxide without losing water. The find might eventually help scientists create more drought-resistant crop plants, the researchers report in the March 17 Science.

Adjustable pores called stomata on the undersides of leaves help plants take in CO2 while minimizing water loss. Like pupils responding to sunlight, plants open and close their stomata in response to changing light, humidity and temperature. Grass stomata can open wider and respond more quickly than those in other plants, which helps grasses photosynthesize more efficiently.
This ability might help explain why grasses grow successfully in so many places on Earth, says Brent Helliker, a plant ecologist at the University of Pennsylvania who wasn’t part of the new study. For instance, grasses are particularly well equipped to deal with the rapidly changing weather and strong winds that can hit plains and prairies.

In most plant stomata, two kidney bean–shaped cells, one on each side of the pore, swell or deflate like balloons to control the size of the opening. But in grass, each of these cells is shaped like a dumbbell instead. And each dumbbell is linked to two other cells called subsidiary cells.
Scientists have long suspected that grasses’ subsidiary cells might give the dumbbells, known as guard cells, an assist by making it easier for them to open and close. But that’s been hard to test in a controlled way.
When a stoma opens, “it’s elbowing its way into the neighbor cells,” says study coauthor Dominique Bergmann, a biologist at Stanford University. “If the neighbors don’t want to move, you’re stuck.” But subsidiary cells have some squish. As guard cells inflate, their neighboring subsidiary cells deflate.
Bergmann and her colleagues mutated a gene called MUTE in purple false brome (Brachypodium distachyon) so that the grass didn’t make the MUTE protein. Without MUTE, plants didn’t make subsidiary cells. And without the helping hand, the plants were less efficient than usual at opening and closing their stomata.

Grasses aren’t the only plants that have the MUTE gene, Bergmann says. But in other plants, the gene provides instructions to help make guard cells, not subsidiary cells. At some point in grasses’ evolution, the MUTE gene took on a function that differs from the rest of the plant kingdom.

Although the new work confirms that subsidiary cells and guard cells work together to make grass stomata more responsive, more research is still needed to understand exactly how subsidiary cells lend a hand. “It would be really nice to show that there’s actually an exchange of ions between the two cell types,” says Michael Blatt, a plant physiologist at the University of Glasgow in Scotland. Sharing ions could incentivize water to flow from one cell type to the other, controlling which one is more inflated.

More responsive stomata may have helped grasses survive during periods when Earth’s climate was warm and dry. “Grasses got lucky,” says study coauthor Michael Raissig, also at Stanford. As Earth’s climate continues to change, Raissig says, these genetic innovations might be exploited to help other plants make it through, too.

Dengue fever spreads in a neighborly way

Dengue is a bit of a homebody. By mapping the spread of the virus across Bangkok, scientists found that infections were most likely to occur within a few minutes’ walk of the home of the first person infected.

Pinpointing where dengue is likely to be transmitted can better focus efforts to stop the spread of the disease, the researchers report in the March 24 Science.

“We often think of transmission and infection as occurring in this ubiquitous, pervasive and amorphous way,” says study coauthor Derek Cummings. But there is a pattern to how dengue spreads. This study, he adds, shows that scientists are “starting to have the tools and methods to really track how infectious diseases move across a population.”
Dengue is a viral disease transmitted by Aedes aegypti mosquitoes and can cause fever and muscle pain so excruciating that it’s also known as “breakbone fever.” In some cases, it can be deadly, resulting in more than 20,000 deaths per year.
Cummings and colleagues looked at both the genetics and locations of about 18,000 cases of dengue from 1994 to 2010 in Thailand, most from the capital Bangkok. If two cases of dengue evolved from the same parent strain of the virus within a season, or about six months, researchers considered the pair to belong to the same transmission chain, which connects dengue infections that spread from one person to the next. About 160 chains occur in Bangkok in a season.

The researchers found that 60 percent of dengue cases within a 200-meter radius in Bangkok were closely related. These infections with a particular dengue strain belonged to the same transmission chain, says Cummings, an epidemiologist at the University of Florida in Gainesville. In contrast, only three percent of cases separated by a greater distance, between one to five kilometers, were from the same transmission chain.
The new study’s combination of genetic and location information provides more details on the ecology of dengue than previous research, says Caroline Buckee, an infectious disease epidemiologist at the Harvard School of Public Health. “It would be great to see this kind of approach become a standard for studies of dengue transmission and epidemiology.”

When the researchers mapped the locations of cases within the same transmission chain, they found that the home of the person originally infected by a mosquito bite, the first link in the chain, is a good indicator of where new cases of dengue will occur.

Thailand’s Ministry of Public Health responds to dengue infections by spraying to kill mosquitoes. “Now, we have some quantitative details to start targeting control technologies,” Cummings says, to better focus spraying in high-priority areas.

The data may also be helpful for a vaccine. Though there is a dengue vaccine licensed for use in Thailand, Cummings says, researchers don’t know yet whether the vaccine will need to be updated with more strains of the virus over time, like the flu shot. Understanding the diversity of dengue strains and how they spread across Bangkok in a season may help researchers address this vaccine concern, he adds.

“Once we can understand these detailed patterns of how things spread, then we might be able to refine how we respond to the pathogen,” Cummings says.

