Category: 7. Science

Identifying Earth-like planets outside out solar system is a leading research goal in astronomy, but determining if candidate planets have atmospheres, and more importantly if they can retain atmospheres, is still out of reach.

In this paper, we present our study on the impact of enhanced EUV flux on the stability and escape of the upper atmosphere of an Earth-like exoplanet using the Global Ionosphere and Thermosphere Model (GITM). We also investigate the differences between one- and three-dimensional solutions.

We use a baseline case of EUV flux experienced at the Earth, and multiplying this flux by a constant factor going up to 50. Our results show a clear evidence of an inflated and elevated ionosphere due to enhanced EUV flux, and they provide a detailed picture of how different heating and cooling rates, as well as the conductivity are changing at each EUV flux level.

Our results also demonstrate that one-dimensional solutions are limited in their ability to capture a global atmosphere that are not uniform. We find that a threshold EUV flux level for a stable atmosphere occurs around a factor of 10 times the baseline level, where EUV fluxes above this level indicate a rapidly escaping atmosphere. This threshold EUV flux translates to about 0.3AU for a planet orbiting the Sun.

Thus, our findings indicate that an Earth-like exoplanet orbiting its host star in a close-in orbit is likely to lose its atmosphere quickly.

Lukas Hanson, Ofer Cohen, Aaron Ridley, Alex Glocer

Comments: 13 pages, 9 figures
Subjects: Earth and Planetary Astrophysics (astro-ph.EP)
Cite as: arXiv:2508.21745 [astro-ph.EP] (or arXiv:2508.21745v1 [astro-ph.EP] for this version)
https://doi.org/10.48550/arXiv.2508.21745
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Related DOI:
https://doi.org/10.3847/1538-4357/adff7f
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Submission history
From: Lukas Hanson
[v1] Fri, 29 Aug 2025 16:19:14 UTC (2,268 KB)
https://arxiv.org/abs/2508.21745
Astrobiology,

Archaea, a domain of microorganisms found in diverse environments including the human microbiome, represent the closest known prokaryotic relatives of eukaryotes.

This phylogenetic proximity positions them as a relevant model for investigating the evolutionary origins of nucleic acid secondary structures such as G-quadruplexes (G4s), which play regulatory roles in transcription and replication. Although G4s have been extensively studied in eukaryotes, their presence and function in archaea remain poorly characterized.

In this study, a genome-wide analysis of the halophilic archaeon Haloferax volcanii identified over 5, 800 potential G4-forming sequences. Biophysical validation confirmed that many of these sequences adopt stable G4 conformations in vitro. Using G4-specific detection tools and super-resolution microscopy, G4 structures were visualized in vivo in both DNA and RNA across multiple growth phases.

Comparable findings were observed in the thermophilic archaeon Thermococcus barophilus. Functional analysis using helicase-deficient H. volcanii strains further identified candidate enzymes involved in G4 resolution. These results establish H. volcanii as a tractable archaeal model for G4 biology.

Archaeal G-Quadruplexes: A Novel Model for Understanding Unusual DNA/RNA Structures Across the Tree of Life

Astrobiology, Genomics,

Linguists have long known that when cultures collide, languages rub off on one another. We borrow words, swap sounds, and even reshape grammar. But charting those exchanges across centuries and continents is hard when the written record is patchy or nonexistent.

A new study flips the problem on its head: instead of starting with history books, the researchers read our DNA to reconstruct past human contact – then asked what happened to the languages.

DNA traces human language history

A team led by Anna Graff at the University of Zurich pulled together genetic data from more than 4,700 people in 558 populations. They paired this with two of the world’s largest linguistic databases, which catalogue everything from word order to consonant inventories across thousands of languages.

Genetic “admixture” – the telltale signature of populations mixing – stands in for a reliable, globally comparable record of contact. With that proxy in hand, the team could identify more than 125 instances where groups clearly met and mingled, even if historians never wrote the encounters down.

What they saw was unambiguous: when people mix, their languages tend to move closer together. Unrelated languages spoken by populations with genetic contact were four to nine percent more likely to share features than expected.

That might sound modest, but across entire grammars and sound systems, it’s a strong, consistent nudge toward similarity.

One surprise was how steady that effect proved to be. Whether the contact was vast and recent – say, colonial movements between continents – or ancient and regional, like Neolithic migrations within Eurasia, the degree of linguistic convergence was strikingly similar.

