This Worm Has 100 Butts

In Greek mythology, the hydra is a creature with many heads. In Norse mythology, Odin rides Sleipnir—a horse with many legs. And in the warm, coastal waters of Australia lives Ramisyllis multicaudata, the worm with many butts.

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The creature is shaped somewhat like a tree, with a single head and a body that branches over and over again, each bifurcation gifted with its very own anus. Now, new research on the innards of this mysterious, multi-bottomed beast reveals that it’s even stranger on the inside.

Ramisyllis and one other related branching worm—Syllis—are found exclusively within the pores and canals inside marine sponges. They place their head somewhere near the sponge’s base and run their branched body through tunnels, extending to the outside of the sponge. M. Teresa Aguado, an evolutionary biologist at the University of Göttingen in Germany, and her colleagues think the worm’s forked figure is perfectly adapted for life in this Swiss cheese labyrinth. The branched body wouldn’t be suitable for swimming around in the outside ocean waters.

“However, living inside the sponge, the animal is protected, and explores the canals and easily moves inside,” said Aguado.

While scientists had gathered some understanding of Ramisyllis’ external anatomy since its discovery in 2006, little was known about how the worm’s insides were put together. So, Aguado and a team of researchers from Australia, Spain, and Germany found wild sponges containing the one-worm tangles and brought them into the lab.

There, the researchers used a combination of different imaging strategies to examine the worms and their porous abodes. They used a 3D X-ray method to see how Ramisyllis is arranged within its sponge host. The team also dissected the worms out of the sponges and used different types of microscopes to peer into Ramisyllis’ insides.

Their results—published recently in the Journal of Morphology—revealed that the worms’ rear ends are legion.

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“We were able to count more than 500 [branches] in one specimen, but we think that they can easily reach 1,000,” said Aguado.

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The team also found that the worms’ branching is well beyond skin deep. Incredibly, every time Ramisyllis forks itself, all the internal organs divide, too: The gut, the nerves, everything splits and runs the length of the branch. This also creates a unique, muscular band or “bridge” that threads between the organs every time the critter splits. These bridges can visually demarcate Ramisyllis’ main trunk, which is pretty useful when you’re observing an animal shaped like a tumbleweed.

The farther you get away from the head, the weirder the worm gets. Aguado and her colleagues were able to closely examine the tips of the branches, which are crucial for the species’ reproduction.

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When Ramisyllis decides it’s time to procreate, its abundance of wandering derrières go through a transformation. The branch ends basically convert into genitals, filling with eggs or sperm. These reproductive units (or “stolons”) grow eyes and their own brains. When mature, the stolons detach and swim away, their freshly acquired “head” and eyes steering them to mate with stolons of the opposite sex. What started as a wriggling snarl of buttholes becomes a swarm of autonomous, sex-seeking torpedoes.

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Non-branching worms in same family as Ramisyllis also use stolons in a similar manner, Aguado points out. But Ramisyllis is unique in the sheer volume of its carnal armada, thanks to its many hundreds of body branches.

Alexander Tzetlin, an invertebrate zoologist at Moscow State University in Russia who was not involved with this study, lauds the research, noting the obstacles in studying animals like Ramisyllis.

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“In many cases, marine annelid [worms] are a very difficult object for research and observation, because they lead a secretive lifestyle,” said Tzetlin. “They live in shelters in pipes, burrows, or they simply dig in the thickness of the sediment, almost never appearing on the surface.”

Tzetlin also points out one big remaining mystery with Ramisyllis: its diet. No food has ever been found inside the worms’ intestines, just empty visceral real estate. It’s particularly baffling in an animal so ludicrously rich in anuses. There’s an awful lot of digestive infrastructure here to be building intestines to nowhere.

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“We don’t know how this animal keeps its huge body having only one minute mouth,” says Aguado. “It may use the organic material in water that goes inside the [sponge] canals due to the currents generated by the sponge.”

Previous research showed that Ramisyllis has lots of long, microscopic extensions from its outer covering. These may absorb nutrients straight from the water.

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Aguado says she and her colleagues are designing experiments to address this feeding question. The team is also investigating how genes are expressed in different parts of the worm’s branching body and in its relatives, gaining insight into how a creature with but one rear gave rise to Ramisyllis’ majestic bramble of butts.

