Sex differences in attention are present at birth, study finds

Amazing stuff!

"... In this new study, infants were presented with side-by-side videos containing a social stimulus, namely a human face with natural movement, and a non-social object, namely a set of metallic balls swinging due to gravity and their mechanical properties (a Newton’s cradle). 

The team found that, regardless of sex, newborn infants generally preferred to look at the social stimulus. However, on average, female infants spent a greater proportion of the time looking at the social stimulus compared to male infants, while male infants spent a greater proportion of time looking at the non-social stimulus compared to female infants. ..."

From the abstract:

"While sex differences in behaviour have attracted considerable scientific interest, their underlying causes are complex and remain poorly understood.

One approach to understand whether early biological factors might play a partial role is to study newborns, who have limited postnatal experiences.

Previous research on neonatal sex differences is extremely limited, and studies that do exist have yielded mixed results, raised methodological concerns, and are yet to be replicated.

To assess these gaps, the present study aimed to reevaluate sex differences in neonatal attention. 130 neonates (67 males, 63 females; mean age = 33 h) were presented with a video of a human face and a non-social object. When analysing percentage looking times, on average, females allocated a greater percentage of time looking at the face relative to males (d = 0.40).

When analysing absolute looking times, females showed a preference for the face compared to the non-social object, while males showed no preference for either. However, no differences were observed between males’ and females’ absolute looking times for the face or object, indicating that sex differences are most prominent in the relative allocation of attention.

Since sex differences in relative attentional patterns are present from the earliest days of life, one possible explanation for this effect may be due to contributions from prenatal factors (e.g., sex hormones). However, alternative explanations may be that these differences reflect general maturational differences between males and females or arise from low-level visual properties of the stimuli rather than their social versus non-social content."

Sex differences in attention are present at birth, study finds | University of Cambridge "Cambridge scientists have shown that girls and boys show differences in what they pay attention to, even at birth. Since these differences are present so early, it is possible they emerge due to prenatal factors."

Sex differences in face looking preferences at birth (open access)

A screen-clipping from the stimulus video depicting the dynamic face and object presented to infants

A majority of larval cells fundamentally transform in metamorphosis

Amazing stuff!

"In brief

• A new study revealed that the majority of larval cells in the marine worm “Schizocardium californicum” appeared to fundamentally transform in metamorphosis, against prior understanding of the process.
• Genetic sequencing of thousands of cells showed evidence of this cellular reprogramming, with larval nerve and gut cells taking on different functions in the adult.
• The findings are the strongest evidence yet of developmental reprogramming in bilaterally symmetrical animals, where one side of the body mirrors the other.

...

Unlike humans, about 80% of animal species undergo metamorphosis, a stepped development from egg to larva to adult, but how it works at a cellular level is not well understood. Some theories and prior research suggested that the original cells in the larva die and are replaced with newly generated adult cells. Other work pointed to cells growing into their same function – for example, larval skin cells would become adult skin cells.

Instead, a ... [new] study has found strong evidence in an acorn worm called Schizocardium californicum that most larval cells were reprogrammed, with even neurons taking on a new role in the adult organism. ...

Cellular reprogramming is thought to happen after an injury or in some species that regenerate organs or whole limbs – but not as a feature of normal development. ..."

From the abstract:

"A major gap in our understanding of animal development is how adult body plans arise in animals with indirect development, where adults emerge from the transformation of a distinct larval form during metamorphosis.

We address this question by examining cellular changes in the enteropneust hemichordate Schizocardium californicum, a species with a complex lifecycle and dramatic metamorphosis.

Employing whole-body single-cell RNA sequencing, we chart the cellular composition and transcriptional dynamics of larval, metamorphic, and adult stages. Our tissue-level atlas reveals that ectodermal and endodermal cell types in larvae and adults occupy distinct transcriptional spaces, showing greater similarity to other cell types within the same life stage than to their counterparts in the opposite stage.

In contrast, mesodermal cell types from both larvae and adults cluster closely together, indicating conserved transcriptional profiles.

These findings demonstrate that the extensive morphological reorganization during metamorphosis is accompanied by broad shifts in transcriptional identity and reveal life-history stage as a major organizing axis of cellular state during the larva-to-adult transition."

Study reshapes understanding of metamorphosis | Stanford Report "Many cells in an acorn worm reprogram into different cell types instead of dying or staying the same, the first evidence of this process in bilaterally symmetrical animals."

