Bones show Dolly’s arthritis was normal for a sheep her age

In the scientific version of her obituary, Dolly the Sheep was reported to have suffered from severe arthritis in her knees. The finding and Dolly’s early death from an infection led many researchers to think that cloning might cause animals to age prematurely.

But new X-rays of Dolly’s skeleton and those of other cloned sheep and Dolly’s naturally conceived daughter Bonnie indicate that the world’s first cloned mammal had the joints of normal sheep of her age. Just like other sheep, Dolly had a little bit of arthritis in her hips, knees and elbows, developmental biologist Kevin Sinclair of the University of Nottingham in England and colleagues report November 23 in Scientific Reports.
The researchers decided to reexamine Dolly’s remains after finding that her cloned “sisters” have aged normally and didn’t have massive arthritis (SN: 8/20/16, p. 6). No formal records of Dolly’s original arthritis exams were kept, so Sinclair and colleagues got Dolly’s and Bonnie’s skeletons and those of two other cloned sheep, Megan and Morag, from the National Museums Scotland in Edinburgh. Megan and Bonnie were both older than Dolly at the time of their deaths and had more bone damage than Dolly did. Morag died younger and had less damage.
Dolly’s arthritis levels were similar to those of naturally conceived sheep her age, indicating that cloning wasn’t to blame. “If there were a direct link with cloning and osteoarthritis, we would have expected to find a lot worse, and it would be more extensive and have a different distribution than what we’re finding in ordinary sheep,” says study coauthor Sandra Corr, a veterinary orthopedic specialist at the University of Glasgow in Scotland.
Dolly’s slightly creaky joints may have stemmed from giving birth to six lambs, including Bonnie. Pregnancy is a risk factor for arthritis in sheep.

Meet the giants among viruses

For decades, the name “virus” meant small and simple. Not anymore. Meet the giants.

Today, scientists are finding ever bigger viruses that pack impressive amounts of genetic material. The era of the giant virus began in 2003 with the discovery of the first Mimivirus (SN: 5/23/09, p. 9). The viral titan is about 750 nanometers across with a genetic pantry boasting around 1.2 million base pairs of DNA, the information-toting bits often represented with A, T, C and G. Influenza A, for example, is roughly 100 nanometers across with only about 13,500 base pairs of genetic material.

In 2009, another giant virus called Marseillevirus was identified. It is different enough from mimiviruses to earn its own family. Since 2013, mega-sized viruses falling into another eight potential virus families have been found, showcasing a long-unexplored viral diversity, researchers reported last year in Annual Review of Virology and in January in Frontiers in Microbiology.

Giant viruses mostly come in two shapes: polyhedral capsules and egglike ovals. But one, Mollivirus, skews more spherical. Pacmanvirus was named for the broken appearance of its outer shell. Both represent potential families. Two newly discovered members of the mimivirus family, both called tupanviruses and both with tails, have the most complete set of genes related to assembling proteins yet seen in viruses (SN Online: 2/27/18). Once unheard of, giant viruses may be common in water and soils worldwide. Only time — and more discoveries — will tell.
Virus length and genome size for a representative from each of two recognized giant virus families (mimivirus and marseillevirus families) and eight potential families are shown. Circles are scaled to genome size and shaded by size range, with influenza A and E. coli bacterium included for comparison. Years indicate when the first viruses were described.

Graphic: C. Chang; Sources: P. Colson, B. La Scola and D. Raoult/Annual Review of Virology 2017; J. Andreani et al/Frontiers in Microbiology 2018

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.”

The oldest known pollen-carrying insects lived about 280 million years ago

The oldest known fossils of pollen-laden insects are of earwig-like ground-dwellers that lived in what is now Russia about 280 million years ago, researchers report. Their finding pushes back the fossil record of insects transporting pollen from one plant to another, a key aspect of modern-day pollination, by about 120 million years.

The insects — from a pollen-eating genus named Tillyardembia first described in 1937 — were typically about 1.5 centimeters long, says Alexander Khramov, a paleoentomologist at the Borissiak Paleontological Institute in Moscow. Flimsy wings probably kept the creatures mostly on the forest floor, he says, leaving them to climb trees to find and consume their pollen.