Netflix’s Awake Trailer Has a Worldwide Sleeping Disorder

See, if Gina Rodriguez had gotten some sleep she’d remember you don’t hold guns that way.

See, if Gina Rodriguez had gotten some sleep she’d remember you don’t hold guns that way.
Screenshot: Netflix

Trailer FrenzyA special place to find the newest trailers for movies and TV shows you’re craving.

In Awake, a mysterious event causes all electronics to stop working… as well as people’s inability to sleep. I have no idea what could possibly cause both these things, and if there’s an answer, it’s absolutely not in the movie’s first trailer.

Seems like society goes to hell rather quickly once the event happens, which is bad news for ex-soldier Jill (Gina Rodriguez) and her daughter Mathilda (Ariana Greenblatt), the latter of whom seems to be the only person on the planet who can go to sleep. Especially since the trailer implies that the only way a group of very tired scientists can figure how to get people to start sleeping again is by very literally sacrificing her. I also don’t know why learning how she’s managing to go night-night requires the child to die, but clearly there’s a lot I don’t understand about this movie.

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Perhaps director Mark Raso (Kodachrome) will give us the answers—perhaps—when Awake debuts on Netflix on June 9.


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Polar Bear-Grizzly Hybrids, Aka Pizzly Bears, May Be Growing More Common Due to Climate Crisis

Illustration for article titled Polar Bear-Grizzly Hybrids, Aka Pizzly Bears, May Be Growing More Common Due to Climate Crisis

Image: Guy Clavel/AFP and Dani Pozo/AFP (Getty Images)

What do you get when you cross a polar bear and a grizzly bear? A fluffy reminder of how climate change is transforming our planet at an alarming rate.

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These hybrids, sometimes called pizzly bears or grolar bears, have been spotted in the wild as far back as 2006. But with global temperatures rising as a result of carbon pollution, the two species’ habitats are overlapping more often. While the heat pushes grizzly bears north, polar bears have been traveling south in search of food as arctic sea ice continues to shrink to historic levels. And odds are the two aren’t just bumping elbows—they seem to be increasingly engaging in “opportunistic mating,” as Vanderbilt University’s Larisa DeSantis put it in a recent video released by the institute. One study in 2017 documented at least eight pizzlies that were traced back to a single female polar bear and two separate grizzly bears.

“We’ve known about pizzlies for quite some time, but their occurrence may be more common with ongoing Arctic warming,” said DeSantis, an associate professor of biological sciences. “As grizzlies move north, they are more likely to come in contact with polar bears in regions where their ranges overlap. Further, polar bears are increasingly having to search for other food sources, when hunting seals from sea ice become untenable.”

Both polar bears and grizzlies are known to congregate at whale carcass sites, she said. And since the two species only diverged about 500,000 or 600,000 years ago, their offspring are capable of reproducing. One study revealed a hybrid that was a result of a pizzly mating with a grizzly, according to DeSantis.

How well are these hybrids suited for survival in the wild? Researchers are still trying to figure that out.

“Most of the time, hybrids are not more vigorous than either of the two species,” DeSantis said, explaining that species generally evolve adaptions best suited to their individual habitats. However, there are instances where hybrid species can be more vigorous than their predecessors, “particularly if that environment is deviating from what it once was.”

If carbon emissions follow their current trajectory, experts predict the global temperature will rise roughly 5.4 degrees Fahrenheit (3 degrees Celsius) by the end of this century. With that increase comes some pretty catastrophic side effects, including massive ecological upheaval, ocean acidification, and sea-level rise, among others. And, though significantly less catastrophic, more pizzly bears.

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Scientists Dive Into Axolotl Genome, Looking for Secrets to Regeneration

An axolotl in a regenerative therapy lab in Dresden in 2015.

An axolotl in a regenerative therapy lab in Dresden in 2015.
Photo: ROBERT MICHAEL/AFP (Getty Images)

Its adorableness aside, the Mexican axolotl is a salamander of particular interest to scientists. On the molecular level, the animal seems to have a cheat code for life: It can regenerate its limbs and vital organs, an ability researchers are desperate to better understand for medical applications.