Distinct cell states define larval and adult body plans in a hemichordate (open access)

Fig. 1: Indirect developing hemichordates as a model to study the transition between larval and adult body plans.

Fig. 2: Single-cell sequencing reveals the broad diversity of hemichordate cell types.

Fig. 5: Genetic makeup of cell type diversity across life history stages.

Hidden Switch in Cell Division May Point to New Cancer Treatments

Amazing stuff!

"When a cell gets ready to divide, it shuts down its gene-reading machinery almost entirely. ...

For decades, the mechanism behind that shutdown was only partially understood. A new study ... identifies a missing piece: an enzyme best known for tagging RNA molecules that turns out to be wired into the cell division machinery itself. The findings ... may point toward new cancer therapies. ...

The new paper shows this same chain reaction [as in RNA transcription] is triggered the moment a cell commits to division. An enzyme called CDK1 activates METTL3, which sets off the same cascade of events. However, in this case, the goal is to complete transcription and clear mRNA molecules from DNA, rather than making new proteins. ...

The window for all of this is narrow. "Mitosis only lasts about an hour," ... Cells have to condense their chromosomes, segregate them, and complete the whole process within a short period of time. “So it has to be very tightly controlled and very quick [???]." ..."

From the highlights and abstract:

"Highlights

• CDK1 phosphorylates the m6A methyltransferase METTL3 at Ser43 upon mitotic entry

• METTL3 phosphorylation allows 7SK methylation and P-TEFb release for transcription

• METTL3 phosphorylation is required for timely mitotic exit and chromosome segregation

• CDK1-METTL3-7SK-P-TEFb axis integrates RNA methylation into mitotic progression

Summary

Transcriptional elongation undergoes extensive remodeling at mitotic entry, yet how elongation control is integrated into core cell-cycle kinase networks remains unclear.

Here, we identify the m6A methyltransferase METTL3 as a direct substrate of the mitotic kinase CDK1 in mammalian cells.

CDK1-dependent phosphorylation of METTL3 at Ser43 is sharply induced at mitotic entry and promotes m6A methylation of the noncoding RNA 7SK, resulting in release of positive transcription elongation factor b (P-TEFb) from the inhibitory 7SK small nuclear ribonucleoprotein particle (snRNP) complex.

This activation of the m6A/7SK/P-TEFb axis facilitates genome-wide clearance of RNA polymerase II and supports timely mitotic progression.

Endogenous mutation of METTL3 Ser43 or disruption of 7SK methylation impairs elongation dynamics, delays mitotic exit, and increases chromosome missegregation.

These findings integrate RNA methylation into the CDK1-driven mitotic program and reveal a mechanism by which transcriptional elongation is coordinated with chromosome segregation fidelity."

Hidden Switch in Cell Division May Point to New Cancer Treatments | Yale School of Medicine

METTL3 promotes cell-cycle progression via activation of transcriptional elongation (open access)

Graphical abstract

Figure 1 METTL3 is required for cell-cycle progression and is phosphorylated at mitosis

Figure 4 The METTL3/7SK/HEXIM1/P-TEFb axis regulates cell-cycle progression

A study of more than 1,100 mammal and bird species found females outlast males in 72% of mammal species. Really!

Amazing stuff! However, this research is dated, published in October 2025!

" ... In birds, it’s the reverse."

"Females, whether they be human or some other type of mammal, like primates or even whales, tend to outlive men by an average of 5.4 years. ..."

"To the point

• Mammals vs birds: Among the 1,176 species studied, female mammals live on average 13 percent longer than males, while among birds, males live about five percent longer than females.
• Mating strategies play a role: In species with strong competition for mates – as is the case with most mammals – males die earlier. In monogamous species, such as many birds, males often live longer.
• Findings from zoos: Sex differences are more pronounced in wild populations than in zoos. This suggests that both genetic and environmental factors contribute to the discrepancy in life expectancy.

...

An international team ... conducted the most comprehensive analysis of sex differences in lifespan across mammals and birds to date.  ...

Across mammals, females usually live longer—for instance, in baboons and gorillas females often outlive males.

Yet this pattern is not universal: in many birds, insects, and reptiles, males are the longer-lived sex.

