Genetic methods for counting new species may be a little too good at their jobs, a new study suggests.

Computer programs that rely on genetic data alone split populations of organisms into five to 13 times as many species as actually exist, researchers report online January 30 in Proceedings of the National Academy of Sciences. These overestimates may muddy researchers’ views of how species evolve and undermine conservation efforts by claiming protections for species that don’t really exist, say computational evolutionary biologist Jeet Sukumaran and evolutionary biologist L. Lacey Knowles.
The lesson, says Knowles, “is that we shouldn’t use genetic data alone” to draw lines between species.

Scientists have historically used data about organisms’ ecological distribution, appearance and behavior to classify species. But the number of experts in taxonomy is dwindling, and researchers have turned increasingly to genetics to help them draw distinctions. Large genetic datasets and powerful computer programs can quickly sort out groups that have become or are in the process of becoming different species. That’s especially important in analyzing organisms for which scientists don’t have much ecological data, such as insects in remote locations or recently extinct organisms.

Knowles and Sukumaran, both of the University of Michigan in Ann Arbor, examined a commonly used computer analysis method, called multispecies coalescent, which picks out genetic differences among individuals that have arisen recently in evolutionary time. Such differences could indicate that a population of organisms is becoming a separate species. The researchers used a set of known species and tested the program’s ability to correctly predict the right number of species given certain variables. The program is good — maybe too good — at detecting the differences, Knowles says. If scientists don’t take other factors, such as geographical separation, into account, they may call genetically different groups separate species when they are merely subgroups of the same species.

Then again, it depends on what you mean by a “species,” says Rampal Etienne, an evolutionary community ecologist at the University of Groningen in the Netherlands. He developed the method that Knowles and Sukumaran analyzed. By one definition, a species is a genetically distinct lineage. “If that’s your species concept then, no, it’s not true that there are more species discovered by this method than there actually are,” Etienne says.

Biologists have long defined species primarily based on mating behavior and physical traits, not genetic similarity. Species are said to be reproductively isolated when they don’t mate either because they can’t or because they don’t for some reason (such as female fish choosing to mate with only red or blue males). Reproductive isolation doesn’t exclude two species from mating once in a while, says evolutionary biologist Ole Seehausen of the University of Bern in Switzerland. What’s important is that species that breed in the same area remain distinct.
What’s more, “speciation is not a one-way road,” Seehausen says. When ecological conditions change, groups that had been going their separate ways may breed with each other again. For instance, female fish that choose mates based on color may breed with males of the non-preferred color when water becomes murky and obscures their vision. Computer programs can predict when speciation has started but can never forecast whether the groups will remain separate or will come back together, Seehausen says.

Using the biological criteria, the genetic method may seem to fall short, but genetic analyses simply aren’t designed to address such questions, Seehausen says. He agrees with Knowles and Sukumaran that genetic data should be used in combination with ecological and other studies to identify species.

Characterizing species based on their genes could still be a useful conservation tool, Etienne says, helping to preserve genetic diversity. A diverse set of genes can help a species adapt to changing environments, and a lack of diversity can doom it to extinction. Identifying diverse groups within a population could help researchers decide where to focus conservation efforts, Etienne says. “Whether they are two species or not is less important,” he says.

Estimates of global biodiversity are not affected by any shortcomings with the genetic analysis programs, Knowles says. Scientists use many types of data to determine the total number of species in a region or on Earth.

A cautionary tale in evolutionary theory is coming straight from the horse’s mouth. When ancient horses diversified into new species, those bursts of evolution weren’t accompanied by drastic changes to horse teeth, as scientists have long thought.

A new evolutionary tree of horses reveals three periods when several new species emerged, scientists report in the Feb. 10 Science. The researchers found that changes in teeth morphology and body size didn’t change very much during these periods of rapid speciation.
“This knocks traditional notions that rapid diversification of new species comes with morphological diversification as well,” says paleontologist Bruce MacFadden of the University of Florida in Gainesville. “This is a very sophisticated and important paper.”