Recently, Khramov and his colleagues scrutinized 425 fossils of Tillyardembia in the institute’s collection. Six had clumps of pollen grains trapped on their heads, legs, thoraxes or abdomens, the team reports February 28 in Biology Letters. A proportion that small isn’t surprising, Khramov says, because the fossils were preserved in what started out as fine-grained sediments. The early stages of fossilization in such material would tend to wash away pollen from the insects’ remains.
The pollen-laden insects had only a couple of types of pollen trapped on them, the team found, suggesting that the critters were very selective in the tree species they visited. “That sort of specialization is in line with potential pollinators,” says Michael Engel, a paleoentomologist at the University of Kansas in Lawrence who was not involved in the study. “There’s probably vast amounts of such specialization that occurred even before Tillyardembia, we just don’t have evidence of it yet.”

Further study of these fossils might reveal if Tillyardembia had evolved special pollen-trapping hairs or other such structures on their bodies or heads, says Conrad Labandeira, a paleoecologist at the National Museum of Natural History in Washington, D.C., also not part of the study. It would also be interesting, he says, to see if something about the pollen helped it stick to the insects. If the pollen grains had structures that enabled them to clump more readily, for example, then those same features may have helped them grab Velcro-like onto any hairlike structures on the insects’ bodies.

Chemical signals from fungi tell bark beetles which trees to infest

Fungi may help some tree-killer beetles turn a tree’s natural defense system against itself.

The Eurasian spruce bark beetle (Ips typographus) has massacred millions of conifers in forests across Europe. Now, research suggests that fungi associated with these bark beetles are key players in the insect’s hostile takeovers. These fungi warp the chemical defenses of host trees to create an aroma that attracts beetles to burrow, researchers report February 21 in PLOS Biology.

This fungi-made perfume might explain why bark beetles tend to swarm the same tree. As climate change makes Europe’s forests more vulnerable to insect invasions, understanding this relationship could help scientists develop new countermeasures to ward off beetle attacks.
Bark beetles are a type of insect found around the world that feed and breed inside trees (SN: 12/17/10). In recent years, several bark beetle species have aggressively attacked forests from North America to Australia, leaving ominous strands of dead trees in their wake.

But trees aren’t defenseless. Conifers — which include pine and fir trees — are veritable chemical weapons factories. The evergreen smell of Christmas trees and alpine forests comes from airborne varieties of these chemicals. But while they may smell delightful, these chemicals’ main purpose is to trap and poison invaders.

Or at least, that’s what they’re meant to do.

“Conifers are full of resin and other stuff that should do horrible things to insects,” says Jonathan Gershenzon, a chemical ecologist at the Max Planck Institute for Chemical Ecology in Jena, Germany. “But bark beetles don’t seem to mind at all.”

This ability of bark beetles to overcome the powerful defense system of conifers has led some scientists to wonder if fungi might be helping. Fungi break down compounds in their environment for food and protection (SN: 11/30/21). And some type of fungi — including some species in the genus Grosmannia — are always found in association with Eurasian spruce bark beetles.
Gershenzon and his colleagues compared the chemicals released by spruce bark infested with Grosmannia and other fungi to the chemical profile of uninfected trees. The presence of the fungi fundamentally changed the chemical profile of spruce trees, the team found. More than half the airborne chemicals — made by fungi breaking down monoterpenes and other chemicals that are likely part of the tree defense system — were unique to infected trees after 12 days.

This is surprising because researchers had previously assumed that invading fungi hardly changed the chemical profile of trees, says Jonathan Cale, a fungal ecologist at the University of Northern British Columbia in Prince George, Canada, who was not involved with the research.
Later experiments revealed that bark beetles can detect many of these fungi-made chemicals. The team tested this by attaching tiny electrodes on bark beetles’ heads and detecting electrical activity when the chemicals wafted passed their antennae. What’s more, the smell of these chemicals combined with beetle pheromones led the insects to burrow at higher rates than the smell of pheromones alone.