One genetic explanation, the heterogametic sex hypothesis, points to differences in sex chromosomes. In mammals, females have two X chromosomes, while males have only one X and one Y (making them the heterogametic sex). ...

Still, there was remarkable variation with many exceptions. “Some species showed the opposite of the expected pattern,” ... “For example, in many birds of prey, females are both larger and longer-lived than males. So sex chromosomes can only be part of the story.” ...

In addition to genetics, reproductive strategies also play a role. Through sexual selection, males in particular develop conspicuous characteristics such as colorful plumage, weapons, or large body size, which increase reproductive success but can shorten lifespan.

The new study supports this assumption: In polygamous mammals with strong competition, males generally die earlier than females.

Many birds, on the other hand, are monogamous, which means that competitive pressure is lower and males often live longer.

Overall, the differences were smallest in monogamous species, while polygamy and pronounced size differences were associated with a more pronounced advantage for females. ...

Parental care also plays a role. The researchers found evidence that the sex that invests more in raising offspring—in mammals, this is often the females—tends to live longer. In long-lived species such as primates, this is likely to be a selective advantage: females survive until their offspring are independent or sexually mature. 

Zoo life reduces—but does not erase—lifespan gaps

A long-standing idea is that environmental pressures—such as predation, pathogens, or harsh climates—drive the observed gaps between males and females. To test this, the researchers turned to zoo populations, where such pressures are largely absent. They found that lifespan gaps persisted even under these protected conditions.

Comparing zoo and wild populations showed that the gaps were often smaller in zoos but rarely disappeared—mirroring the human case, where advances in medicine and living conditions have narrowed but not eliminated the lifespan gap.

The findings suggest that sex differences in lifespan are deeply rooted in evolutionary processes—shaped by sexual selection and parental investment and that genetic differences in the sex determination system may also play a role. ..."

From the abstract:

"Across human cultures and historical periods, women, on average, live longer than men, a pattern best understood from a comparative evolutionary perspective. Here, we analyzed adult life expectancy in 528 mammal and 648 bird species in zoos. Like humans, 72% of mammals exhibited a female life expectancy advantage, while 68% of birds showed a male advantage, as expected from the harmful effects of sex chromosomes described by the heterogametic sex hypothesis.

Yet, sex differences varied widely. 

In zoos, we found strong evidence that this variation generally correlated with both the mating system and sexual size dimorphism.

Although with weaker evidence, the patterns remained consistent in populations from the wild, with an even larger effect of the mating system.

Thus, even in zoos, where environmental pressures are largely reduced, precopulatory sexual selection seems to play a fundamental role in shaping sex differences in life expectancy in mammals and birds."

Tuesday, September 1, 2026 - Join The Flyover

Why Do Women Live Longer Than Men?

Why women live longer than men - evolutionary insights on longevity (original news release, October 2025)

Sexual selection drives sex difference in adult life expectancy across mammals and birds (open access) "Study traces the evolutionary roots of the lifespan gap between women and men"

Tying RNA into many pseudoknots using AI

Amazing stuff! Just a charming exercise or toy academic experiments? Maybe not.

"... Another kind of molecule is employed by cells for a staggering variety of odd jobs: RNA. And determining how sequences of these nucleic acids bend and loop has proven to be a much more formidable challenge.

Especially tricky to predict are RNA pseudoknots: strands that fold and connect in complex ways ... It was precisely because of this knotty problem that a team of researchers tested the latest RNA-designing AIs by asking them to create molecules that fold into 57 pseudoknot structures. Remarkably, the platforms came up with properly folding sequences for 55 of them. ..."

From the editor's summary and abstract:

"Editor’s summary

RNA molecules can fold into intricate three-dimensional shapes that drive much of their biology, but designing new structured RNAs from scratch has remained out of reach.

Townley et al. show that complex RNA structures called pseudoknots can now be designed reliably using artificial intelligence (AI).

In a year-long competition on the citizen science platform Eterna, AI methods solved more than 95% of 57 design challenges, matching the performance of expert human players ... 

Cryo–electron microscopy revealed that the molecules folded into entirely new three-dimensional architectures, sometimes featuring intricate interactions that the AI had not been instructed to build. RNA design has thus entered the deep-learning era. ...

Abstract

RNA design has been hindered by the limited accuracy of three-dimensional (3D) structure prediction. In this study, we show that intricate RNA structures can be generated with current deep learning tools through accurate de novo design of pseudoknot secondary structures.