The emergence of several new species in a relatively short time is often accompanied by the evolution of special new traits. Classic notions of evolution say that these traits — such as longer teeth with extensive enamel — are adaptive, enabling an animal to succeed in a particular environment. In horses, the evolution of such teeth might permit a shift from browsing on leafy, shrubby trees to grazing on grasses in open spaces with windblown dust and grit.

“You can’t live on a grassland as a grazer and have short teeth,” says MacFadden, an expert in horse evolution. “You’ll wear your teeth down and that’s not a recipe for success as a species.”

Similarly, a big change in body size can indicate a move to a new environment. Animals that live in forests tend to be smaller and more solitary than the larger herd animals that live in open grasslands.

Paleontologist Juan Cantalapiedra and colleagues compiled decades of previous work to create an evolutionary tree of 138 horse species (seven of which exist today), spanning roughly 18 million years. The tree reveals three major branchings of new species: a North American burst between 15 million and 18 million years ago, and two bursts coinciding with dispersals into Eurasia about 11 million and 4.5 million years ago.
The researchers expected to see evidence of an “adaptive radiation,” major changes in teeth and body size that allowed the new horse species to succeed. But rates of body size evolution didn’t differ much in sections of the family tree with low and high speciation rates. And rates of change in tooth characteristics were actually lower in sections of the tree with fast speciation rates, the team reports.

“It’s very tempting to see some change in body size, for example, and say, ‘Oh, that’s adaptive radiation,’” says Cantalapiedra, of the Leibniz Institute for Evolution and Biodiversity Science at the Museum für Naturkunde in Berlin. “But that’s not what we see.”

Cantalapiedra and his collaborators speculate that during the periods of rapid speciation, the environment was so expansive and productive that there just wasn’t a lot of competition to drive the evolution of adaptive traits. Perhaps, for example, North American grasslands were so rich and dense that there was enough energy for various species to evolve without having to develop traits that gave them an edge.

That scenario might be special to horses, says MacFadden, but it might not. Similarly, classic adaptive radiation scenarios might be true in many cases, but as this work shows, not always.

BOSTON — Rooted in place, plants can’t run away from arsenic-tainted soil — but they’re far from helpless. Scientists have identified enzymes that help rice plant roots tame arsenic, converting it into a form that can be pushed back into the soil. That leaves less of the toxic element to spread into the plants’ grains, where it can pose a health risk to humans, researchers reported February 17 at the annual meeting of the American Association for the Advancement of Science.

Once arsenic worms its way into rice plant roots and gets into the vascular system, “it’s transported into the leaves and the grain,” David Salt, a biologist at the University of Nottingham in England who conducted the recent research, said during a news conference. Inside the plant, arsenic “can accumulate to levels where it can potentially be toxic if it accumulates over long times.”
Since arsenic occurs naturally in soil, understanding the genetic basis for plants’ natural defense mechanisms might help researchers engineer plants that take in less arsenic, said Mary Lou Guerinot, a biologist at Dartmouth College.
Arsenic in the soil switches between two different forms — ions with different electric charges. That form depends on soil conditions, which in a rice field fluctuate between wetter and drier. Plants are more likely to pull in arsenite from the soggy soil of a flooded rice paddy, and arsenate when that soil dries out a bit. The plants use different chemical mechanisms to take in and process the different arsenic ions.

In arsenate-rich soil, the ion sneaks into the outer layer of root cells through specialized passageways, called transport channels, that normally carry phosphate ions through root cell membranes. Transforming arsenate into arsenite lets the roots push the element back into the soil through a process called efflux, but scientists weren’t sure how the plant changed arsenic’s form.
Salt’s team found that rice plants without working genes for enzymes called HAC1;1 and HAC1;2 couldn’t turn arsenate into arsenite. So more arsenate accumulated in the plants’ shoots. When the scientists made HAC1;1 and HAC1;2 genes in other rice plants produce more of the enzymes than usual, grains from those plants had lower concentrations of any form of arsenic.

It’s just one defense of many, Salt said, and it’s not bulletproof. Arsenate can still spread into plants’ vascular systems from the roots via phosphate channels.

When the soil is rich in arsenite, rice roots take arsenite up through the same channels that take in silicon. Although efflux is an efficient way for roots to get rid of arsenite, there’s a limit to how quickly the cells can push the ion out.