50 years ago, contraception options focused on women

The pill is a sledgehammer approach to contraception…. A second-generation of [drugs] is being designed to do the job without upsetting a woman’s normal cycle of ovulation and menstruation…. A contraceptive administered to the man can be given only for a short time without actually affecting the development of sperm … and, therefore, is not being considered for actual clinical use. —Science News, April 15, 1967

Update
Contraceptives have come a long way since 1967. Women can choose low-dose pills, hormonal rings, implants and intrauterine devices — effective methods that can be less disruptive to normal menstrual cycles. Men have far fewer options, but that may eventually change. A long-acting gel injected into 16 adult male rhesus monkeys’ reproductive tracts completely prevented pregnancy in their partners over one to two breeding periods. The gel works like a vasectomy but is less invasive and can be reversed more easily, researchers report February 7 in Basic and Clinical Andrology.

Parents may one day be morally obligated to edit their baby’s genes

A doctor explains to a young couple that he has screened the pair’s in vitro fertilized embryos and selected those that had no major inheritable diseases. The couple had specified they want a son with hazel eyes, dark hair and fair skin. Then the doctor announces that he has also taken the liberty of eliminating the “burden” of genetic propensities for baldness, nearsightedness, alcoholism, obesity and domestic violence.

The prospective mother replies that they didn’t want those revisions. “I mean diseases, yes, but …” Her husband jumps in to say, “We were just wondering if it’s good to leave a few things to chance.”
But the doctor reminds the would-be parents why they came to him in the first place. They want to give their child “the best possible start.”

That’s a scene from the movie Gattaca, which premiered 20 years ago in October. But thanks to recent advances in gene-editing tools such as CRISPR/Cas9, genetic manipulation of human embryos is becoming reality.

Soon, designer babies like those described in the film may even become morally mandatory, some ethicists say.

Gattaca’s narrator tells us that such genetic manipulation of in vitro fertilized embryos has become “the natural way of giving birth” in the near future portrayed in the film. It has also created an underclass of people whose parents didn’t buy those genetic advantages for their children.
Until recently, that sort of fiddling with human DNA was only science fiction and allegory, a warning against a new kind of eugenics that could pit the genetic haves and have-nots against each other. At a symposium sponsored by the Hastings Center on October 26 before the World Conference of Science Journalists in San Francisco, ethicists and journalists explored the flip side of that discussion: whether parents have a moral obligation to make “better” babies through genetic engineering. Technology that can precisely change a baby’s genes is quickly becoming reality. This year, scientists reported using CRISPR/Cas9 in viable human embryos to fix mutations that cause heart and blood disorders. CRISPR/Cas9 acts as a molecular scissors that relatively easily and precisely manipulates DNA. Scientists have honed and developed the tool in the roughly five years it has been around, creating myriad “CRISPR” mice, fish, pigs, cows, plants and other creatures. Its use in human embryos has been hotly debated. Should we or shouldn’t we?

For many people, the fear of a class of genetically enhanced people is reason enough not to tinker with the DNA of the human germline — eggs, sperm, embryos and the cells that give rise to eggs and sperm. By all means, correct diseases, these folks say, but don’t add extras or meddle with characteristics that don’t have anything to do with health. A panel of ethicists convened by the U.S. National Academies of Medicine and Science also staked out that position in February, ruling that human germline engineering might someday be permissible for correcting diseases, but only if there are no alternatives and not for enhancements.

But the question “should we?” may not matter much longer, predicted the Hastings Center’s Josephine Johnston at the symposium. As science advances and people become more comfortable with gene editing, laws prohibiting tinkering with embryos will fall, she said, and it will be up to prospective moms and dads to decide for themselves. “Will editing a baby’s genes be mandatory, the kind of thing you’re supposed to do?”

For Julian Savulescu, an ethicist at the University of Oxford, the answer is yes. Parents are morally obligated to take steps to keep their children healthy, he says. That includes vaccinating them and giving them medicine when they’re ill. Genetic technologies are no different, he argues. If these techniques could make children resistant to infections, cancer or diabetes, then parents have an obligation to use them, he says.

For now, he cautions, CRISPR’s safety and efficacy haven’t been established, so parents shouldn’t subject their children to the risks. He also points out that this sort of editing would also require in vitro fertilization, which is prohibitively costly for many people. (And couples could pretty much forget about having the perfect baby through sexual intercourse. Designer darlings would have to be created in the lab.)

But someday, possibly soon, gene editing could become a viable medical intervention. “If CRISPR were safe and not excessively costly, we have a moral obligation to use it to prevent and treat disease,” Savulescu says.

Using gene editing to cure genetic diseases is something retired bioethicist Ronald Green of Dartmouth College can get behind. “I fully support the reproductive use of gene-editing technology for the prevention and elimination of serious genetic diseases,” Green said at the symposium. “If we could use gene editing to remove the sequences in an embryo that cause sickle cell disease or cystic fibrosis, I would say not only that we may do so, but in the case of such severe diseases, we have a moral obligation to do so.”

But that’s where a parent’s obligation stops, Green said. Parents and medical professionals aren’t required to enhance health “to make people who are better than well,” he said.

Savulescu, however, would extend the obligation to other nondisease conditions that could prevent a kid from having a full set of opportunities in life. For instance, children with poor impulse control may have difficulty succeeding in school and life. The drug Ritalin is sometimes prescribed to such kids. “If CRISPR could do what Ritalin does and improve impulse control and give a child a greater range of opportunities,” he says, “then I’d have to say we have the same moral obligation to use CRISPR as we do to provide education, to provide an adequate diet or to provide Ritalin.”