In an Eterna competition involving 57 pseudoknots, generative artificial intelligence (AI) methods matched experienced human designers in solving most blind challenges, evaluated by single nucleotide–resolution chemical mapping, compensatory mutagenesis, and cryo–electron microscopy.

AI-generated molecules with accurate secondary structures formed well-ordered 3D folds stabilized by noncanonical tertiary interactions not modeled during design.

Success was guided by an RNet foundation model trained on prior chemical mapping data, suggesting that some difficult RNA design tasks may be tractable without first solving RNA 3D structure prediction."

ScienceAdviser

OpenKnot (Eterna competition) "Many important biological processes depend on RNAs that form pseudoknots, and they are among the most conserved structures in evolutionary history. However, scientists still have much to learn about their properties, structure, and functions."

RNet: a network strategy to predict RNA binding preferences (open access)

De novo design of RNA pseudoknots with deep learning (no public access)

De novo design of RNA pseudoknots with deep learning (preprint, open access)

Figure 2 The workflow of RNet.

(A) RNA native structures or 

(B) simulation trajectories are transformed into networks. 

(C) A machine learning-based algorithm decomposes the local and global network properties to identify binding sites.

(D) A distance-based dynamical graph algorithm can accurately describe the binding dynamical motions.

(E, F) Local and Global network properties.

(G) The diagram of the DDNC.

Some of the RNA pseudoknots

Fig 4 Cryo-electron microscopy of AI-designed pseudoknotted RNA.

(A) Secondary structure of Kissing Multiloops (target P20 in Round 3), colored by stem.

(B) AlphaFold 3 3D informed secondary structure and predicted model, colored by stem.

(C-E) For the tested designs from (C) Struct2SeQ-SHAPE, 

(D) MPNN-fixbb, and

(E) gRNAde, cryo-EM derived secondary structures (top), cryo-EM maps (unsharpened) and fitted coordinates, colored by stem (bottom), show high accuracy in recovering the target pseudoknot secondary structure while also highlighting distinct topologies from AlphaFold 3 prediction and noncanonical interactions (insets under (D) and (E)).

Cells use a little-known molecule to protect themselves from iron overload

Amazing stuff! Biological iron is no irony! 😊

Notice the charts in this study are unusually very well done. They tell a consistent story about the function of polyamines.

"... When too much of [iron] is left free inside cells, it can trigger destructive reactions that break down DNA, proteins, and even cell membranes.

Now, ... have discovered that cells rely on an unexpected protector against this threat: small molecules called polyamines.

The researchers’ detailed findings ... reveal that polyamines act like storage lockers for iron, safely holding the metal in a non-reactive state until cells need it.

These findings solve a decades-old mystery about why cells maintain such extraordinarily high levels of polyamines and uncover a previously unknown defense mechanism that protects cells from toxic iron overload. ..."

From the highlights and abstract:

"Highlights

• Genome-wide CRISPR screen identifies polyamine-GPX4 synthetic lethality

• Polyamine depletion raises labile iron and ferritin without altering total iron

• Live-cell labile iron sensor shows inverse coupling with polyamines

• Spermine and spermidine directly coordinate Fe2+ to limit its reactivity

Summary

Polyamines are essential and evolutionarily conserved metabolites present at millimolar concentrations in mammalian cells.

Cells tightly regulate polyamine homeostasis through complex feedback mechanisms, yet the precise role necessitating this regulation remains unclear. Here, we show that polyamines contribute to endogenous buffering of redox-active iron, providing a molecular link between polyamine metabolism and ferroptosis.

Using a genome-wide CRISPR screen, we identified a synthetic lethal dependency between polyamine depletion and the key ferroptosis suppressor, glutathione peroxidase 4 (GPX4).

Mechanistically, we show that polyamine deficiency triggers a redistribution of cellular iron, increasing the labile iron pool and upregulating ferritin.

To directly visualize this iron buffering in living cells, we developed a genetically encoded fluorescent reporter for redox-active iron.

Live-cell analysis revealed a striking inverse correlation between intracellular polyamine levels and redox-active iron at single-cell resolution.

These findings reposition polyamines as key regulators of iron homeostasis, with implications for ferroptosis-linked disease states and cellular redox balance."