So to create rice plants that are better at dealing with arsenic, Salt and other scientists are looking not just at how roots push out arsenic once it gets in, but how they keep the toxin out to begin with. For example, engineering channels that are better at pulling in just phosphate or just silicon could lessen the amount of arsenic that co-opts those channels.

Since soil conditions in a rice field switch between dry and wet, plants need defense mechanisms for both forms of arsenic. “Once we know what forms the plant takes in and how it’s doing that, we’ll need a solution for arsenate and arsenite,” Guerinot says. “There’s no easy fix.”

Certain birth defects were 20 times more prevalent in babies born to Zika virus–infected mothers in the U.S. in 2016 than they were before the virus cropped up in the United States, a CDC study suggests. The finding strengthens the evidence that a mother’s Zika infection during pregnancy raises her baby’s risk of microcephaly and other brain malformations.

The study, published March 3 in the CDC’s Morbidity and Mortality Weekly Report, examined data collected through birth defect surveillance programs in Massachusetts; North Carolina; and Atlanta, Georgia, in 2013 and 2014. In that timeframe — before Zika appeared in the United States — microcephaly, brain abnormalities or another Zika-associated birth defect appeared in just 3 out of every 1,000 live births.

But from January to September 2016, 26 babies out of 442 born to mothers with suspected Zika virus infection during pregnancy showed these defects, according to data from the U.S. Zika Pregnancy Registry. That’s an incidence of nearly 60 per 1,000 pregnancies carried by women with Zika, far higher than the pre-Zika level.

Though the two datasets were collected using different measures and so aren’t directly comparable, the findings bolster previous evidence suggesting that certain brain defects appear much more frequently in babies born to Zika-infected mothers.

Saturn serves up the closest thing to space pasta, the latest round of images from NASA’s Cassini probe, released March 9, show.

On March 7, the spacecraft snapped a series of portraits of Pan, Saturn’s small moon that orbits within a 325-kilometer gap in one of the planet’s rings. Taken at a distance of 24,572 kilometers from the moon, these are the closest images of Pan to date.

The close-ups could help refine astronomers’ understanding of the mini moon’s geology and shape. Pan has a distinctive ridge along its equator, which in the past has prompted astronomers to liken the moon’s shape to that of a flying saucer. In the new images, Pan’s ridge isn’t uniform like that of a fictional alien spacecraft. Instead, it’s uneven, creating an overall shape that more closely resembles a ravioli or wrinkly walnut.

Still, the ridge’s distinctness is “what is so spectacular and eye-opening in these images,” says imaging team leader Carolyn Porco of the Space Science Institute in Boulder, Colo. That supports the theory that the ridge is made of material from Saturn’s rings that continued to rain down on Pan’s equator after it formed.

Cassini captured the images on one of a series of ring-grazing orbits, as part of its final few months orbiting Saturn. Though it won’t get this close to Pan again, the probe is scheduled to swing past Saturn’s other “flying saucer” moon, Atlas, on April 12.

Physicists have snagged a bounty of five new particles in one go.

Members of the LHCb experiment, located at the Large Hadron Collider near Geneva, reported the prolific particle procurement in a paper posted online March 14 at arXiv.org. The five particles are each composed of three quarks — a class of particle that makes up larger particles such as protons and neutrons. Each of the new particles comprises two “strange” quarks and one “charm” quark.

The five particles are in various excited, or high-energy, states — giving each particle a different mass and a different arrangement of quarks within. Such particles are expected to exist according to the theory of the strong nuclear force, which bundles quarks together into larger particles.

The five excited particles are named after their low-energy relative, Ωc0 or omega-c-zero. Their rather uninspiring monikers are Ωc(3000)0, Ωc(3050) 0, Ωc(3066) 0, Ωc(3090) 0 and Ωc(3119) 0. Each number in parentheses indicates the mass of the particle in millions of electron volts.

Nomadic warriors and herders known as the Huns are described in historical accounts as having instigated the fifth century fall of the Roman Empire under Attila’s leadership. But the invaders weren’t always so fierce. Sometimes they shared rather than fought with the Romans, new evidence suggests.