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Now, geneticists have gotten a clearer view of the smiling salamander’s genome, rendering it on the chromosomal scale. The research was published this week in the Proceedings of the National Academy of Sciences.

Understanding a genetic structure in complete detail takes a lot of time, far longer than it takes to first report the mapping of a genome, as we did with humans in 2003 and the duck-billed platypus in 2008. Secrets remain shrouded in those purportedly finished genetic codes, so geneticists keep tinkering. Decrypting the axolotl’s genome in particular was a tall order; where bits of a human genome charged with making a protein may span hundreds to thousands of base pairs, in an axolotl, it takes hundreds of thousands of base pairs. Nevertheless, the complete axolotl genome was announced in 2019 by the same team who published the recent research.

“We used some techniques that were related to our earlier classical genetic mapping techniques,” said co-author Jeramiah Smith, a geneticist at the University of Kentucky, in a video call. “But that allowed us to stitch these million base pair things into billion, billion-plus base pair scaffolds that represented the length of chromosomes.”

Axolotls are evolutionary ascetics. While the rest of the salamanders learned how to live amphibiously, the axolotl stayed in the water and evolved to basically stay in its larval phase throughout its life. Comparing the axolotl to a Pokémon is uncannily accurate; a century ago, researchers found that when you fed thyroid tissue to axolotls, they’d occasionally undergo metamorphosis, losing the fern-like gills that sprout from their heads and the tadpole-esque tailfin.

The recent paper specifically looked at how the genome is folded away inside the animal on the molecular level and where the DNA sequences that regulate genes are located in relation to the places where gene transcription starts. That’s remarkable when you consider the scale and extreme compactness of the folding; a human DNA strand is about 6 feet when stretched out, but an axolotl’s would be over 30 feet. All that genetic material is being sequestered in the cells of an animal 200 times smaller than the average human—it’s a mind-boggling example of efficiency in packing, all on a microscopic scale.

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“The work has ordered the sequenced pieces of axolotl genomic DNA sequence in the correct order, as it is on the chromosome,” Elly Tanaka, a biochemist at the Vienna BioCenter’s Institute of Molecular Pathology who also works on axolotl genetics but is unaffiliated with the research, said in an email. “This is important because, in all animals with vertebrae, genes are turned on and off by control sequences that are actually lying pretty far away from the gene itself.” The research, she added, will be important for seeing if the ability to regenerate could ever be activated in humans.

A wild axolotl in a conservation lab in Mexico City in 2014.

A wild axolotl in a conservation lab in Mexico City in 2014.
Photo: RONALDO SCHEMIDT/AFP via Getty Images (Getty Images)

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How the genes fold is important in figuring out how the axolotl grows its initial bits and pieces and then what sequences are kicked into second gear when any one of those components needs replacing. To figure out the locations of different DNA strands, the team made different proteins in the animal fluoresce, highlighting the loci of interest.

“There are a lot of details involved with regenerating a limb,” Smith said. “We’re not only now thinking about the genome as a linear structure, but also the higher orders of 3D structures that it takes on.”

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Today, there are populations of axolotls kept at various research institutions, not to mention the animals sold in pet shops. But captive populations suffer from inbreeding, and the number of wild animals, which exclusively inhabit the waters of and surrounding Lake Xochimilco in Mexico City, are dwindling. “They’re endangered in their native habitat,” Smith said. “We should be considering that this is a real species that lives in a real habitat.”

Conservation and genetic inquiry are obviously not in opposition, but if we want to continue learning about and eventually benefitting from this species’ superpowers, we should make sure the wild population continues to survive and thrive.

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Early Humans Were Walking Around With Ape-Like Brains, Study Finds

One of the Dmanisi skulls on exhibit in Leiden in 2009.

One of the Dmanisi skulls on exhibit in Leiden in 2009.
Photo: VALERIE KUYPERS/AFP via Getty Images (Getty Images)

Humans can be distinguished from other apes in many ways, such as our general hairlessness, our upright bipedalism, and, of course, our powerful brains. But it turns out that our cognitive ability didn’t evolve as early as previously thought, according to new research by an international team of researchers.