Cells use a little-known molecule to protect themselves from iron overload | MIT News | Massachusetts Institute of Technology "This discovery points toward new combination strategies against cancer, and may explain the iron buildup seen in disorders such as early-onset Parkinson’s disease."

Polyamines buffer labile iron to suppress ferroptosis (no public access)

Polyamines buffer labile iron to suppress ferroptosis (preprint, open access)

Graphical abstract

Fig. 1 CRISPR screen identifies modulators of polyamine sensitivity

Fig. 2 Polyamine depletion promotes ferroptosis

Fig 3 Polyamines act independently of canonical ferroptosis regulators

Fig 4 Polyamine deficiency increases redox-active iron

Fig 5 Genetically encoded sensor for redox-active iron

Why do we get sleepy? How neurons control sleep drive

Amazing stuff!

"... researchers from Beth Israel Deaconess Medical Center and Auburn University, have now identified specific neurons that are crucial for this balanced relationship between sleep and wakefulness.

"We have identified neuronal populations that monitor prolonged wakefulness and actively promote sleep," ... "This is an important missing piece of the puzzle in understanding why we become sleepy." ...

This highlighted specific brain areas that reflected time spent awake. Within one of these regions, they further identified two distinct neuronal populations that influence sleep drive: GABAergic and serotonergic neurons in the brainstem.

The activation of both neuronal populations increased the longer the animals stayed awake and declined again after sleep onset. ..."

From the abstract:

"Prolonged wakefulness increases sleep drive and is normally compensated for by increased sleep. This homeostatic regulation of sleep shapes our lives profoundly, but the underlying neural circuit mechanisms remain poorly understood.

Here, we identify wake-activated neurons that regulate sleep drive in mice, using whole-brain activity mapping, targeted neuronal manipulations and electrophysiology.

By comparing whole-brain responses to sleep deprivation, recovery sleep and circadian behaviour, we identify the anterior medial preoptic area and the median raphe as candidate regions that encode sleep deficit. Activating sleep-deprivation-responsive cells in these regions induces increases in sleep duration and intensity that resemble recovery sleep. Conversely, inhibiting deprivation-responsive cells reduces sleep and abolishes the increased sleep propensity usually observed during deprivation.

Neurons in the median raphe that are responsive to sleep deprivation project to subcortical sleep-associated regions and act through the preoptic hypothalamus. These deprivation-sensitive cells include serotonergic neurons and a distinct population of GABAergic neurons, whose intrinsic excitability increases during sleep deprivation.

Co-activation of GABAergic and serotonergic neurons synergistically promotes sleep, whereas 

co-inhibition chronically decreases sleep by nearly 70%.

Remarkably, most mice survive despite this marked reduction in sleep, without the compensatory increases in sleep drive or the behavioural deficits typically associated with severe sleep deprivation.

Together, these results define neuronal populations that are activated during wakefulness and are crucial for sleep drive."

Why do we get sleepy? How neurons control sleep drive

Why do we get sleepy? How neurons control sleep drive (original news release) "Why does staying awake inevitably make us sleepy? Researchers ... have identified neuronal populations in the brain that become activated during prolonged wakefulness and are crucial for sleep drive. Their findings provide new insights on how the brain generates the need for sleep."

Wake-activated neuronal populations that regulate sleep drive (open access)

Sleep-promoting neurons (green) and recently activated neurons (magenta) in the mouse brain.

Fig. 1: Mapping of whole-brain activity reveals correlates of sleep deprivation and recovery.

Fig. 2: Deprivation-TRAP cells promote NREM sleep and slow-wave activity.

Engineers connect bacteria to create living transistors

Amazing stuff! Are we getting closer to artificial biological intelligence? You bet!

The human brain is a lot more energy efficient than machine learning & artificial intelligence. The human brain does not need a voracious water and energy consuming data center!

"MIT researchers have engineered bacteria that can function as transistors, allowing the team to create living “circuit boards” that can be printed onto a growth medium in a Petri dish. ...

The research team designed two different transistors, along with three bacterial strains that relay information between the transistors, giving them the building blocks they need to design nearly any type of circuit. In a new study, they used these cells to create circuits that can add two or three inputs, or send one input to a specific location in the circuit. ..."

From the abstract:

"The multicellular forms and functions seen in biology are controlled by cellular communication and collective computation.