The study suggests that these fungi-made chemicals can help beetles tell where to feed and breed, possibly by advertising that the fungi has taken down some of the tree’s defenses. The attractive nature of the chemicals could also explain the beetle’s swarming behavior, which drives the death of healthy adult trees.

But while the fungi aroma might doom trees, it could also lead to the beetles’ demise. Beetle traps in Europe currently use only beetle pheromones to attract their victims. Combining pheromones with fungi-derived chemicals might be the secret to entice more beetles into traps, making them more effective.

The results present “an exciting direction for developing new tools to manage destructive bark beetle outbreaks” for other beetle species as well, Cale says. In North America, mild winters and drought have put conifer forests at greater risk from mountain pine beetle (Dendroctonus pendersoae) attacks. Finding and using fungi-derived chemicals might be one way to fend off the worst of the bark beetle invasions in years to come.

What has Perseverance found in two years on Mars?

In August 2021 on a lonely crater floor, the newest Mars rover dug into one of its first rocks.

The percussive drill attached to the arm of the Perseverance rover scraped the dust and top several millimeters off a rocky outcrop in a 5-centimeter-wide circle. From just above, one of the rover’s cameras captured what looked like broken shards wedged against one another. The presence of interlocking crystal textures became obvious. Those textures were not what most of the scientists who had spent years preparing for the mission expected.
Then the scientists watched on a video conference as the rover’s two spectrometers revealed the chemistry of those meshed textures. The visible shapes along with the chemical compositions showed that this rock, dubbed Rochette, was volcanic in origin. It was not made up of the layers of clay and silt that would be found at a former lake bed.

Nicknamed Percy, the rover arrived at the Jezero crater two years ago, on February 18, 2021, with its sidekick helicopter, Ingenuity. The most complex spacecraft to explore the Martian surface, Percy builds on the work of the Curiosity rover, which has been on Mars since 2012, the twin Spirit and Opportunity rovers, the Sojourner rover and other landers.

But Perseverance’s main purpose is different. While the earlier rovers focused on Martian geology and understanding the planet’s environment, Percy is looking for signs of past life. Jezero was picked for the Mars 2020 mission because it appears from orbit to be a former lake environment where microbes could have thrived, and its large delta would likely preserve any signs of them. Drilling, scraping and collecting pieces of the Red Planet, the rover is using its seven science instruments to analyze the bits for any hint of ancient life. It’s also collecting samples to return to Earth.
Since landing, “we’ve been able to start putting together the story of what has happened in Jezero, and it’s pretty complex,” says Briony Horgan, a planetary scientist at Purdue University in West Lafayette, Ind., who helps plan Percy’s day-to-day and long-term operations.

Volcanic rock is just one of the surprises the rover has uncovered. Hundreds of researchers scouring the data Perseverance has sent back so far now have some clues to how the crater has evolved over time. This basin has witnessed flowing lava, at least one lake that lasted perhaps tens of thousands of years, running rivers that created a mud-and-sand delta and heavy flooding that brought rocks from faraway locales.

Jezero has a more dynamic past than scientists had anticipated. That volatility has slowed the search for sedimentary rocks, but it has also pointed to new alcoves where ancient life could have taken hold.

Perseverance has turned up carbon-bearing materials — the basis of life on Earth — in every sample it has abraded, Horgan says. “We’re seeing that everywhere.” And the rover still has much more to explore.
Perseverance finds unexpected rocks
Jezero is a shallow impact crater about 45 kilo­meters in diameter just north of the planet’s equator. The crater formed sometime between 3.7 billion and 4.1 billion years ago, in the solar system’s first billion years. It sits in an older and much larger impact basin known as Isidis. At Jezero’s western curve, an etched ancient riverbed gives way to a dried-out, fan-shaped delta on the crater floor.

That delta “is like this flashing signpost beautifully visible from orbit that tells us there was a standing body of water here,” says astrobiologist Ken Williford of Blue Marble Space Institute of Science in Seattle.