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The team’s findings, published today in the journal Science, are based on five 1.8-million-year-old skulls from a roughly 10-acre site near the Georgian town of Dmanisi. The brains of these early arrivals into Europe and Asia—hominin species that evolved well before Homo sapienswere already known to be small, but in the recent inspection, the researchers made endocasts of the ancient skulls. Basically, they created topographical maps of the brain cases, which can reveal minute differences in shape that provide insights about the development of different regions of the long-decomposed brains. Understanding ancient brain structures helps flesh out the genesis of our species; whether we inched or sprinted to our modern morphology and what road we took to get here.

Endocasts of the five 1.8-million-year-old crania from Dmanisi.

Endocasts of the five 1.8-million-year-old crania from Dmanisi.
Image: M. Ponce De León and Ch. Zollikofer, University of Zurich

“These structures are extremely interesting, because they constitute the neural substrate for complex cognitive tasks, such as toolmaking and use, social cognition, and, most importantly, spoken language,” said study authors Marcia Ponce de León and Christoph Zollikofer, both paleoanthropologists at the University of Zurich, in an email. “We don’t know whether these hominins had language in the modern sense, but the brain structures were there, and likely have co-evolved with language capabilities.”

The saga of human origins is clouded by a fragmentary fossil record, like an old book so worn with time that only a few handfuls of sentences are being used to guess the whole story. But guess we do, and our accuracy gets better with every newly found fossil and newly invented technology to analyze them. The skulls investigated in the new paper were excavated between 1991 and 2008 and are housed at the Georgian National Museum in Tbilisi.

Comparing the Georgian Homo endocasts to ones taken from skulls of about the same age and younger from Africa and the Indonesian island of Java, the team found that the Georgian hominins’ brains looked more similar to those of great apes than modern humans. This suggests that modern brain structures emerged from Africa later than early wanderers out of the continent by at least 100,000 years.

“There must have been two ‘out-of-Africa’ dispersals of early Homo: the first is documented by the fossil evidence from the site of Dmanisi in today’s Georgia” about 2 million years ago, the researchers said in their email. “These Homo populations had primitive brains. The second dispersal is documented by the fossils from Java; these populations had modern brains.”

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A Dmanisi specimen (left) compared with a more cognitively developed Homo erectus from Indonesia (right).

A Dmanisi specimen (left) compared with a more cognitively developed Homo erectus from Indonesia (right).
Image: M. Ponce De León and Ch. Zollikofer, University of Zurich

Since the earliest fossil attributed to the genus Homo dates to nearly 3 million years ago, the Georgian skulls signify that at least some of the earliest humans lacked the developed brains we normally think of as defining our genus. It was a moment, the researchers said, of “realizing the emperor had no clothes,” the clothes here being a reorganized brain.

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The researchers were particularly interested in the frontal lobes of the Dmanisi individuals, a region of the brain that likely played a vital role in the early human endeavors of language development and toolmaking. Both innovations were springboards for early humans, who were able to do more than survive; at some point, we began to communicate with nuance, organize as larger groups, and created tools that allowed us to hunt more effectively, live in greater comfort, and eventually become the most dominant species on the planet (for better or worse).

“It does not really change our understanding of Homo sapiens, but it definitely changes the way we look at early human brain evolution,” said Amélie Beaudet, a paleoanthropologist at the University of Cambridge who was not affiliated with the recent study, in an email. Beaudet noted that despite knowledge of the primitive Australopithecine brain structure possessed by the Lucy individual, among others, and the more-developed crania of recent humans (dating to about half a million years ago), “we did not really know what happened in between. With this study we have a better idea, even if there are still some gaps.”

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More fossils always help in better understanding our evolutionary arc, but in lieu of new finds, new technology tends to step up. The gap in our knowledge of human cognitive development is narrowing. We should be grateful for our predecessors’ evolution, because now we have the brains to figure out how it all happened.

Eagles Are Filled With Rat Poison

The face of a bird who’s cranky about rodenticide.

The face of a bird who’s cranky about rodenticide.
Photo: David Zalubowski (AP)

Eagles are majestic, beautiful, and full of toxins that we’ve pumped into the environment. A new study finds that 82% of dead eagles examined between 2014 and 2018 had detectable levels of rat poison in their systems.