“No matter where in the world populations come into contact, their languages become more alike to remarkably consistent extents,” said senior author Chiara Barbieri, now at the University of Cagliari.

That consistency cuts against a common assumption that only intense, prolonged encounters reshape grammar and sound systems, or that small-scale neighborly contact leaves barely a trace.

The genetic lens suggests languages are sensitive instruments, registering social touchpoints across the full spectrum – from trade and intermarriage to conquest and diaspora.

Not all grammar is transferable

Of course, not every part of a language is equally malleable. Some features seem to travel more readily. Word order patterns and certain consonant sounds were more likely to converge than deeper layers of morphology or prosody.

But here, too, the study counsels caution. The researchers didn’t find a one-size-fits-all rulebook that says, for example, “Nouns move; verb endings don’t.”

That challenges decades of “borrowability hierarchies” that rank which features can be shared across languages. Instead, the authors argue, social dynamics – prestige, power, identity, and the practicalities of multilingual life – can override structural inertia.

If a community prizes a dominant group’s speech, it may adopt conspicuous elements quickly; if it resists assimilation, the most “borrowable” features might barely budge.

You can see the everyday version of this push and pull in familiar loanwords. English picked up “sausage” from French after the Norman Conquest; centuries later, French borrowed “sandwich” from English.

Vocabulary swaps like these are the visible tip. Beneath the surface, the new study shows, subtler shifts in sound and syntax can ripple outward whenever people share space and stories.

The team even found the mirror image of borrowing: divergence on purpose. In some places, features became less alike after contact, not more.

That happens when communities lean into linguistic differences to mark who they are – tightening vowel systems, restoring older word orders, or reinforcing local pronunciations as a badge of identity. In other words, contact doesn’t always melt boundaries; sometimes it sharpens them.

This duality – convergence alongside intentional distancing – is central to how languages evolve. It helps explain why some neighboring tongues grow steadily more alike, while others cling to distinctiveness despite centuries of cohabitation.

DNA tells story of language

Methodologically, the study’s move is elegant. Historical documents and oral traditions can be rich but patchy, and for many regions and eras they simply don’t exist.

Genes keep a different kind of ledger. When populations intermix, they leave a durable statistical imprint that persists for thousands of years.

By aligning those genetic signals with language structures, the authors could quantify contact and its linguistic consequences on a global canvas – from Amazonia and the Sahel to the Pacific and the Arctic.

The approach also helps disentangle coincidence from contact. Two unrelated languages might independently develop similar features for internal reasons. But when that similarity lines up with clear genetic admixture between the speakers, the balance of probability shifts toward historical interaction.

Languages evolve in real time

Beyond satisfying our curiosity about how English, Hausa, Quechua, or Hmong came to be what they are, the findings carry a warning for the present. Contact has always been part of human life, but the pace and scale are accelerating.

Globalization, urbanization, climate-driven displacement, and land-use change are bringing communities together – and pushing others apart – in new ways. As that churn intensifies, we should expect languages to converge more in some respects and to splinter or vanish in others.

It also reframes the stakes of language loss. We often focus on shrinking vocabularies and disappearing oral literatures.

This study suggests that deeper, structural layers – sound patterns, grammatical architectures, the hidden wiring of a language – can erode under sustained contact, even when a language survives on the surface.

Protecting linguistic diversity, then, isn’t only about counting how many languages remain; it’s about preserving the full range of their internal variety.

DNA and language share histories

The research tells a familiar human story with fresh evidence. When people meet – through trade or conquest, migration or marriage – we share more than DNA. We pass around technologies, beliefs, recipes, and ways of speaking.

Some of those exchanges are voluntary, others are imposed; some knit communities together, others spark efforts to stand apart. Our languages, like our DNA, carry the scars and gifts of those encounters.

By treating genes as a time machine, this study gives linguistics a new global baseline. It doesn’t replace fieldwork, historical scholarship, or typological theory.

It makes them sharper, pointing to where contact likely mattered and how deeply. And it leaves us with a clear takeaway for the century ahead: as our lives intertwine ever more tightly, the sounds and structures we use to make meaning will change with them.

The study is published in the journal Science Advances.

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We stroll past wheat, clover, and grass and see only the green half of the story. The other half – the roots – do the heavy lifting: anchoring plants, pulling up water and nutrients, and locking away carbon in the soil.

Yet because roots are hidden, scientists have spent decades using muddy, labor-intensive methods to guess their size and spread, often missing the finest, most active threads. According to a team of researchers at Aarhus University, that guesswork can finally stop.