Huns and farmers living around the Roman Empire’s eastern border, where the Danube River runs through present-day Hungary, borrowed ways of life from each other during the fifth century, say archaeologist Susanne Hakenbeck of the University of Cambridge and colleagues. Nomadic Huns on the Roman frontier raised relatively small numbers of animals and grew some crops, while border-zone farmers incorporated more meat into what had been a wheat- and vegetable-heavy diet, the scientists report March 22 in PLOS ONE.
“Our data show that the dietary strategies of the people on both sides of the Roman frontier were not fundamentally different,” Hakenbeck says.

Their findings challenge a traditional view of the Huns as marauders who roamed hundreds of kilometers from Central Asia to Europe. There’s no evidence of major social upheavals or a geographically distinctive group of newcomers at the frontier sites, so at least some Huns may have been homegrown, Hakenbeck suggests. Rapidly forming groups of Hun warriors and herders on horseback could have emerged in southeastern Europe not far from the Roman Empire’s border, perhaps supplemented by nomadic newcomers from farther east near the Black Sea, she proposes.

Still, geographic origins of the Huns are tough to pin down, says archaeologist Ursula Brosseder of the University of Bonn in Germany. The Huns developed as a political movement that picked up members from various ethnic groups as it spread, she explains. Brosseder suspects the “Hun phenomenon” formed on the grasslands of Western Eurasia, a territory that includes regions cited by Hakenbeck. The earliest evidence of Huns in that region dates to about 2,400 years ago.
The new study supports the idea that herding communities adapted flexibly to new environments, sometimes relying only on their livestock and at other times farming to varying extents, Brosseder says. Nomadic herders in Asia probably cultivated millet, a fast-growing cereal that can be used to feed people and horses, Hakenbeck says.
Her group studied skeletons of 234 people buried at five previously excavated sites on or near the Roman frontier. Each site contained evidence of contact with Huns, including bronze artifacts and adult skulls with elongated braincases created by binding the head during childhood. Reasons for this practice are poorly understood. It may have signified affiliation with the Huns or social status of some kind.

Graves at a Roman fort and a nearby cemetery lay on Roman land, about 150 kilometers from the frontier. Another two cemeteries were situated on the banks of the Danube River, directly on the Roman frontier. A final graveyard fell outside Roman territory. It was located about 150 kilometers east of the border.

Measurements of ratios of specific forms of carbon, nitrogen and oxygen in teeth and ribs enabled the scientists to identify what types of plants and how much meat or milk individuals ate during childhood, early adulthood and toward the end of their lives.

Results pointed to considerable consumption of cultivated plants, most likely millet, as well as meat or milk at all five sites. Variations on this general pattern occurred across sites and among individuals at each site, suggesting that groups and individuals rapidly adjusted how much they farmed or herded as circumstances dictated. “This mixing and matching was likely a kind of economic insurance policy in violent and unstable times,” Hakenbeck says.

Hakenbeck’s group also measured another tooth element, strontium, to determine whether individuals at four of the sites had grown up drinking water and eating food in the locales where they were buried. Between 30 and 50 percent of individuals studied at those sites weren’t locals, and the birthplaces of these people remain a mystery, Hakenbeck says.

In many cases, both newcomers and natives to the Roman frontier substantially changed their eating habits over the course of their lives, the researchers find. That fits Hakenbeck’s “mix and match” scenario, in which a fluctuating diet aided survival on the empire’s edge.

Most visitors to a large natural history museum don’t know it, but they are only scratching the surface of the museum’s holdings, even if they check out every exhibition. Most of the scientific treasures are tucked away in collection rooms filled with millions of specimens, which scientists use in their research.

The Field Museum in Chicago, home to Sue, the famous T. rex, is displaying some of its secreted goodies in its new exhibit “Specimens: Unlocking the Secrets of Life.” The museum has more than 30 million biological specimens, mummies, minerals, cultural artifacts and other objects in its collections. At any one time, only 0.5 to 1.5 percent of the holdings are on display. For the new exhibit, curators brought out about 5,600 additional items — from preserved deep-sea creatures and fossilized brains to meteorites — to show the diversity of the museum’s hidden collections, says Rusty Russell, director of collections.
“Specimens” not only provides access to these items, but it also informs the public about what natural historians do for a living. “Field Museum’s scientists do collections-based research. Without our vast collections, we could not carry out our science,” says William Simpson, head of geological collections and collections manager of fossil vertebrates. “In fact, almost none of our collecting is done for exhibit.”