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The study, published on Wednesday in PLOS One, was, happily, made possible by the fact that eagle populations are actually rebounding across the U.S. The 303 birds examined in the study, a mix of bald and golden eagles, were collected by state and federal agencies that are part of the Southeastern Cooperative Wildlife Disease Study, a project based out of the University of Georgia that analyzes carcasses of wild animals from across the country for disease and other problems.

“When you have populations increasing, of course some are going to get into trouble, and that’s how they come across our shop here,” said Mark Ruder, an assistant professor at the College of Veterinary Medicine at the University of Georgia and a co-author of the study.

Ruder and his team saw an opportunity with the increased number of samples they were getting. “There had been a lot of attention on this type of rodenticide in other raptor species like barn owls, screech owls, hawks, but none specifically for eagles,” he said. “We knew anticoagulant rodenticide was a problem, so we had the anticipation that this is going to be worthy of an investigation.”

The study examined the eagle carcasses for evidence of what’s known as second-generation anticoagulant rodenticide, a heavy-duty solution for pests that acts as a blood thinner and eventually kills the animal after they eat it. Before the 1970s, anticoagulant rodenticides worked less well than current rodent killers. The rodents would often have to eat a lot more of the poison over several days to make it have an effect. Manufacturers began strengthening their products and introduced a second generation of the poison, which could kill rats and mice much quicker. This version of the rodenticide, however, is “stickier,” Ruder explained, meaning it stays in animals’ bodies—and can enter the bodies of predators that feed on rats and mice that may eat the poison.

“It’s the ability to persist in those tissues for a long time that creates the problem,” Ruder said. “Being efficient predators and scavengers, eagles are more at risk for accumulating this toxin through their system, basically just by being eagles—eating dead stuff or killing things and eating them.”

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While 82% of the creatures in the study had measurable amounts of the poison in their bodies, it’s worth noting that anticoagulant rodenticide was determined to be the cause of death for only 4% of the sample of eagles examined. (The paper asserts that the mortality figure could be an underestimate, especially since around half the eagles in the sample died by trauma like gunshots, car accidents, or electrocution.) But the fact that such a high proportion of the animals had traces of rodenticide at all was “surprising,” Ruder said—and worrisome. Because of the danger posed to other animals, the Environmental Protection Agency has restricted the sale of anticoagulant rodenticide to just commercial markets and professional pest controls.

“If you go to the hardware store, you and I just can’t buy it willy-nilly,” Ruder said.

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This control has had some good effects: Ruder said a study of barn owls in Kentucky had found that the birds’ level of exposure to anticoagulant rodenticide decreased after the EPA restricted use of the pesticide. Eagles, however, don’t generally prey directly on the main targets of the rodenticide like other raptor birds do, suggesting that the toxin got into their bodies another way.

“It’s not super common to look out the window and see a bald eagle hunting for the mouse that lives in your crawl space, or whatever,” Ruder said. “These are food webs—everything is connected—and the eagles are likely getting exposed to these compounds through ingestion of much more natural prey that have, in turn, eaten something else in order to be exposed.”

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And this infection of the food web, the study suggests, is a widespread problem for wildlife across the country. The eagles came from 18 different wildlife management agencies from different regions, with no difference in levels of rodenticide between states.

“There is definitely recognition by many that these second-generation anticoagulant rodenticides have the potential to extend beyond their population of pest rodent species, and this study will certainly reinforce that understanding,” Ruder said. “Despite current management and policy efforts to mitigate that risk to wildlife, it still appears that we’re getting quite a bit of non-target exposure and intoxication in non-target species. We need to keep examining what pathways for exposure are for wildlife and figure out how to lower that risk.”

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A Dangerous Toxin From Pond Scum Can Go Airborne, Study Finds

A blue-green algae bloom documented along the St. Lucie River in Port Saint Lucie, Florida, on July 5, 2016.

A blue-green algae bloom documented along the St. Lucie River in Port Saint Lucie, Florida, on July 5, 2016.
Photo: Rhona Wise (Getty Images)

A potent toxin released by algae blooms has the potential to become airborne, recent research suggests. In what’s said to be a first, the study found traces of the toxin in the air near pond water in Massachusetts. Though it’s unclear whether this and similar toxins are harmful to people and animals when airborne, the scientists warn that the discovery is definitely worrying.