Green rejected the idea that parents should, or even could, secure a better life for their kids through genetic manipulation. Scientists haven’t identified all the genes that contribute to good lives — and there are plenty of factors beyond genetics that go into making someone happy and successful. Already, Green said, “the healthy natural human genome has enough variety in it to let any child successfully navigate the world and fulfill his or her own vision of happiness.” (A version of his remarks was posted on the Hastings Center’s Bioethics Forum.)

Many traits that would help a person make more money or have an easier life are associated with social prejudices and discrimination, says Marcy Darnovsky, the executive director of the Center for Genetics and Society in Berkeley, Calif. People who are taller and fair-skinned tend to make more money. If parents were to engineer their children to have such traits, “I think we would be inscribing those kinds of social prejudices in biology,” she says. “We get to very troubled waters very quickly as a society once we start down that road.”

Creating a class of “genobility,” as Green calls genetically enhanced people, would increase already staggering levels of inequality, Darnovsky says. That, says Savulescu, “is the Gattaca objection I often get.”

Yes, he acknowledges, “it could create even greater inequalities, there’s no doubt about that.” Whenever money is involved, people who have more of it can afford better treatments, diets and healthier lifestyles — and disparities will exist. “However, this is not inevitable,” Savulescu says. Countries with national health care systems could provide such services for free. Such measures could even correct natural inequalities, he argues.

Johnston worries that genetic manipulation could change family dynamics. Parents might be disappointed if their designer baby doesn’t turn out as desired. That’s a variation of the old problem of unfulfilled parental expectations, Savulescu says. “It’s a problem that deserves attention, but it’s not a problem that deserves banning CRISPR,” he says.

How oral vaccines could save Ethiopian wolves from extinction

Deep in the Bale Mountains of Ethiopia, wildlife workers trek up above 9,800 feet to save some of the world’s most rare carnivores, Ethiopian wolves.

“It’s cold, tough work,” says Eric Bedin, who leads the field monitoring team in its uphill battle.

In this sparse, sometimes snowy landscape, the lanky and ginger-colored wolves (Canis simensis) reign as the region’s apex predators. Yet the combined threats of rabies, canine distemper and habitat reduction have the animals cornered.

Bedin and his colleagues, traveling by horse and on foot through dramatically shifting temperatures and weather, track these solitary hunters for weeks at a time. Team members know every wolf in most packs in these mountains. The team has vaccinated some wolves against rabies, only to have hopes dashed when the animals died of distemper months later.
“These guys work their asses off to protect these wolves,” says Claudio Sillero, a conservation biologist at the University of Oxford who heads up the Ethiopian Wolf Conservation Programme, of which the field monitoring team is an integral part. Down the line, humans stand to benefit from all this work too.

Sillero and his colleagues have been at this for 30 years. They’ve seen four major outbreaks of rabies alone, each leaving dozens of carcasses across the highlands and cutting some populations by as much as 75 percent.

Today, fewer than 500 Ethiopian wolves exist — around half of them in the Bale Mountains. A new oral rabies vaccine program aims to give the endangered animals a fighting chance. It may be their best hope for survival, Sillero says.

Later this year, if all goes well, oral vaccines hidden in hunks of goat meat will be scattered across wolf ranges and eaten by the animals. One dose every two years should bolster immunity against rabies among these iconic animals immortalized on several of their country’s postage stamps.
One Health
Vaccinating endangered animals en masse in the wild is rarely attempted. Making the case for vaccination takes years of testing. And even when the case is strong for stepping in, the tools needed to vaccinate wildlife aren’t often available, says Tonie Rocke, an epizootiologist with the U.S. Geological Survey in Madison, Wis. On the opposite side of the globe from Bale, on North America’s Great Plains, Rocke’s lab is testing an oral vaccine to protect prairie dogs and endangered ferrets from plague.
A recent synergy has made these new oral vaccine efforts possible: improvements in vaccine technology (developed for humans and domesticated animals) and growing public and scientific interest in “One Health.” The conservation buzzword refers to efforts to help one species that also benefit others, including humans.

The researchers pushing for a green light in Ethiopia point to the one shining success in oral vaccines for wild animals, and to its One Health benefits. From 1978 to 2010, oral vaccines sprinkled across parts of Europe eliminated rabies in red foxes. Europe’s rabies cases in humans and other animals dropped by 80 percent from 1984 to 2014. But rabies is still common in certain parts of the world, including Ethiopia. Worldwide, more than 59,000 people die from the disease each year.

Successes on the plateaus of Bale and the prairies of North America could open the door for other vaccines to protect threatened species. Vaccines against Ebola in great apes and white-nose syndrome in bats are in the works.

But introducing vaccines into natural environments is a hard sell and can come with controversy and unexpected consequences.
A last resort
To the average U.S. vet or dog owner, vaccination is a no-brainer. But for endangered species, the stakes are high. Some conservationists are reluctant to intervene with disease-preventing vaccines in the wild, says Karen Laurenson, an epidemiologist and veterinarian with the Frankfurt Zoological Society.

Disease has its place in ecosystems. It can control population levels and put pressure on species to develop natural resistance, says Laurenson, who started working with the wolf project in the mid-1990s. Using a vaccine to take a disease out of the mix could leave a population vulnerable to future outbreaks should the vaccine become ineffective or stop being used. In an ecosystem with multiple power players, one vaccinated predator could gain an unnatural advantage over its competitors.