Visitors wandering the exhibit will notice that all of this collecting has helped shed light on life millions of years ago, as well as stories ripped from today’s headlines.
Remember the Miracle on the Hudson in 2009? Pilot Chesley B. “Sully” Sullenberger safely landed a plane after its engines failed in a bird strike. To identify the birds, a scientist compared the remains recovered from the plane’s engines with tissues from known birds in the museum’s collection, some of which are on display in “Specimens.” The researcher determined that the birds were migratory Canada geese, not year-round Big Apple residents.
Museum collections play central roles in all kinds of identifications, especially for classifying new species. The museum has more than 20,000 holotypes — specimens that researchers have used to define species — in its collections, most of which were identified by museum scientists. The new exhibit features about 10 of these.

One example: dinosaur bones discovered in 1900 in the Colorado Rockies. In his lab, Elmer Riggs, the Field Museum’s first paleontology curator, removed rock covering the bones and realized he had unearthed a dinosaur bigger than Brontosaurus, the largest dinosaur known at the time. Riggs named the new dinosaur Brachiosaurus altithorax.

Another holotype on display is a skull and jaw of the early mammal Morganucodon oehleri, named in 1963, from the early Jurassic Period some 200 million years ago. The fossils show evidence of key evolutionary changes in early mammal history.

Several parts of “Specimens” are more hands-on. Visitors are urged to touch a giant, 160-kilogram clamshell from the Philippines, and they can peruse a drawer full of now-extinct butterflies with silvery-blue wings. Visitors also can sort seashells into different species. An interactive touch screen offers a look at ancient insects trapped in amber a la Jurassic Park.

When specimens are collected, researchers often don’t know how they’ll be used in the future. In one recent case, researchers analyzed two Arctic ivory gulls collected in 1896 to show that mercury levels in the ocean are now 45 times higher than a century ago. In another example in the exhibit, rodent and marsupial bones found in owl pellets recovered from Australian caves document wildlife before European settlement. Managers are now using the fossils as a blueprint to re-create ecosystems with species that still live in Australia.

All of these specimens show Field visitors a world they may not have known existed behind museum walls. Other large museums would do well to highlight their hidden bounty, too.

A common and usually harmless virus may trigger celiac disease. Infection with the suspected culprit, a reovirus, could cause the immune system to react to gluten as if it was a dangerous pathogen instead of a harmless food protein, an international team of researchers reports April 7 in Science.

In a study in mice, the researchers found that the reovirus, T1L, tricks the immune system into mounting an attack against innocent food molecules. The virus first blocks the immune system’s regulatory response that usually gives non-native substances, like food proteins, the OK, Terence Dermody, a virologist at the University of Pittsburgh, and colleagues found. Then the virus prompts a harmful inflammatory response.
“Viruses have been suspected as potential triggers of autoimmune or food allergy–related diseases for decades,” says Herbert Virgin, a viral immunologist at Washington University School of Medicine in St. Louis. This study provides new data on how a viral infection can change the immune system’s response to food, says Virgin, who wasn’t involved in the study.

Reoviruses aren’t deadly. Almost everyone has been infected with a reovirus, and almost no one gets sick, Dermody says. But if the first exposure to a food with gluten occurs during infection, the virus may turn the immune system against the food protein, the researchers found.

The immune system can either allow foreign substances, such as food proteins, to pass through the body peacefully, or it can go on the attack. In people with celiac disease, gluten is treated like a harmful pathogen; the immune system response damages the lining of the small intestine, causing symptoms like bloody diarrhea.

Celiac disease has been associated with two genetic features. Though 30 to 40 percent of people in the United States have one or both of these features, only 1 percent of the population has been diagnosed with the disease. This disparity suggests that some environmental factor triggers it.

Dermody and colleagues found that the T1L reovirus may be a trigger. In mice engineered to have one of those genetic features, the virus appeared to trick the immune system into seeing gluten as an enemy.
The key interaction occurs in the mesenteric lymph nodes, where gluten meets up with dendritic cells, which are like the “orchestra conductors” of the immune system, Dermody says. These cells dictate whether the immune system ignores a substance or mounts a defense against it.