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Algae blooms and the toxins they produce have become an increasingly common problem. These blooms are showing up more often and more intensely than they did decades ago, often in lakes or freshwater sources, and when they do, they can cause mass poisonings and die-offs in the local ecosystem. People and their pets exposed to these toxins aren’t safe, either—dogs dying after swimming in or ingesting algae-contaminated freshwater has sadly become an annual event.

One particularly scary toxin is called anatoxin-a (ATX), also known by its edgier name, “Very Fast Death Factor.” ATX is produced by species of blue-green algae—a group of bacteria that survive through photosynthesis, like plants (the blue-green refers to the color they usually display in massive numbers). ATX is known to have killed birds, dogs, and other animals since its discovery in the 1960s; it’s also suspected of having poisoned people. In humans, it’s been linked to blurred vision, dizziness, headache, and gastrointestinal symptoms like vomiting and diarrhea.

Though ATX has never been observed to go airborne, the researchers behind this new study theorized that it could happen under the right conditions. Their study, published in Lake and Reservoir Management Friday, seems to show that it can.

In the summer of 2019, they periodically visited Capaum Pond, found on the tiny island of Nantucket off Massachusetts. When an algae bloom appeared, they collected samples of pond water as well as air nearby, using a prototype device that collected air through a glass fiber filter. They consistently found ATX in the water throughout the summer. And during a trip in mid-September, they found the toxin in the air as well.

“This study is the first to report ATX captured on glass fiber filters adjacent to a waterbody experiencing a [harmful algae bloom],” the study authors wrote.

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Other algae-related toxins have been shown to become airborne as well, but there’s a lot left unknown about how this process would work with ATX. It could have gotten suspended inside water droplets, for instance, or the bacteria producing it could have become airborne themselves. The researchers think that heavy winds the night before their collection played a part, while the fog that happened the next day might have helped it stay afloat as long as it did.

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It’s unclear how much of a health risk airborne ATX might be to animals and humans. Though dangerous, ATX is produced in high amounts less often than other toxins associated with blue-green algae (one likely reason is that it degrades easily in the environment). And aside from one documented cluster of cases in France, it hasn’t been shown to harm people frequently. But since climate change will only make these blooms more frequent and harder to combat, any potential added risks from ATX and other toxins have to be studied now, the researchers say, adding that the general public should be warned about the possible dangers of these toxins.

“People often recreate around these lakes and ponds with algal blooms without any awareness of the potential problems,” said study author, James Sutherland, an environmental scientist with the Nantucket Land Council, in a statement released by the study’s publisher. “Direct contact or inhalation of these cyanotoxins can present health risks for individuals, and we have reported a potential human health exposure not previously examined.”

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Airborne DNA Could Help Scientists Find Elusive Animals

The hope is that airborne DNA collection could expand the field of environmental DNA.

The hope is that airborne DNA collection could expand the field of environmental DNA.
Photo: RADEK MICA/AFP via Getty Images (Getty Images)

A UK-based team says they were able to pull genetic material from the air and correctly identify the species it belonged to, an exciting leap for the field of environmental DNA. The technique of sampling an environment for DNA to figure out what organisms inhabit it, known as environmental DNA or eDNA, is regularly used to study terrestrial and marine environments: Simply see what molecular fragments can be found on a forest floor or floating in the sea, and you’ll know what creature recently passed through. Now, they’ve taken DNA directly from the air in an animal’s burrow.

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Published today in the journal PeerJ, the research describes a lab set-up in which they were able to detect airborne DNA. The test organisms were a group of naked mole rats, set up in a makeshift burrow of pipes and tanks at the Queen Mary University of London. The research team stuck a hose into the animals’ tank and pulled air into it, which fed into a filter usually used for marine eDNA sampling. Then, the researchers ran genetic testing on the filter (which substitutes for the animal tissue that normally would be tested for genetic material) and, to their surprise, were able to identify the rats purely from genetic material that was floating around in the burrow’s airspace.