Perseverance landed on the crater floor about two kilometers from the front of the delta. Scientists thought they’d find compacted layers of soil and sand there, at the base of what they dubbed Lake Jezero. But the landscape immediately looked different than expected, says planetary geologist Kathryn Stack Morgan of NASA’s Jet Propulsion Laboratory in Pasadena, Calif. Stack Morgan is deputy project scientist for Perseverance.
For the first several months after the landing, the Mars 2020 mission team tested the rover’s movements and instruments, slowly, carefully. But from the first real science drilling near the landing location, researchers back on Earth realized what they had found. The texture of the rock, Stack Morgan says, was “a textbook igneous volcanic rock texture.” It looked like volcanic lava flows.

Over the next six months, several more rocks on the crater floor revealed igneous texture. Some of the most exciting rocks, including Rochette, showed olivine crystals throughout. “The crystal fabric was obviously cooled from a melt, not transported grains,” as would be the case if it were a sedimentary sample, says Abigail Allwood of the Jet Propulsion Lab. She leads the rover’s PIXL instrument, which uses an X-ray beam to identify each sample’s composition.

Mission scientists now think the crater floor is filled with igneous rocks from two separate events — both after the crater was created, so more recently than the 3.7 billion to 4.1 billion years ago time frame. In one, magma from deep within the planet pushed toward the surface, cooled and solidified, and was later exposed by erosion. In the other, smaller lava flows streamed at the surface.
Sometime after these events, water flowed from the nearby highlands into the crater to form a lake tens of meters deep and lasting tens of thousands of years at least, according to some team members. Percy’s instruments have revealed the ways that water altered the igneous rocks: For example, scientists have found sulfates and other minerals that require water to form, and they’ve seen empty pits within the rocks’ cracks, where water would have washed away material. As that water flowed down the rivers into the lake, it deposited silt and mud, forming the delta. Flooding delivered 1.5-meter-wide boulders from that distant terrain. All of these events preceded the drying of the lake, which might have happened about 3 billion years ago.

Core samples, which Perseverance is collecting and storing on board for eventual return to Earth, could provide dates for when the igneous rocks formed, as well as when the Martian surface became parched. During the time between, Lake Jezero and other wet environments may have been stable enough for microbial life to start and survive.

“Nailing down the geologic time scale is of critical importance for us understanding Mars as a habitable world,” Stack Morgan says. “And we can’t do that without samples to date.”

About a year after landing on Mars, Perseverance rolled several kilometers across the crater floor to the delta front — where it encountered a very different geology.

The delta might hold signs of ancient life
Deltas mark standing, lasting bodies of water — stable locales that could support life. Plus, as a delta grows over time, it traps and preserves organic matter.

Sand and silt deposited where a river hits a lake get layered into sedimentary material, building up a fan-shaped delta. “If you have any biological material that is trapped between that sediment, it gets buried very quickly,” says Mars geologist Eva Scheller of MIT, a researcher with the Percy team. “It creates this environment that is very, very good for preserving the organic matter.”

While exploring the delta front between April 2022 and December 2022, Perseverance found some of the sedimentary rocks it was after.
Several of the rover’s instruments zoomed in on the textures and shapes of the rocks, while other instruments collected detailed spectral information, revealing the elements present in those rocks. By combining the data, researchers can piece together what the rocks are made of and what processes might have changed them over the eons. It’s this chemistry that could reveal signs of ancient Martian life — biosignatures. Scientists are still in the early stages of these analyses.

There won’t be one clear-cut sign of life, Allwood says. Instead, the rover would more likely reveal “an assemblage of characteristics,” with evidence slowly building that life once existed there.

Chemical characteristics suggestive of life are most likely to hide in sedimentary rocks, like those Perseverance has studied at the delta front. Especially interesting are rocks with extremely fine-grained mud. Such mud sediments, Horgan says, are where — in deltas on Earth, at least — organic matter is concentrated. So far, though, the rover hasn’t found those muddy materials.