But the virus engages with the dendritic cells as well, fooling the cells into thinking that gluten, like the virus, is in some way dangerous. And then the immune system attacks the gluten.

Dermody and colleagues also found that the reovirus stimulated activity of an enzyme called tissue transglutaminase. In people with celiac disease, the enzyme makes gluten more able to trigger a harmful immune system response.

Celiac patients also had higher levels of reovirus antibodies than those found in people without the disease.

Dermody doesn’t think that the T1L reovirus is the only virus that can stimulate celiac disease. Future research will analyze the potential of other viruses and also determine whether T1L is a true trigger of the disease in humans. If it is, then a reovirus vaccine could be developed for at-risk children, which could potentially block the development of celiac disease, “and that would be pretty amazing,” Dermody says.

Some Pakistani people are real knockouts, a new DNA study finds. Knockouts in this sense doesn’t refer to boxing or a stunning appearance, but to natural mutations that inactivate, or “knock out” certain genes. The study suggests that human knockouts could prove valuable evidence for understanding how genes work and for developing drugs.

Among 10,503 adults participating in a heart disease study in Pakistan, 1,843 people have at least one gene of which both copies have been knocked out, researchers report online April 12 in Nature. Researchers also drew blood from many of the participants and used medical records to study more than 200 traits, such as heart rate, blood pressure and blood levels of sugar, cholesterol, hormones or other substances. Studying how the knockout mutations affect those traits and health could point to genes that are potentially safe and effective targets for new drugs.
Combining genetic data with medical information will provide “a rich dataset for many applications,” says Robert Plenge, a human geneticist formerly with the pharmaceutical company Merck.

Scientists have traditionally learned about genes’ roles by deleting the genes from mice and then cataloging abnormalities in how those mice developed and behaved. Such animal research will always be needed, but studies of people naturally lacking certain genes “will change the nature of the scientific investigation of the genetic basis of human disease,” Plenge wrote in a commentary in the same issue of Nature.

Often, a person will inherit a broken copy of a gene from one parent and a healthy copy from the other. But 39 percent of the people in this study had parents who were closely related — often first cousins — increasing the odds of inheriting two mutant copies of a gene. Of this study’s 1,843 participants, 1,504 had both copies of a single gene knocked out. The rest had more than one gene knocked out, including one person in whom six genes were predicted to be completely nonfunctional.
In one example from the new study, geneticist Sekar Kathiresan and colleagues found four people in which both copies of the APOC3 gene had inactivating mutations. Kathiresan and colleagues had previously found that people with one mutated copy of APOC3 are protected against heart disease. Normally, the ApoC3 protein made from the gene stops dietary fat from being cleared from the body. People who had one mutant copy of the gene were able to get rid of fat more quickly than normal, reducing the amount left to clog arteries, says Kathiresan, of the Broad Institute of MIT and Harvard. Scientists reasoned that drugs that inactivate the ApoC3 protein would also reduce heart attack risk in people who have two working copies of the gene.
But there was a problem. Scientists worried that drugs that completely abolish the activity of the ApoC3 protein might be dangerous. Previous genetic studies encompassing nearly 200,000 people had never found a person with both copies of APOC3 knocked out, indicating that people might not be able to do without the gene entirely. Finding people who have almost no ApoC3 protein in their blood indicates that it is probably safe to get rid of its activity.

Further tests on 28 family members of one man who had both copies of APOC3 knocked out showed that his wife (who was his first cousin) and all nine of the couple’s children also lacked APOC3. The researchers fed fat-filled milkshakes to 13 members of the family — six who lacked APOC3 and seven who had two functional copies of the gene. Within six hours after the milkshake, levels of triglyceride— a type of fat in the blood — shot up two to three times over premilkshake levels in people with two functional copies of the gene. But in people in which the gene was knocked out, “triglyceride levels didn’t go up. It didn’t budge at all,” Kathiresan says. That finding suggests APOC3 could be a good target for drugs that reduce triglyceride levels in the blood and fend off heart disease, he says.