“I tend to think of it a bit like soup,” said lead author Elizabeth Clare, a molecular ecologist at Queen Mary University of London, in a video call. “We’re in the soup, and it contains dust and pollen and bits of DNA floating around… It’s one of those things where you have to have a leap of faith to even try it.”

The team wasn’t sure they’d get anything from the experiment. While eDNA is commonplace in the realms of land and sea research, things move differently in the air. Molecular fragments need to be filtered out of the medium they’re floating in to be read, and things dissipate in air quickly if you’re not in an enclosed space (hence why outdoor coronavirus transmission is less likely than indoors). That’s why Clare’s team started with the mole rats, an enigmatic species that scuttles about in networks of narrow subterranean tunnels. After they successfully detected mole rat DNA in the tunnel’s air, they broadened their testing to the lab itself. They were able to pick up human DNA in the air—their own.

“The first question was pretty risky: Is there DNA in the air? The answer is yes, and we can capture it,” Clare said. “The next question has to get more risky: Can we do it under more difficult circumstances?”

The implications for airborne DNA detection are large. Clare does fieldwork with bats, whose habit of staying in dark, cavernous spaces or tiny chambers often prevents researchers from accessing bat colonies. eDNA in the air (to be called airDNA or maybe eDNAir—they’re working on it) would allow researchers to broaden their observational horizons. Wherever it’s employed, the molecular detection method serves as a sort of biological roll call where species can phone in rather than needing to be directly observed.

eDNA is a source of optimism for conservationists desperate to get a pulse on endangered or elusive animals. It’s useful for knowing all the characters in an ecological niche or understanding which animals survived disasters like the Australian wildfires. Down the road—way down it—Clare hopes that airborne DNA collection could help create a live map of biodiversity in a chosen area.

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There’s an Ancient Connection Between Our Saliva and Snake Venom

The Taiwan habu has venom glands that are rooted in a distant genetic past.

The Taiwan habu has venom glands that are rooted in a distant genetic past.
Image: OIST/Steven Aird

Humans and other mammals have the same genetic foundations for developing oral venom that snakes have, according to a paper published today in the Proceedings of the National Academy of Sciences.

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This connection was discovered by a research team looking at venom-producing tissue from 30 habus, a pit viper from East Asia. The researchers were scrutinizing the animals’ genes to understand which had a hand in expressing the complex proteins that make up the snakes’ venom.

The toxins in snake venom evolve quickly, and it’s hard to get a sense of how ancient toxins may have differed from the ones sequestered in the animals’ glands today. Instead of searching for those earlier states, the researchers—Agneesh Barua and Alexander S. Mikheyev of Japan’s Okinawa Institute of Science and Technology—instead looked at the genes that are instrumental in making the toxins. It’s almost like not being able to hear an old piece of music but instead getting a gist of how other music derived from it based on the common rules of its tempo, time signature, and key.

After learning how genes expressed toxin-related proteins, the next step was to establish correlations between the genes (which genes were most or least often associated). The researchers found that the venom genes were ones that worked to maintain protein structure and cultivate a biological environment that allowed a lot of proteins to be produced.

“This makes perfect sense, because venom is a cocktail made up of toxin proteins,” said Barua in an email. “It is vital that the protein structure of these toxins is maintained. Otherwise, the venom won’t work, and the animal would not be able to catch its prey.”

“This suggests that there is a common molecular framework between venom glands in snakes and salivary tissue in non-venomous mammals,” Barua said, adding that the shared attribute represents an ancient genetic makeup inherited by both modern animal groups.

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A Russel viper at a venom extraction center in India in 2016.

A Russel viper at a venom extraction center in India in 2016.
Photo: ARUN SANKAR/AFP (Getty Images)

Some mammals do have venom; both living types of monotreme have glands for injecting toxins, though only the platypus’s are functional. Shrews and slow lorises can also unleash a toxic bite—the latter’s involves combining saliva with secretions from the sweat gland. On the whole, though the reptilian world has mammalian life beat, producing a diverse array of species with a repertoire of different venoms. The salivary glands of mice, dogs, and humans still genetically resemble those of our distant, slithery cousins on the tree of life. It’s not yet known why serpents became such experts of toxicity, while mammals just dabbled with the helpful trait.