Reprogramming natural systems is difficult because they comprise many signaling molecules connecting a web of regulatory networks within cells.

Here we apply principles from pass transistor logic (PTL) to design bacteria that can be easily reconfigured to perform computations on a solid surface. Strains of Pantoea agglomerans were built to encode two transistors (N-type and P-type) whose inputs and outputs are small molecules. They are connected by three relay strains that convert molecular diffusion to unidirectional flow.

To build circuits, an acoustic liquid handler prints patterns of these five strains on a surface.

By changing the pattern, not requiring any genetic changes, different operations are implemented, including multi-input multioutput logic, demultiplexor, half-adder and full-adder.

This work demonstrates that only five cell types, each encoding a simple operation, can be scaled to create complex computational operations."

MIT engineers connect bacteria to create living transistors | MIT News | Massachusetts Institute of Technology "By wiring together colonies of these bacteria, the researchers built circuits that can perform complicated calculations."

Living circuit boards built by printing bacterial transistors (no public access)

What Drove Life Into The Trees during evolution?

Recommendable!

The host's silver shining nose ring is a little distracting! 😊

(1) What Drove Life Into The Trees? - YouTube

Inheritable, fragmented DNA can transfer from mammalian cell to neighboring cell and change how they function via tunneling nanotubes

Amazing stuff! This could be a major milestone!

"... A new study ... reveals just that: an alternate, previously unknown, route for DNA to travel between cells. Scientists ... found that in some cases when chromosomes failed to divide equally, DNA fragments remained behind in tiny sacs called micronuclei, which float in the cell's cytoplasm rather than the nucleus. Using fluorescently tagged ... cell lines, the researchers observed these micronuclei migrating from one cell to another carrying their DNA passengers with them, which was a surprising discovery. ...

“This has been well-established in organisms such as bacteria through a process called horizontal gene transfer, where bacteria share DNA with neighboring bacteria, allowing them to acquire a new function, such as resistance to antibiotics,” ... “But we were not aware of this type of transfer before in human cells.” ...

in cases of genomic instability, donor cells transferred micronuclei to recipient cells through bridge-like structures called nanotubes. The transfer occurred across multiple human cell types, including retinal pigment epithelial cells, kidney cells, and cancer cells. ...

To test whether this new DNA that came from another cell had a functional impact on the new cell, the scientists engineered donor cells with resistance to a specific antibiotic. After combining donor and recipient cells in culture and inducing chromosome damage, they found that recipient cells acquired the same antibiotic resistance – direct evidence that mammalian cells can trade genetic material through simple cell-to-cell contact. ..."

"In a recent Cell paper ... show that genomic instability drives human cells to transfer fragmented chromosomes to neighbors via tunneling nanotubes (TNTs), with heritable functional consequences, raising fundamental questions about intercellular communication, genome surveillance, and cancer evolution."

From the highlights and abstract:

"Highlights

• Genomic instability generates micronuclei and chromosome fragments in the cytoplasm

• Direct cell-cell contact triggers intercellular transfer of genomic DNA

• Transferred DNA fragments are functional and maintained within recipient cell genomes

• Intercellular DNA transfer can confer heritable phenotypic changes

Summary

The mammalian genome is safeguarded within the confines of the interphase nucleus. However, genomic instability can trigger the mislocalization of nuclear DNA to the cytoplasm within micronuclei or as fragmented chromosomes.

Beyond activating cell-autonomous signaling programs, whether such cytoplasmic DNA can elicit non-cell-autonomous consequences to nearby cells remains unclear. Here, we show that cytoplasmic DNAs undergo intercellular transfer through contact-dependent, cytoskeleton-based nanotube structures connecting adjacent human cells.

Diverse sources of genomic instability—including exposure to mitotic spindle poisons, ionizing radiation, and Cas9-induced chromosome breakage—promote nanotube-mediated DNA transfer in both cancerous and non-cancerous cells. Transferred DNA fragments are stably inherited as functional extrachromosomal genetic elements in the recipient host genome, thereby conferring heritable phenotypic traits to the recipient cell. 

Our findings uncover a horizontal gene transfer-like mechanism through which direct cell-cell contact can propagate genomic instability and reshape mammalian genomes."