Some vaccines also bring direct risks. Injectable vaccines often require trapping the animal — a costly endeavor that’s stressful and dangerous for both wild animals and the humans doing the vaccinating. Oral vaccines could be scooped up and eaten by other animals. Plus, for an oral or injectable attenuated vaccine, which contains a living but harmless version of a virus, there’s a slim possibility that evolutionary pressure could eventually drive the virus, now distributed through the population, to become lethal again.

Because room for error is slim for a species on the brink of extinction, most instances of vaccine use have been limited to emergency responses during ongoing outbreaks.

Projects that don’t go well can have lasting repercussions. In 1990, researchers tried to vaccinate some packs of endangered African wild dogs (Lycaon pictus) in Tanzania and Kenya against rabies, assuming the disease was behind a recent dip in numbers. Every dog in the study died. The stress of getting vaccinated, shot by dart from a distance, may have made the dogs more susceptible to disease, though that theory was never proven. The incident increased skepticism about vaccines and caused some African countries to tighten vaccine regulations. “It left a terrible legacy,” says veterinarian Richard Kock of the University of London.

The long game
The uphill battle faced by Sillero’s team involves more than the challenges of canvassing the Ethiopian highlands. Making a case to government officials that oral vaccines are necessary conservation tools took decades of fieldwork, genetic testing and meetings upon meetings. “The credit really goes to Claudio and the others for persisting,” Laurenson says. “Even when the doors have been shut, sometimes they’ve kept banging.”

Sillero arrived in Ethiopia in 1987 to study the wolves. A rabies outbreak hit in late 1989. Just as it does in dogs and humans, the disease attacks a wolf’s brain, causing aggressive behavior and, eventually, death. Canine distemper appeared in 1992. Marked by severe diarrhea, vomiting and coughing, the disease appears to hit wolves harder than dogs, Sillero says. The Ethiopian packs have faced four more major flare-ups of rabies and two of distemper. Two of the eight populations of wolves he came to study have gone extinct in that time.

“This is a human-caused problem, not a natural dynamic,” Laurenson says. Each year, shepherds and farmers move higher up into the wolves’ habitat, bringing grazing livestock. These people also bring domesticated dogs — the primary carriers of rabies and canine distemper (SN Online: 9/30/16). In one area of Ethiopia, wolf habitat shrunk by 34 percent from 1985 to 2003. Islands of wolf populations persist in remote highland areas surrounded by oceans of free-ranging dogs.

Vaccinating the wolves was plan B, after the lower-risk approach of vaccinating domestic dogs didn’t cut it. Because the dogs roam far and wide, dog vaccination programs didn’t reach enough animals to generate prolonged protection and prevent outbreaks in wolves. “I’m sure we were improving the situation and reducing the chance of spillovers in wild carnivores, but we weren’t preventing them altogether,” Sillero says.

Going with oral vaccines was plan C. In 2003, the government approved use of an injectable vaccine only in response to outbreaks. Sillero’s team first had to collect samples and send them to international labs to confirm that an outbreak was happening. The researchers were always behind. An oral option that proactively protects the animals started to sound like a smart way to go.

Deliver the dose
On paper, the wolves look like good candidates for an oral vaccine intervention. Few other animals brave the highlands habitat, so the odds are low that a vaccine distributed in bait would get eaten by the wrong creatures. And not vaccinating is arguably riskier than making the effort. Consecutive rabies and distemper outbreaks recently cut one of the smallest known wolf populations down to two individuals, Sillero’s team reported in December in Emerging Infectious Diseases.

The Ethiopian team chose to test an oral rabies vaccine, called SAG2, that had been used successfully in red foxes. Twenty million baits had been dropped across Europe with no vaccine-induced rabies cases or reported deaths. SAG2 also passed safety tests in a slew of different species, including African wild dogs. “That work was absolutely fundamental,” Laurenson says.
Getting the vaccine into the animals is the trickiest part. Animals have to bite into the bait to puncture an internal packet that contains the vaccine, rather than swallow the bait whole. “You’ve got to make the bait such that the [wolf] would chew it,” says Anthony Fooks, a vaccine researcher who runs a U.K. government lab that handles sample tests for the wolf project.

So Sillero and his team launched a series of pilot studies of an oral SAG2. “We set up cafeteria-type experiments, with different baits and delivery methods,” Sillero says. The researchers dropped 445 baits in locations around Bale. Hiding the vaccine in goat meat and distributing the goods at night worked better than other options, the team reported in 2016 in Vaccine. Of 21 wolves trapped a couple of weeks later, 14, or 67 percent, carried a biomarker showing the vaccine was in the wolf’s system. Of those, 86 percent had developed immunity against rabies. The impact on other wildlife was low: Only a few raptors snatched up vaccines meant for the wolves.

With all that data in hand, Sillero’s team finally won over Ethiopia’s Wildlife Conservation Authority in December, receiving an official thumbs-up to move forward. This month, 4,000 vaccines arrived; the mass vaccination program could get off the ground this summer.

It’ll be the first mass oral vaccination program to target an endangered species in the wild. The basic plan: Distribute the oral vaccines at night once every two years, vaccinate at least 40 percent of a chosen wolf population and use motion-sensing cameras to see if each pack’s high-ranking males and females — the primary pup producers — take the bait. It’s important to keep the top producers healthy.
Drones and peanut butter
Having a readily available oral vaccine for the wolves was a lucky break for the researchers in Ethiopia. A research team in the United States had no such luck. Tonie Rocke and her colleagues had to develop their own oral plague vaccine for prairie dogs. The team devised a raccoon poxvirus that produces plague proteins once inside the prairie dog body. The proteins train the immune system to fight the plague-causing Yersinia bacteria.