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“It is likely that the ancestor of venomous snakes had a particular advantage in developing oral secretions, the kind of advantage that ancestors of shrews or mice didn’t have,” Barua said. “It could be imagined that the conditions for the non-venomous ancestors of snakes were ‘just right’ to develop venom.”

It’s theoretically possible that non-venomous mammalian salivary glands, like those of humans or mice, could eventually become so. (But it’s hard to imagine what adaptive purpose venom might serve for us, what with the global supply chain and all.)

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For now, at least, the research is a reminder that complex life on this planet has very ancient shared roots, and even reptiles and mammals are genetically tethered. Our similarities will always be more than skin (or scale) deep.

These Mutant Rabbits Walk on Two Legs, and Geneticists Now Know Why

A sauteur d’Alfort rabbit walking on its front feet, the result of a genetic mutation.

A sauteur d’Alfort rabbit walking on its front feet, the result of a genetic mutation.
Photo: S. Boucher

An entire lineage of French rabbits has been doing handstands for nearly a century. The acrobatic bunnies are not so much performing a stunt as they are a product of stunted genetics, according to a paper published this week in PLOS Genetics.

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First discovered in a domesticated rabbit living in a Parisian suburb in 1935, the recessive trait is the product of a genetic mutation that could have been hidden in the animals’ genetic code for generations, only to surface then. It’s not a superpower. The rabbit variety—the “sauteur d’Alfort,” or “the Alfort jumper”—is also more likely to develop cataracts and become blind.

“The strain has been kept since then to study ocular malformations and pathological locomotion,” said co-author Miguel Carneiro, a geneticist at the University of Porto in Portugal, in an email. “Rabbits carrying this mutation would not be able to survive long in the wild due to its deleterious effects.”

The bunnies are bipedal and often blind.

The bunnies are bipedal and often blind.
Image: Carneiro et al. 2021 (Other)

The rabbits walk on all fours when moving slowly, but in a rush, turn to the handstand method. Now, a team of geneticists have identified the root of all those problems in the breed’s DNA.

Illustration for article titled These Mutant Rabbits Walk on Two Legs, and Geneticists Now Know Why

Photo: S. Boucher

To figure out the origins of the animal’s abnormalities, the team of geneticists and developmental biologists bred the Alfort jumper with rabbits that hop normally and sequenced the DNA of their descendants. They found the rabbits that ended up bipedal had a mutation on the first chromosome; specifically, a warped gene called RORB, which expresses a protein of the same name.

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“With modern technology, it’s straightforward to go from a simple recessive disorder to finding the genes,” said co-author Leif Andersson, a geneticist at Uppsala University in Sweden, in a video call. “The expectation was there was something wrong with the spinal cord, because they don’t coordinate their forelegs and the hind legs.”

Among the Alfort jumping rabbits (perhaps a misnomer, given the bunnies have no hops), this was proven true. The RORB protein is a transcription factor, meaning it has a hand in a number of genes, which all end up being expressed in traits. The proteins are ordinarily produced in inhibitory interneurons that cease communications moving through the body. (Imagine an operator refusing to service your calls.) In the weird-walking rabbits, the interneurons either were less present or completely absent, and, in the latter case, the rabbits would overflex their hind legs, rendering them incapable of hopping.

“What’s happening when you’re moving is that you have these neurons firing all the time, and they coordinate muscle contractions and receive feedback on the balance of the different limbs,” Andersson said. “This coordination of muscle contraction is not correct in these rabbits.”

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You can think, the rabbits’ handstand is not itself the mutation, but a workaround to an otherwise debilitating inhibition of the animal’s iconic means of locomotion. Andersson said the two-footed locomotion caused the animals no pain of which he was aware.

It’s not the only animal to experience gait disruption due to genetic mutations. Similar behavior was seen in mice with a RORB mutation, and previous work of Andersson’s found that a mutation in the gene DMRT3 disrupts the gait of mice and horses. (Interestingly, it is that mutation at work when you look at the different gait patterns of certain horse breeds, from Tennessee Walkers to Louisiana Fox Trotters.)

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Thanks to genetic science, these mysteries can be decrypted on microscopic scales and could aid in better understanding the communication centers of our own (human) spinal cords, for medical research going forward.