Rogue DNA can move from cell to cell and change how they function "Scientists ... discover an important new way that cells trade genetic material"

Broken chromosomes don’t stay home: Tunneling nanotubes carry damaged DNA between human cells (no public access)

Human cells can exchange genomic DNA that alters cell behavior (original news release) "Children’s Research Institute scientists discover that DNA transferred between cells can be inherited, remain biologically active"

Genome instability triggers intercellular DNA transfer between human cells (open access)

Graphical abstract

Figure 1 Intercellular DNA transfer via nanotube-like connections in human cells

Did poop/gut evolve with helped fuel the Cambrian explosion?

Amazing stuff! How did bowel movement and excrement develop in the first place? Still an open question, I believe.

One animal's poop is another animal's treasure!

"The driving force behind this biological big bang, they argue in a recent Trends in Ecology & Evolution review paper, just might have been feces.

While many early animals had already appeared in the fossil record during the preceding Ediacaran period, the Cambrian explosion marked the emergence of animal guts, which naturally produced a whole bunch of animal poop. Even so, fossilized turds—known as coprolites—from this time period are hard to come by, and those that are unearthed tend not to attract much attention. Many are left to gather dust in archives, ... or simply abandoned at the dig site.

For the new study, Kimmig and co-author Russell Bicknell analyzed coprolites recovered from more than 35 deposits around the globe, all dating back to before and during the Cambrian explosion. The prehistoric poo came in all shapes and sizes, from microscopic pellets to coprolites measuring several centimeters long and packed with crushed shells and other bits of undigested food. Some had dissolved upon striking the seafloor, creating something evocatively referred to as an “exploded fecal carpet.” (Maybe those marine critters should have laid off the iceberg lettuce...)

The researchers discovered that, as the Cambrian progressed, animal dung became larger, more common, and more complex, reflecting the development of more sophisticated digestive systems. As more and more of this excrement accumulated, the study authors reason, it would have carried organic matter and valuable nutrients from the rich shallows down into the deep ocean, potentially making these environments more habitable. “Together, these fossils show animals were beginning to process and then redistribute organic matter using entirely novel pipelines ,” ... Such a “fecal revolution,” they explain, may have set the stage for an eruption of new life. ..."

From the highlights and abstract:

"Highlights

The ‘Cambrian Radiation’ comprises the rapid diversification of marine organisms and ecological niches during the Ediacaran to Cambrian Periods. It is also the time during which animals with guts first appear. The appearance of guts, in turn, leads to fecal matter, fossils of which are preserved as coprolites.

Fecal matter is rarely preserved in the Cambrian. However, in a few assemblages, the diversity and development of fecal matter are observed. There was little fecal matter available at the onset of the Cambrian, while larger and more diverse fecal matter became available by the middle Cambrian.

We assess the effect that increased availability of fecal matter had on deeper water environments and how this made such environments habitable for Cambrian organisms.

Combining these observations with data on digestive tracts and biogeochemistry of nutrient cycling in the Cambrian demonstrates that fecal matter played a significant role in driving the Cambrian Radiation.

Abstract

Coprolites—fossil material extruded from an animal’s digestive system—represent a rare insight into trophic interactions in deep time. However, while the first animals appeared about 600 million years ago, the first coprolites are only observed in the earliest Cambrian.

Conversely, in modern oceans, fecal pellets are an important part of the particulate organic carbon in the water column and the global flux of organic carbon to deep water.

In this review, we analyze the impact of the advent of fecal matter on the Cambrian Radiation by examining coprolites, analyzing animal biology, and contextualizing this through the role of fecal pellets in the oceanic nutrient cycle. We illustrate the central position of coprolites in driving the Cambrian Radiation."

ScienceAdviser

On the origin of feces: how animal poo drove Earth’s greatest evolutionary event

How an ‘explosion of excrement’ changed Earth's ecosystems forever

The Cambrian fecal revolution: Fueling the Cambrian Radiation (no public access)

A curious collection of Cambrian coprolites (fossilized poop)

Collagen structure of the porcine eye revealed

Good, but older news!

The fascia consists of collagen.

"Collagen fibers are found in various forms throughout the body, forming the foundational extracellular structure of tissues.

Despite nearly a century of study, high-resolution views of functional, macromolecular collagen fibers have remained elusive because of compositional heterogeneity and data-processing limitations.

Lou et al. analyzed the relatively uniform fibrils from the vitreous body of the eye and were able to determine a high-resolution structure that reveals layers of individual fibrils wrapped in a fourfold symmetric helix.