Saving plague-ridden prairie dogs (Cynomys spp.) is an indirect way to protect the real target: an endangered predator, black-footed ferrets (Mustela nigripes) of the Great Plains. The ferrets survive on a diet of mostly prairie dogs and had nearly gone extinct in the 1970s due to centuries of habitat loss, prey declines and plague.
On top of captive breeding and reintroduction programs to keep the ferret species afloat, the U.S. Fish and Wildlife Service traps and vaccinates wild ferrets directly. But it’s not enough.

Rocke and her colleagues went ahead and developed a peanut butter–flavored oral plague vaccine. They distributed it by drones and four-wheelers in small test plots in seven states to limit prairie dog carriers. (Plague can threaten prairie dog populations too, so everybody wins.)

Last June, the researchers published the results of these successful small-scale field trials in EcoHealth. A prairie dog’s odds of surviving in plague-ridden areas just about doubled. And the peanut butter pellets were as good at reducing plague levels as traditional insecticides that kill plague-carrying fleas. It’s unclear just how many prairie dogs in colonies need to be vaccinated to protect the ferrets from plague.

Getting the vaccine approved wasn’t as tortuous as it has been in Ethiopia. Collaborators at Colorado Parks and Wildlife already had a cheap way to make the baits, and in 2017, Colorado Serum Company licensed the product through the U.S. Department of Agriculture.

This year, Rocke hopes to conduct larger-scale field trials to determine the levels of immunity required for success in a mass vaccination. Ultimately, the application will be limited — just selected populations of prairie dogs that are either in ferret territory or endangered themselves, such as the Utah prairie dog (C. parvidens). Plague infects a handful of humans and domesticated animals each year as well, and the team is looking into using the vaccine in areas where humans spend time, like national parks.
Encouraging others
Success for one species could be good news for others. Similar preventative strategies might work in other threatened animals, including other members of the dog family dealing with rabies and ungulates like zebras at risk of catching anthrax while grazing. Researchers are testing preventative vaccines to protect wild Hawaiian monk seals from a seal-specific distemper virus.

Oral vaccines aren’t the only nontraditional delivery method. Rocke’s lab is working on a topical vaccine against white-nose syndrome, which threatens bats (SN Online: 3/31/16), and one to combat rabies in common vampire bats (Desmodus rotundus). Vampire bats in particular nuzzle each other during social grooming. “It’s an easy way to get the vaccine distributed amongst members of the colony,” Rocke says.

In October in PLOS Neglected Tropical Diseases, her lab reported that the vaccine works in captured big brown bats (Eptesicus fuscus), but it still hasn’t been tested in vampire bats, key rabies carriers in South America. Rocke and colleagues hope to start trials in vampire bats this year in Mexico and Peru.

Great apes can fall victim to some of the same pathogens as humans, such as measles and Ebola. In March 2017 in Scientific Reports, a research team published successful lab tests of an oral vaccine against Ebola in captive chimpanzees (Pan troglodytes). The vaccine relies on the rabies virus to deliver Ebola proteins that elicit an immune response in chimps, but it hasn’t been tested in the field yet.

Such a vaccine should be used selectively, Kock says. Vaccinating great apes against Ebola in preserves where the animals might encounter human carriers makes sense. But vaccinating gorillas across large forests in the Congo “is just silly,” he says.

Protecting isolated species on the brink of extinction is where vaccines could do the most good. Endangered Amur tigers (Panthera tigris altaica) have been hit hard by canine distemper, their numbers falling to around 500 individuals in their Siberian habitat. Vaccines have been debated as a potential option and injectables have been tested in captive tigers.

Sillero doesn’t expect to see any oral options developed against distemper in the future, because there’s not a big economic incentive. Unlike rabies, the disease doesn’t cause problems in humans. So he’s working with the shots available. Genetic analyses of locally circulating distemper strains published in July 2017 suggest the injectable distemper vaccines should work for the Ethiopian wolves, Fooks says. Sillero’s team is testing one in the field now. Preliminary data suggest the shot elicits a good immune response.
What’s good for the wildlife
Greater awareness about the overlap of human, livestock and wildlife health on shared lands underlies many of these projects. Ethiopia has one of the highest rabies death rates among humans in the world, and lowering the disease prevalence in any animals that humans come in contact with has benefit.

“This will have positive impacts for the threatened animals, for the welfare of domestic dogs and livestock, and for the health and finance of the human community,” Sillero argues. The One Health mind-set is also behind programs run in a few areas of Ethiopia’s northern highlands, to teach local farmers how to build more efficient stoves that require less firewood, and thus, less foraging in wolf territory.

“Vaccination and eradication of things like rabies … needs a whole of society approach,” Kock says. “It cannot be done piecemeal.”

For Ethiopia’s impending oral vaccine launch that has been so many years in the making, Sillero is optimistic. But he’s still holding his breath.

“I have to see the wolves taking up the baits before I can congratulate the team,” he says. “But I think we’re nearly there.”

Volcanic sulfur may make barn owls grow redder feathers

Life on a volcanic isle appears to give barn owls a blush of red-brown plumage.

The high-sulfur environment on such islands influences the birds’ coloration, researchers report March 13 in the Journal of Biogeography. Darker feathers might also play a role in detoxifying harmful sulfur-based chemicals or help the owls blend in better with the islands’ humid, shadowy forest backdrop. The findings are among the first evidence that environmental sources of sulfur — such as the soil — can influence the color of integument like fur or feathers.
Barn owls (Tyto alba) are found across most continents and on many islands. The owls’ plumage varies considerably across the globe, with bellies ranging from almost completely white to a much darker copper color.