A high-tech root census

“It’s a bit like studying marine ecosystems without ever being able to dive,” said senior author Henrik Brinch-Pedersen, a professor in the Department of Agroecology.

Until now, the standard approach was to carve out big blocks of soil, wash away the dirt, sort and dry what remained, and weigh the roots. It’s slow, destructive, and misses the fine roots that absorb nutrients and release carbon to the soil.

The new approach swaps spades for droplet digital PCR (ddPCR), a DNA technology that partitions a teaspoon of soil into tens of thousands of microscopic droplets. Each droplet then answers a yes/no question: Does it contain plant DNA with a specific genetic signature?

The team uses a marker called ITS2 – think of it as a barcode that differs among species – so a single run can reveal not just that roots are present, but whose roots they are. Crucially, it also shows how much underground biomass each species contributes.

“It’s a bit like giving the soil a DNA test,” Brinch-Pedersen said. “We can suddenly see the hidden distribution of species and biomass without digging up the whole field.”

Mapping roots with precision

Because ddPCR counts DNA molecules across thousands of droplets, it can quantify roots that would otherwise be pulverized or rinsed away.

That makes it possible to map root communities at high resolution in living fields, pastures, and mixed-species grasslands and to repeat measurements over time without disturbing the site.

The payoff spans several fronts. For climate research, it lets scientists measure how much carbon different crops actually push belowground – data that’s been frustratingly hard to pin down but is essential for credible climate accounting in agriculture.

For plant breeding, the digital DNA method creates a path to select varieties that invest more in roots without sacrificing grain or forage aboveground.

And for biodiversity science, the technology finally illuminates the underground dynamics in species mixes – who’s competing, who’s complementing – insights that were “almost impossible before,” Brinch-Pedersen noted.

Roots matter for the climate

We tend to picture wind turbines and EVs when we think of climate solutions, but roots are a vast, quiet carbon pump.

As plants photosynthesize, some of the captured carbon flows belowground into roots and the surrounding soil. Depending on the crop, soil type, and management, a fraction of that carbon can persist for decades or even centuries.

Farmers and policymakers talk about “soil carbon sequestration,” but without precise measurement tools it’s been hard to document gains in ways that stand up to scrutiny. A rapid, species-resolved root assay changes that equation.

DNA test in soil

In practice, researchers collect small soil cores, extract DNA, and run ddPCR with species-specific probes keyed to the ITS2 barcode. The number of positive droplets scales with root biomass for that species in that sample.

Because the test targets DNA directly in soil, it captures fine roots and root fragments as well as thicker roots that are tough to wash and weigh.

There are, however, limits. Close relatives can be tricky to tell apart when their barcodes are nearly identical – ryegrass and Italian ryegrass hybrids, for instance, can blur the signal.

And the method recognizes only what it’s trained to find. Researchers must validate a probe for each species, so expanding the “DNA library” is both the hurdle and the goal.

“For us, the most important thing is that we have shown it can be done,” Brinch-Pedersen said. “Our vision is to expand the library so we can measure many more species directly in soil samples.”

Rapid answers from soil

Speed is the other advantage. Traditional root studies hinge on days to weeks of field and lab work per site. The ddPCR method turns around results in hours, making it practical to scale from a few experimental plots to entire farms, seasons, and regions.

That opens the door to experiments that were previously unrealistic. Researchers can compare cover crops for their belowground carbon contributions across soil types.

They can track how drought shifts root allocation among species in a pasture. They can also screen hundreds of breeding lines for deeper, denser root systems.

Plants that work smarter

Brinch-Pedersen sees a straight line from measurement to design. If breeders can quantify underground investment as easily as they count kernels or measure protein, they can begin to select for crops that are not only high-yielding but also high-sequestering. These are plants that do more of the climate work for us.

The same logic applies to mixtures. With species-level root data, agronomists can compose plant communities that pack more carbon belowground while maintaining forage or grain output above.

The bigger picture is simple: half a plant lives out of sight, and that half shapes soil health, farm resilience, and the climate. With a “DNA test for dirt,” researchers can finally watch that hidden half at work – no shovels required.

The study is published in the journal Plant Physiology.