But the sedimentary rocks studied have revealed carbonates, sulfates and unexpected salts — all materials indicating interaction with water and important for life as we know it. Percy has found carbon-based matter in every rock it has abraded, Horgan says.

“We’ve had some really interesting results that we’re pretty excited to share with the community,” Horgan says about the exploration of the delta front. Some of those details may be revealed in March at the Lunar and Planetary Science Conference.

Perseverance leaves samples for a future mission
As of early February, Perseverance has collected 18 samples, including bits of Mars debris and cores from rocks, and stored them on board in sealed capsules for eventual return to Earth. The samples come from the crater floor, delta front rocks and even the thin Martian atmosphere.

In the final weeks of 2022 and the first weeks of 2023, the rover dropped — or rather, carefully set down — half of the collected samples, as well as a tube that would reveal whether samples contained any earthly contaminants. These captured pieces of Mars are now sitting at the front of the delta, at a predetermined spot called the Three Forks region.
If Perseverance isn’t functioning well enough to hand over its onboard samples when a future sample-return spacecraft arrives, that mission will collect these samples from the drop site to bring back to Earth.

Researchers are currently working on designs for a joint Mars mission between NASA and the European Space Agency that could retrieve the samples. Launching in the late 2020s, it would land near the Perseverance rover. Percy would transfer the samples to a small rocket to be launched from Mars and returned to Earth in the 2030s. Lab tests could then confirm what Perseverance is already uncovering and discover much more.

Meanwhile, Percy is climbing up the delta to explore its top, where muddy sedimentary rocks may still be found. The next target is the edge of the once-lake, where shallow water long ago stood. This is the site Williford is most excited about. Much of what we know about the history of how life has evolved on Earth comes from environments with shallow water, he says. “That’s where really rich, underwater ecosystems start to form,” he says. “There’s so much going on there chemically.”

How fingerprints form was a mystery — until now

Scientists have finally figured out how those arches, loops and whorls formed on your fingertips.

While in the womb, fingerprint-defining ridges expand outward in waves starting from three different points on each fingertip. The raised skin arises in a striped pattern thanks to interactions between three molecules that follow what’s known as a Turing pattern, researchers report February 9 in Cell. How those ridges spread from their starting sites — and merge — determines the overarching fingerprint shape.
Fingerprints are unique and last for a lifetime. They’ve been used to identify individuals since the 1800s. Several theories have been put forth to explain how fingerprints form, including spontaneous skin folding, molecular signaling and the idea that ridge pattern may follow blood vessel arrangements.

Scientists knew that the ridges that characterize fingerprints begin to form as downward growths into the skin, like trenches. Over the few weeks that follow, the quickly multiplying cells in the trenches start growing upward, resulting in thickened bands of skin.

Since budding fingerprint ridges and developing hair follicles have similar downward structures, researchers in the new study compared cells from the two locations. The team found that both sites share some types of signaling molecules — messengers that transfer information between cells — including three known as WNT, EDAR and BMP. Further experiments revealed that WNT tells cells to multiply, forming ridges in the skin, and to produce EDAR, which in turn further boosts WNT activity. BMP thwarts these actions.

To examine how these signaling molecules might interact to form patterns, the team adjusted the molecules’ levels in mice. Mice don’t have fingerprints, but their toes have striped ridges in the skin comparable to human prints. “We turn a dial — or molecule — up and down, and we see the way the pattern changes,” says developmental biologist Denis Headon of the University of Edinburgh.

Increasing EDAR resulted in thicker, more spaced-out ridges, while decreasing it led to spots rather than stripes. The opposite occurred with BMP, since it hinders EDAR production.

That switch between stripes and spots is a signature change seen in systems governed by Turing reaction-diffusion, Headon says. This mathematical theory, proposed in the 1950s by British mathematician Alan Turing, describes how chemicals interact and spread to create patterns seen in nature (SN: 7/2/10). Though, when tested, it explains only some patterns (SN: 1/21/14).