In 2021, evolutionary ecologist Andrea Romano and his colleagues discovered that barn owls on some islands are paler than mainland populations. “However, such a difference disappears on small and remote islands and archipelagos, where in some cases, owls are darker than the continental ones,” says Romano, of the University of Milan.

The researchers wondered if there was something special about these smaller, more isolated islands that was causing a color pattern reversal in the owls: sulfur. Many of the remote islands are volcanic in origin, with volcanoes loading the air and soil with sulfur dioxide. Sulfur also has a crucial role in the development of some melanin pigments. For instance, pheomelanin — which is biochemically built using sulfur compounds — imparts a reddish hue in vertebrate soft tissues, while eumelanin, which creates blacks and dark browns, doesn’t rely on sulfur.

Some studies have linked sulfur-rich diets or artificial sulfur sources like pollution to plumage and fur color, Romano says. So the team hypothesized that a volcanic environment full of sulfur might encourage the owls to produce more pheomelanin, making their plumage darker.

The researchers examined the preserved, feather-covered skins of more than 2,000 barn owl museum specimens from dozens of island groups. They scored the relative redness of the owls’ belly plumage, finding an average color for each geographic location. On islands with sulfur-rich volcanic soils or recently active volcanoes — such as Sulawesi in Indonesia or the Canary Islands — the owls had darker, redder plumage than those on nonvolcanic islands such as Tasmania, the team found.

The influence of volcanic sulfur on barn owl colors explains less than 10 percent of the color variation, the researchers estimate. Other inputs like genetics play a major role. For instance, one gene called MC1R is responsible for as much as 70 percent of the color variation, says Thomas Kvalnes, an ecoevolutionary biologist at the Norwegian Institute for Nature Research in Trondheim who was not involved with this study.

“Still there is variation left to explain, both within and between populations,” Kvalnes says. “This is where different environmental factors need to be taken into account.”
It’s possible that sulfur-driven colors provide benefits to the owls, Romano says. Volcanic islands are often thick with vegetation supported by dark, fertile soil. Darker feathers might help the predatory owls disappear into their forest surroundings. The owls might also avoid the toxic effect of high sulfur exposure by shuttling a glut of sulfur into making more pheomelanin. Melanin has been previously tied to detoxifying pollutants in sea snakes, for instance (SN: 8/14/17).

Among birds, the connection between plumage color and volcanic sulfur might not be limited to just barn owls. Multiple bird species in Iceland, for example, are getting a pheomelanin boost from environmental sulfur, another group reported February 25 in the Journal of Ornithology. But some of these are migratory birds, Kvalnes points out, which dilutes the link between the local setting and the level of pigmentation.

It’s also possible the volcanic sulfur–pheomelanin relationship is even more widespread in vertebrates. “Studies on different species are highly needed to confirm whether this pattern is general,” Romano says. “Theoretically, however, the same process should apply to at least other birds and mammals.”

Romano is also interested in investigating how the sulfur is moving from the environment into the plumage pigmentation. Is it through the diet? The water? Maybe the air? “We know nothing about how sulfur reaches the soft tissues of this top predator,” he says.

The biggest planet orbiting TRAPPIST-1 doesn’t appear to have an atmosphere

A rocky planet that circles a small star nearly 40 light-years from Earth is hot and has little or no atmosphere, a new study suggests. The finding raises questions about the possibility of atmospheres on the other orbs in the planetary system.

At the center of the system is the red dwarf star dubbed TRAPPIST-1; it hosts seven known planets with masses ranging from 0.3 to 1.4 times Earth’s, a few of which could hold liquid water (SN: 2/22/17; 3/19/18). The largest, TRAPPIST-1b, is the closest to its parent star and receives about four times the radiation Earth receives from the sun, says Thomas Greene, an astrobiologist at NASA’s Ames Research Center at Moffett Field, Calif.
Like all other planets in the system, TRAPPIST-1b is tidally locked, meaning that one side of the planet always faces the star, and one side looks away. Calculations suggest that if the stellar energy falling on TRAPPIST-1b were distributed around the planet — by an atmosphere, for example — and then reradiated equally in all directions, the planet’s surface temperature would be around 120° Celsius.

But the dayside temperature of the planet is actually around 230° C, Greene and colleagues report online March 27 in Nature. That, in turn, suggests that there’s little or no atmosphere to carry heat from the perpetually sunlit side of the planet to the dark side, the team argues.

To take TRAPPIST-1b’s temperature, Greene and his colleagues used the James Webb Space Telescope to observe the planet in a narrow band of infrared wavelengths five times in 2022. Because the observations were made just before and after the planet dodged behind its parent star, astronomers could see the fully lit face of the planet, Greene says.

The team’s results are “the first ‘deep dive’ look at this planet,” says Knicole Colon, an astrophysicist at NASA’s Goddard Space Flight Center in Greenbelt, Md, who was not involved with the study. “With every observation, we expect to learn something new,” she adds.

Astronomers have long suggested that planets around red dwarf stars might not be able to hold onto their atmospheres, largely because such stars’ frequent and high-energy flares would blast away any gaseous shroud they might have during their early years (SN: 12/20/22). Yet there are some scenarios in which such flares could heat up a planet’s surface and drive volcanism that, in turn, yields gases that could help form a new atmosphere.