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Most people recognize Alzheimer’s from its devastating symptoms such as memory loss, while new drugs target pathological aspects of disease manifestations, such as plaques of amyloid proteins. Now a sweeping new study in the Sept. 4 edition of Cell by MIT researchers shows the importance of understanding the disease as a battle over how well brain cells control the expression of their genes. The study paints a high-resolution picture of a desperate struggle to maintain healthy gene expression and gene regulation where the consequences of failure or success are nothing less than the loss or preservation of cell function and cognition.

The study presents a first-of-its-kind, multimodal atlas of combined gene expression and gene regulation spanning 3.5 million cells from six brain regions, obtained by profiling 384 post-mortem brain samples across 111 donors. The researchers profiled both the “transcriptome,” showing which genes are expressed into RNA, and the “epigenome,” the set of chromosomal modifications that establish which DNA regions are accessible and thus utilized between different cell types.

The resulting atlas revealed many insights, described in a paper that appears in the September 4^th issue of Cell, and shows that the progression of Alzheimer’s is characterized by two major epigenomic trends. The first is that vulnerable cells in key brain regions suffer a breakdown of the rigorous nuclear “compartments” they normally maintain to ensure some parts of the genome are open for expression but others remain locked away. The second major finding is that susceptible cells experience a loss of “epigenomic information,” meaning they lose their grip on the unique pattern of gene regulation and expression that gives them their specific identity and enables their healthy function.

Accompanying the evidence of compromised compartmentalization and the erosion of epigenomic information are many specific findings pinpointing molecular circuitry that breaks down by cell type, by region, and gene network. They found, for instance, that when epigenomic conditions deteriorate, that opens the door to expression of many genes associated with disease, whereas if cells manage to keep their epigenomic house in order, they can keep disease-associated genes in check. Moreover, the researchers clearly saw that when the epigenomic breakdowns were occurring people lost cognitive ability but where epigenomic stability remained, so did cognition.

To understand the circuitry, the logic responsible for gene expression changes in Alzheimer’s disease, we needed to understand the regulation and upstream control of all the changes that are happening, and that’s where the epigenome comes in. This is the first large-scale single-cell multi-region gene-regulatory atlas of AD, systematically dissecting the dynamics of epigenomic and transcriptomic programs across disease progression and resilience.”

Manolis Kellis, senior author, professor in the Computer Science and Artificial Intelligence Lab and head of MIT’s Computational Biology Group

By providing that detailed examination of the epigenomic mechanisms of Alzheimer’s progression, the study provides a blueprint for devising new Alzheimer’s treatments that can target factors underlying the broad erosion of epigenomic control or the specific manifestations that affect key cell types such as neurons and supporting glial cells.

“The key to developing new and more effective treatments for Alzheimer’s disease depends on deepening our understanding of the mechanisms that contribute to the breakdowns of cellular and network function in the brain,” said Picower Professor and co-corresponding author Li-Huei Tsai, director of The Picower Institute for Learning and Memory and a founding member of MIT’s Aging Brain Initiative, along with Kellis. “This new data advances our understanding of how epigenomic factors drive disease.”

Kellis Lab members Zunpeng Liu and Shanshan Zhang are the study’s co-lead authors.

Compromised compartments and eroded information

Among the post-mortem brain samples in the study, 57 came from donors to the Religious Orders Study or the Rush Memory and Aging Project (collectively known as “ROSMAP”) who did not have AD pathology or symptoms, while 33 came from donors with early-stage pathology and 21 came from donors at a late stage. The samples therefore provided rich information about the symptoms and pathology each donor was experiencing before death.

In the new study, Liu and Zhang combined analyses of single cell RNA sequencing of the samples, which measures which genes are being expressed in each cell, and ATACseq, which measures whether chromosomal regions are accessible for gene expression. Considered together, these transcriptomic and epigenomic measures enabled the researchers to understand the molecular details of how gene expression is regulated across seven broad classes of brain cells (e.g. neurons or other glial cell types) and 67 subtypes of cells types (e.g. 17 kinds of excitatory neurons or 6 kinds of inhibitory ones).

The researchers annotated more than 1 million gene-regulatory control regions that different cells employ to establish their specific identities and functionality using epigenomic marking. Then, by comparing the cells from Alzheimer’s brains to the ones without, and accounting for stage of pathology and cognitive symptoms, they could produce rigorous associations between the erosion of these epigenomic markings and ultimately loss of function.

For instance, they saw that among people who advanced to late-stage AD, normally repressive compartments opened up for more expression and compartments that were normally more open during health became more repressed. Worryingly, when the normally repressive compartments of brain cells opened up, they became more afflicted with disease.