Mouse digits, however, are too tiny to give rise to the elaborate shapes seen in human fingerprints. So, the researchers used computer models to simulate a Turing pattern spreading from the three previously known ridge initiation sites on the fingertip: the center of the finger pad, under the nail and at the joint’s crease nearest the fingertip.
By altering the relative timing, location and angle of these starting points, the team could create each of the three most common fingerprint patterns — arches, loops and whorls — and even rarer ones. Arches, for instance, can form when finger pad ridges get a slow start, allowing ridges originating from the crease and under the nail to occupy more space.

“It’s a very well-done study,” says developmental and stem cell biologist Sarah Millar, director of the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai in New York City.

Controlled competition between molecules also determines hair follicle distribution, says Millar, who was not involved in the work. The new study, she says, “shows that the formation of fingerprints follows along some basic themes that have already been worked out for other types of patterns that we see in the skin.”

Millar notes that people with gene mutations that affect WNT and EDAR have skin abnormalities. “The idea that those molecules might be involved in fingerprint formation was floating around,” she says.

Overall, Headon says, the team aims to aid formation of skin structures, like sweat glands, when they’re not developing properly in the womb, and maybe even after birth.

“What we want to do, in broader terms, is understand how the skin matures.”

The deadly VEXAS syndrome is more common than doctors thought

A mysterious new disease may be to blame for severe, unexplained inflammation in older men. Now, researchers have their first good look at who the disease strikes, and how often.

VEXAS syndrome, an illness discovered just two years ago, affects nearly 1 in 4,000 men over 50 years old, scientists estimate January 24 in JAMA. The disease also occurs in older women, though less frequently. Altogether, more than 15,000 people in the United States may be suffering from the syndrome, says study coauthor David Beck, a clinical geneticist at NYU Langone Health in New York City. Those numbers indicate that physicians should be on the lookout for VEXAS, Beck says. “It’s underrecognized and underdiagnosed. A lot of physicians aren’t yet aware of it.”
Beck’s team reported discovering VEXAS syndrome in 2020, linking mutations in a gene called UBA1 to a suite of symptoms including fever, low blood cell count and inflammation. His team’s new study is the first to estimate how often VEXAS occurs in the general population — and the results are surprising. “It’s more prevalent than we suspected,” says Emma Groarke, a hematologist at the National Institutes of Health in Bethesda, Md., who was not involved with the study.
VEXAS tends to show up later in life ­­— after people somehow acquire UBA1 mutations in their blood cells. Patients may feel overwhelming fatigue, lethargy and have skin rashes, Beck says. “The disease is progressive, and it’s severe.” VEXAS can also be deadly. Once a person’s symptoms begin, the median survival time is about 10 years, his team has found.

Until late 2020, no one knew that there was a genetic thread connecting VEXAS syndrome’s otherwise unexplained symptoms. In fact, individuals may be diagnosed with other conditions, including polyarteritis nodosa, an inflammatory blood disease, and relapsing polychondritis, a connective tissue disorder, before being diagnosed with VEXAS.

To ballpark the number of VEXAS-affected individuals, Beck’s team combed through electronic health records of more than 160,000 people in Pennsylvania, in a collaboration with the NIH and Geisinger Health. In people over 50, the disease-causing UBA1 mutations showed up in roughly 1 in 4,000 men. Among women in that age bracket, about 1 in 26,000 had the mutations.

A genetic test of the blood can help doctors diagnose VEXAS, and treatments like steroids and other immunosuppressive drugs, which tamp down inflammation, can ease symptoms. Groarke and her NIH colleagues have also started a small phase II clinical trial testing bone marrow transplants as a way to swap patients’ diseased blood cells for healthy ones.

Beck says he hopes to raise awareness about the disease, though he recognizes that there’s much more work to do. In his team’s study, for instance, the vast majority of participants were white Pennsylvanians, so scientists don’t know how the disease affects other populations. Researchers also don’t know what spurs the blood cell mutations, nor how they spark an inflammatory frenzy in the body.

“The more patients that are diagnosed, the more we’ll learn about the disease,” Beck says. “This is just one step in the process of finding more effective therapies.”