“To be totally sure that this planet has no atmosphere, we need many more measurements,” says Michaël Gillon, an astrophysicist at the University of Liège in Belgium who was not part of the new study. It’s possible that when observed at a wider variety of wavelengths and from other angles, the planet could show signs of a gaseous shroud and thus possibly hints of volcanism.

Either way, says Laura Kriedberg, an astronomer at the Max Planck Institute for Astronomy in Heidelberg, Germany, who also did not participate in the study, the new result “definitely motivates detailed study of the cooler planets in the system, to see if the same is true of them.”

In mice, anxiety isn’t all in the head. It can start in the heart

When you’re stressed and anxious, you might feel your heart race. Is your heart racing because you’re afraid? Or does your speeding heart itself contribute to your anxiety? Both could be true, a new study in mice suggests.

By artificially increasing the heart rates of mice, scientists were able to increase anxiety-like behaviors — ones that the team then calmed by turning off a particular part of the brain. The study, published in the March 9 Nature, shows that in high-risk contexts, a racing heart could go to your head and increase anxiety. The findings could offer a new angle for studying and, potentially, treating anxiety disorders.
The idea that body sensations might contribute to emotions in the brain goes back at least to one of the founders of psychology, William James, says Karl Deisseroth, a neuroscientist at Stanford University. In James’ 1890 book The Principles of Psychology, he put forward the idea that emotion follows what the body experiences. “We feel sorry because we cry, angry because we strike, afraid because we tremble,” James wrote.

The brain certainly can sense internal body signals, a phenomenon called interoception. But whether those sensations — like a racing heart — can contribute to emotion is difficult to prove, says Anna Beyeler, a neuroscientist at the French National Institute of Health and Medical Research in Bordeaux. She studies brain circuitry related to emotion and wrote a commentary on the new study but was not involved in the research. “I’m sure a lot of people have thought of doing these experiments, but no one really had the tools,” she says.

Deisseroth has spent his career developing those tools. He is one of the scientists who developed optogenetics — a technique that uses viruses to modify the genes of specific cells to respond to bursts of light (SN: 6/18/21; SN: 1/15/10). Scientists can use the flip of a light switch to activate or suppress the activity of those cells.
In the new study, Deisseroth and his colleagues used a light attached to a tiny vest over a mouse’s genetically engineered heart to change the animal’s heart rate. When the light was off, a mouse’s heart pumped at about 600 beats per minute. But when the team turned on a light that flashed at 900 beats per minutes, the mouse’s heartbeat followed suit. “It’s a nice reasonable acceleration, [one a mouse] would encounter in a time of stress or fear,” Deisseroth explains.

When the mice felt their hearts racing, they showed anxiety-like behavior. In risky scenarios — like open areas where a little mouse might be someone’s lunch — the rodents slunk along the walls and lurked in darker corners. When pressing a lever for water that could sometimes be coupled with a mild shock, mice with normal heart rates still pressed without hesitation. But mice with racing hearts decided they’d rather go thirsty.

“Everybody was expecting that, but it’s the first time that it has been clearly demonstrated,” Beyeler says.
The researchers also scanned the animals’ brains to find areas that might be processing the increased heart rate. One of the biggest signals, Deisseroth says, came from the posterior insula (SN: 4/25/16). “The insula was interesting because it’s highly connected with interoceptive circuitry,” he explains. “When we saw that signal, [our] interest was definitely piqued.”

Using more optogenetics, the team reduced activity in the posterior insula, which decreased the mice’s anxiety-like behaviors. The animals’ hearts still raced, but they behaved more normally, spending some time in open areas of mazes and pressing levers for water without fear.
A lot of people are very excited about the work, says Wen Chen, the branch chief of basic medicine research for complementary and integrative health at the National Center for Complementary and Integrative Health in Bethesda, Md. “No matter what kind of meetings I go into, in the last two days, everybody brought up this paper,” says Chen, who wasn’t involved in the research.

The next step, Deisseroth says, is to look at other parts of the body that might affect anxiety. “We can feel it in our gut sometimes, or we can feel it in our neck or shoulders,” he says. Using optogenetics to tense a mouse’s muscles, or give them tummy butterflies, might reveal other pathways that produce fearful or anxiety-like behaviors.

Understanding the link between heart and head could eventually factor into how doctors treat panic and anxiety, Beyeler says. But the path between the lab and the clinic, she notes, is much more convoluted than that of the heart to the head.

An antibody injection could one day help people with endometriosis

An experimental treatment for endometriosis, a painful gynecological disease that affects some 190 million people worldwide, may one day offer new hope for easing symptoms.

Monthly antibody injections reversed telltale signs of endometriosis in monkeys, researchers report February 22 in Science Translational Medicine. The antibody targets IL-8, a molecule that whips up inflammation inside the scattered, sometimes bleeding lesions that mark the disease. After neutralizing IL-8, those hallmark lesions shrink, the team found.

The new treatment is “pretty potent,” says Philippa Saunders, a reproductive scientist at the University of Edinburgh who was not involved with work. The study’s authors haven’t reported a cure, she points out, but their antibody does seem to have an impact. “I think it’s really very promising,” she says.

