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Science news in brief: From elephant's skin to the discovery of Planet Nine

And a roundup of other stories from around the world

It appears ants were cultivating crops long before humans
It appears ants were cultivating crops long before humans (Don Parsons)

Ants were millions of years ahead of us in producing antibiotics

The dawn of agriculture did not rise with neolithic humans in Mesopotamia. Or in China. Or in the Levant. No, it bloomed in the rainforests of South America some 60 million years ago. And the first farmers were humble ants.

Long before early humans cultivated wheat, barley, lentils and flax, ancient leafcutter ants raised fungus. And like human farmers, the ants had to fend off crop pests, particularly a parasitic fungal disease.

“If the fungus dies, the ants die,” says Cameron Currie, a microbial ecologist at the University of Wisconsin-Madison who studies the fungus-farming ants and their mutually beneficial relationships with other species.

To fight the pestilence, the ants aligned themselves with a bacteria that produces a chemical capable of subduing the parasite. Now, Currie and his colleagues have found evidence that suggests that the partnership between ants and antimicrobial bacteria has existed for tens of millions of years. The key clues came from two 20-million-year-old ants that were discovered, trapped in amber, in the Dominican Republic.

One of the fossilized ants had specialised pockets on its head, called crypts, that are also seen on modern ants. The crypts are known to house the fungus-protecting bacteria, called actinobacteria. The other ant specimen was entombed with gas bubbles on its body, likely produced by the respiration of the actinobacteria.

“It’s kind of like the ants are walking pharmaceutical factories,” says Currie, who is an author of the study, which appeared last week in the journal Proceedings of the National Academy of Sciences. “This indicates that, like in the way ants predated us in growing crops, they also predated us by tens of millions of years in associating with microbes to produce antibiotics.

(Michel Milinkovitch/NYT) (NYT)

Why elephants don’t shed their skin

The African elephant is known for its thick, wrinkly skin. But look closer and you’ll see an intricate network of tiny crevices that makes the mighty mammal’s hide resemble cracked mud or damaged concrete.

The purpose of those cracks is no mystery. An elephant doesn’t have sweat or sebum glands, so it covers its skin in water or mud to keep cool. The micrometre-wide cracks in its skin retain 10 times more moisture than a flat surface, helping the animal regulate its body temperature. They also help mud adhere to the skin, which protects against parasites and rays from the sun.

Now a team of researchers believe they have discovered that these cracks form as a result of the stress of skin bending, not shrinking. Their explanation, published recently in Nature Communications, might even hold clues to treating a common human genetic skin disorder.

Michel Milinkovitch, an evolutionary biologist at the University of Geneva in Switzerland, and his team found that dead elephant skin cells resemble those of humans suffering from ichthyosis vulgaris, a disease found in 1 out of every 250 people that prevents the shedding of skin. In humans, the condition, for which there is no cure, causes thick, dry scales on the surface of the skin that are usually treated with moisturisers.

But in African elephants, holding on to all that dead skin appears to be beneficial: the lack of shedding causes the skin to build up as the elephant ages, eventually bending and breaking over the layer of papillae, which provides the animal the means to stay cool.

More research is needed to determine whether the lack of skin-shedding in elephants shares a genetic basis with ichthyosis vulgaris in humans. But the confluence of the conditions could suggest a path forward for treating the ailment.

(Roberto Molar Candanosa/Scott Sheppard/Carnegie Institution for Science/NYT) (NYT)

The Goblin points towards Planet Nine

Among some astronomers there is a growing suspicion that our solar system’s distant reaches conceal a large, ninth planet that we have not yet seen. New findings about a minor ice planet far beyond Pluto buttress this idea.

Recently, astronomers led by Scott Sheppard of the Carnegie Institution for Science in Washington revealed the orbital details of the planet, which they have nicknamed the Goblin. Sheppard and his colleagues first spotted the object, which for now carries the official designation of 2015 TG387, as part of a systematic search three years ago for new planets in the outer system, including the hypothesised Planet Nine. But only with additional observations did they realise how far out TG387 really is.

“It took us three years to figure out that it has an interesting orbit,” Sheppard says.

The planet, estimated to have a width of a couple of hundred miles, is currently about 7.4 billion miles from the sun, or about 2.5 times farther away than Pluto. But that is near to the closest it ever gets to the sun.