“For Alzheimer’s patients, repressive compartments opened up, and gene expression levels increased, which was associated with decreased cognitive function,” explained first author Zunpeng Liu.

But when cells managed to keep their compartments in order such that they expressed the genes they were supposed to, people remained cognitively intact.

Meanwhile, based on the cells’ expression of their regulatory elements, the researchers created an epigenomic information score for each cell. Generally, information declined as pathology progressed but that was particularly notable among cells in the two brain regions affected earliest in Alzheimer’s: the entorhinal cortex and the hippocampus. The analyses also highlighted specific cell types that were especially vulnerable including microglia that play immune and other roles, oligodendrocytes that produce myelin insulation for neurons, and particular kinds of excitatory neurons.

Risk genes and ‘chromatin guardians’

Detailed analyses in the paper highlighted how epigenomic regulation tracked with disease-related problems, Liu noted. The e4 variant of the APOE gene, for instance, is widely understood to be the single biggest genetic risk factor for Alzheimer’s. In APOE4 brains, microglia initially responded to the emerging disease pathology with an increase in their epigenomic information, suggesting that they were stepping up to their unique responsibility to fight off disease. But as the disease progressed the cells exhibited a sharp drop off in information, a sign of deterioration and degeneration. This turnabout was strongest in people who had two copies of APOE4, rather than just one. The findings, Kellis said, suggest that APOE4 might destabilize the genome of microglia, causing them to burn out.

Another example is the fate of neurons expressing the gene RELN and its protein Reelin. Prior studies, including by Kellis and Tsai, have shown that RELN- expressing neurons in the entorhinal cortex and hippocampus are especially vulnerable in Alzheimer’s, but promote resilience if they survive. The new study sheds new light on their fate by demonstrating that they exhibit early and severe epigenomic information loss as disease advances, but that in people who remained cognitively resilient the neurons maintained epigenomic information.

In yet another example, the researchers tracked what they colloquially call “chromatin guardians” because their expression sustains and regulates cells’ epigenomic programs. For instance, cells with greater epigenomic erosion and advanced AD progression displayed increased chromatin accessibility in areas that were supposed to be locked down by Polycomb repression genes or other gene expression silencers. While resilient cells expressed genes promoting neural connectivity, epigenomically eroded cells expressed genes linked to inflammation and oxidative stress.

“The message is clear: Alzheimer’s is not only about plaques and tangles, but about the erosion of nuclear order itself,” Kellis said. “Cognitive decline emerges when chromatin guardians lose ground to the forces of erosion, switching from resilience to vulnerability at the most fundamental level of genome regulation.

“And when our brain cells lose their epigenomic memory marks and epigenomic information at the lowest level deep inside our neurons and microglia, it seems that Alheimer’s patients also lose their memory and cognition at the highest level.”

Other authors of the paper are Benjamin T. James, Kyriaki Galani, Riley J. Mangan, Stuart Benjamin Fass, Chuqian Liang, Manoj M. Wagle, Carles A. Boix, Yosuke Tanigawa, Sukwon Yun, Yena Sung, Xushen Xiong, Na Sun, Lei Hou, Martin Wohlwend, Mufan Qiu, Xikun Han, Lei Xiong, Efthalia Preka, Lei Huang, William F. Li, Li-Lun Ho, Amy Grayson, Julio Mantero, Alexey Kozlenkov, Hansruedi Mathys, Tianlong Chen, Stella Dracheva, and David A. Bennett.

Funding for the research came from The National Institutes of Health, The National Science Foundation, the Cure Alzheimer’s Fund, the Freedom Together Foundation, the Robert A. and Renee E. Belfer Family Foundation, Eduardo Eurnekian, and Joseph P. DiSabato.

New research investigates the possibility that different spacecraft could visit Comet 3I/ATLAS, giving scientists a unique on-location view of the interstellar visitor, or even offering the chance to collect material that could be much older than the bodies of our solar system.

Discovered on July 1 by the ATLAS (Asteroid Terrestrial-impact Last Alert System), 3I/ATLAS is just the third-ever object found drifting through our solar system that is believed to have originated from around another star. It therefore offers scientists a unique opportunity to study material from another planetary system. However, recent examination of this interstellar intruder’s trajectory and its velocity of around 130,000 mph (219,000 km/h) has revealed that it could actually originate from a region of our galaxy much older than the solar system and its immediate surroundings.