Many scientists think endometriosis occurs when bits of the uterine lining — the endometrium — slough off during menstruation. Instead of exiting via the vagina, they voyage in the other direction: up through the fallopian tubes. Those bits of tissue then trespass through the body, sprouting lesions where they land. They’ll glom onto the ovaries, fallopian tubes, bladder and other spots outside of the uterus and take on a life of their own, Saunders says.
The lesions can grow nerve cells, form tough nubs of tissue and even bleed during menstrual cycles. They can also kick off chronic bouts of pelvic pain. If you have endometriosis, you can experience “pain when you urinate, pain when you defecate, pain when you have sex, pain when you move around,” Saunders says. People with the disease can also struggle with infertility and depression, she adds. “It’s really nasty.”
Once diagnosed, patients face a dearth of treatment options — there’s no cure, only therapies to alleviate symptoms. Surgery to remove lesions can help, but symptoms often come back.

The disease affects at least 10 percent of girls, women and transgender men in their reproductive years, Saunders says. And people typically suffer for years — about eight on average — before a diagnosis. “Doctors consider menstrual pelvic pain a very common thing,” says Ayako Nishimoto-Kakiuchi, a pharmacologist at Chugai Pharmaceutical Co. Ltd. in Tokyo. Endometriosis “is underestimated in the clinic,” she says. “I strongly believe that this disease has been understudied.”

Hormonal drugs that stop ovulation and menstruation can also offer relief, says Serdar Bulun, a reproductive endocrinologist at Northwestern University Feinberg School of Medicine in Chicago not involved with the new study. But those drugs come with side effects and aren’t ideal for people trying to become pregnant. “I see these patients day in and day out,” he says. “I see how much they suffer, and I feel like we are not doing enough.”

Nishimoto-Kakiuchi’s team engineered an antibody that grabs onto the inflammatory factor IL-8, a protein that scientists have previously fingered as one potential culprit in the disease. The antibody acts like a garbage collector, Nishimoto-Kakiuchi says. It grabs IL-8, delivers it to the cell’s waste disposal machinery, and then heads out to snare more IL-8.

The team tested the antibody in cynomolgus monkeys that were surgically modified to have the disease. (Endometriosis rarely shows up spontaneously in these monkeys, the scientists discovered previously after screening more than 600 females.) The team treated 11 monkeys with the antibody injection once a month for six months. In these animals, lesions shriveled and the adhesive tissue that glues them to the body thinned out, too. Before this study, Nishimoto-Kakiuchi says, the team didn’t think such signs of endometriosis were reversible.
Her company has now started a Phase I clinical trial to test the safety of therapy in humans. The treatment is one of several endometriosis therapies scientists are testing (SN: 7/19/19) . Other trials will test new hormonal drugs, robot-assisted surgery and behavioral interventions.

Doctors need new options to help people with the disease, Saunders says. “There’s a huge unmet clinical need.”

Half of all active satellites are now from SpaceX. Here’s why that may be a problem

SpaceX’s rapidly growing fleet of Starlink internet satellites now make up half of all active satellites in Earth orbit.

On February 27, the aerospace company launched 21 new satellites to join its broadband internet Starlink fleet. That brought the total number of active Starlink satellites to 3,660, or about 50 percent of the nearly 7,300 active satellites in orbit, according to analysis by astronomer Jonathan McDowell using data from SpaceX and the U.S. Space Force.
“These big low-orbit internet constellations have come from nowhere in 2019, to dominating the space environment in 2023,” says McDowell, of the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass. “It really is a massive shift and a massive industrialization of low orbit.”

SpaceX has been launching Starlink satellites since 2019 with the goal of bringing broadband internet to remote parts of the globe. And for just as long, astronomers have been warning that the bright satellites could mess up their view of the cosmos by leaving streaks on telescope images as they glide past (SN: 3/12/20).

Even the Hubble Space Telescope, which orbits more than 500 kilometers above the Earth’s surface, is vulnerable to these satellite streaks, as well as those from other satellite constellations. From 2002 to 2021, the percentage of Hubble images affected by light from low-orbit satellites increased by about 50 percent, astronomer Sandor Kruk of the Max-Planck Institute for Extraterrestrial Physics in Garching, Germany, and colleagues report March 2 in Nature Astronomy.

The number of images partially blocked by satellites is still small, the team found, rising from nearly 3 percent of images taken between 2002 and 2005 to just over 4 percent between 2018 and 2021 for one of Hubble’s cameras. But there are already thousands more Starlink satellites now than there were in 2021.

“The fraction of [Hubble] images crossed by satellites is currently small with a negligible impact on science,” Kruk and colleagues write. “However, the number of satellites and space debris will only increase in the future.” The team predicts that by the 2030s, the probability of a satellite crossing Hubble’s field of view any time it takes an image will be between 20 and 50 percent.
The sudden jump in Starlink satellites also poses a problem for space traffic, says astronomer Samantha Lawler of the University of Regina in Canada. Starlink satellites all orbit at a similar distance from Earth, just above 500 kilometers.

“Starlink is the densest patch of space that has ever existed,” Lawler says. The satellites are constantly navigating out of each other’s way to avoid collisions (SN: 2/12/09). And it’s a popular orbital altitude — Hubble is there, and so is the International Space Station and the Chinese space station.
“If there is some kind of collision [between Starlinks], some kind of mishap, it could immediately affect human lives,” Lawler says.

SpaceX launches Starlink satellites roughly once per week — it launched 51 more on March 3. And they’re not the only company launching constellations of internet satellites. By the 2030s, there could be 100,000 satellites crowding low Earth orbit.

So far, there are no international regulations to curb the number of satellites a private company can launch or to limit which orbits they can occupy.

“The speed of commercial development is much faster than the speed of regulation change,” McDowell says. “There needs to be an overhaul of space traffic management and space regulation generally to cope with these massive commercial projects.”