Because TG387 remains far beyond the pull of the gravitational heavyweights of the solar system – Jupiter, Saturn, Uranus and Neptune – that raises the question of how it got thrown into its current orbit.

In 2016, Michael Brown and Konstantin Batygin of the California Institute of Technology published a detailed prediction of what they called an unseen planet, bigger than Earth yet smaller than Neptune, that was shepherding the movement of these distant objects and could explain the odd journeys around the sun of these faraway astronomical bodies.

They called it Planet Nine. Ann-Marie Madigan, an astronomer at the University of Colorado, has suggested that gravity from a massive ring of small objects early in the solar system’s history could explain the distant orbits. Madigan’s ideas could help explain how the ice planets were cast out there, but not any clustering in their orbits.

(Zachary Lippman/Cold Spring Harbor Laboratory/Howard Hughes Medical Institute/NYT) (NYT)

Coming faster to your market: one fussy fruit

The physalis might look at first look like a purely ornamental plant. The fruit also known as a groundcherry bears papery, heart shaped husks that resemble Chinese lanterns. Within each physalis casing is a small, tart, edible fruit, similar in appearance to a cherry tomato, that is sometimes sold at farmers’ markets.

The fruit might be more common in supermarkets were it not so difficult to grow in large quantities. Physalis bushes sprawl untidily and can drop their fruits early, and the plants possess other undesirable traits. Diminishing these traits through selective breeding would take years.

Recently, a team of researchers reported that, by removing certain portions of the plant’s DNA using common gene-editing techniques, they’ve produced a physalis with a larger fruit and a more ordered bush, greatly speeding the process of domestication. Their work, which appeared in the journal Nature Plants, is part of a scientific initiative called the Physalis Improvement Project.

Joyce Van Eck, a plant geneticist at Cornell University and an author of the paper, and her colleagues had already discovered that, using Crispr, a gene-editing technique that can snip out portions of the genome, they could alter a specific tomato gene and produce plants that flowered more quickly.

The scientists wondered whether the physalis could be similarly altered, to help fast-track the domestication process.

Using Crispr the team removed a small portion of the physalis’s genome. The resulting plants, when they grew, arranged themselves into more compact bushes. Heartened by these successes, the researchers are working to see whether they can control the shape of physalis bushes with more precision. They are also keen to find a solution to the problem of fruit dropping off the bush.

Because Crispr involves only the removal of DNA, not the addition of new material, the resulting produce isn’t considered a genetically modified organism in the US or Canada, Van Eck says.

(Getty (Getty)

Researchers on a drive to reclassify psilocybin

Researchers from Johns Hopkins University in Maryland have recommended that psilocybin, the active compound in hallucinogenic mushrooms, be reclassified for medical use, potentially paving the way for the psychedelic drug to one day treat depression and anxiety and help people stop smoking.

The suggestion to reclassify psilocybin from a US schedule I drug, with no known medical benefit, to a schedule IV drug, which is akin to prescription sleeping pills, was part of a review to assess the safety and abuse of medically administered psilocybin.

Before the country’s Food and Drug Administration (FDA) can be petitioned to reclassify the drug though, it has to clear extensive study and trials, which can take more than five years, the researchers wrote.

The widespread legalisation of marijuana has helped demystify drug use, with many people now recognising the medicinal benefits for those with anxiety, arthritis and other physical ailments.

Psychedelics, like LSD and psilocybin, are illegal and not approved for medical or recreational use. But in recent years scientists and consumers have begun rethinking their use to combat depression and anxiety.

“We are seeing a demographic shift, particularly among women,” says Matthew Johnson, an associate professor of psychiatry and behavioural sciences at Johns Hopkins and one of the study’s authors. Among the research he has conducted, he says, “we’ve had more females in our studies”.

Microdosing, or the use of psychedelics in small, managed doses, has become a popular way to try to increase productivity and creative thinking, particularly among the technorati in Silicon Valley.

Johnson says the FDA had approved a number of trials of psilocybin. If its use is approved for patients, he says, “I see this as a new era in medicine”.

He warned though that psilocybin is not a panacea for everyone. In their analysis, the researchers called for strict controls on its use. There are areas of risk too for patients with psychotic disorders and anyone who takes high doses of the drug.

© New York Times

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