Sugar modifications are interspersed at defined positions within the fiber and alter packing density and hydration.

The specialized function of vitreous body collagen as a transparent medium is enabled by specific modifications and a composition distinct from that known for structural collagens."

"... 

Composition and Stoichiometry

Type V/XI core: Acts as the internal nucleation center that dictates initial fibril geometry.
Type II shell: Forms an antiparallel outer layer that expands the overall diameter of the fibril.
Type IX and opticin: Decorate the outer surface to regulate spacing, surface properties, and interaction with the surrounding gel.

Stabilization and Assembly

Glycan modification: Abundant galactose-glucose disaccharides attach to hydroxylysine residues within conserved motifs, stabilizing interhelical packing.
Vitreous-specific design: Unlike cartilage counterparts, the type IX collagen in the vitreous lacks the NC4 domain and instead possesses an elongated chondroitin sulfate chain, which preserves the transparent, hydrated gel matrix.

..." (Google Search)

From the abstract:

"Collagen, a fundamental constituent of the extracellular matrix, has long remained elusive to high-resolution structural characterization.

Using a tailored system and optimized cryo–electron microscopy processing for long-period filaments, we determined the structure of native collagen fibrils from the porcine vitreous body, with local resolutions extending from 2.6 to 7 angstroms.

Each 67-nanometer periodic unit contains type II, V/XI, and IX collagen triple helices together with opticin, at a stoichiometry of 8:4:4:4, which reveals their detailed higher-order molecular packing.

Abundant galactose-glucose disaccharides modify hydroxylysine residues in conserved -glycine-X-hydroxylysine- motifs, mediating fibril packing and structural stability.

Our structure uncovers the glycan-mediated assembly principle of collagen fibrils and clarifies the structure-function basis of collagens in the vitreous body."

In Science Journals | Science

The molecular architecture of mammalian vitreous body collagen fibrils (no public access)

Chemists find a new pathway to luminescence through mechanochemical force

Amazing stuff!

"In brief

• Computational modeling revealed an unexpected order of bond breaking in the core molecular structure that causes bioluminescence in nature.
• Mechanical force ruptures the dioxetane molecule’s carbon-carbon bond first, which is contrary to previous understanding of how the break in the molecule’s bonded square of oxygen and carbon atoms leads to light emission.
• The findings suggest the potential to develop improved stress sensors as well as gain insight into some forms of biological luminescence.

...

Chemists have long used molecules called dioxetanes to create light. These molecules have the same core structure that enables biological luminescence: two oxygen atoms and two carbon atoms bonded together in a square. Heat or mechanical force can break those bonds, causing light emission. ...

But when ... researchers modeled force applied to dioxetanes, they found that the bond between the carbon atoms breaks first, then the one between the oxygens."

From the abstract:

"1,2-Dioxetanes are well-known for their chemiluminescent decomposition initiated by O–O bond scission.

Under thermal conditions, this chemiluminescence has been used for molecular imaging, while mechanochemical triggering of chemiluminescence can be a powerful tool for studying stress in materials.

It has been widely assumed that mechanochemical activation follows the same O–O scission pathway as the thermal case.

However, our first-principles simulations of the mechanochemically triggered decomposition of 1,2-dioxetane show that the traditional O–O scission pathway is largely insensitive to applied force.

Instead, a thermally inaccessible C–C bond scission pathway is stabilized by applied force and becomes energetically favored above a critical force (∼1.8–3.0 nN). This force-induced mechanistic switch is robust across various pulling directions and substituents, including the experimentally tested adamantyl derivative.

These findings establish a new, fundamentally force-dependent pathway for chemiluminescence.

They demonstrate that mechanical force can be used not only to accelerate a reaction, but to fundamentally change its mechanism. This presents significant opportunities for new mechanophore design and mechanochemical sensing applications."

Chemists find a new path to luminescence | Stanford Report "The molecule behind the glow of fireflies and plankton breaks apart in an unexpected order under force – a discovery that could lead to better stress sensors and help illuminate some mysteries of the natural world."

The Force Awakens a Dormant Chemiluminescent Pathway in 1,2-Dioxetane (no public access)

Graphical abstract

Why Aging May Be a Program, Not a Breakdown

Very recommendable! An interesting hypothesis! Will we one day find the triggers of the aging program in humans?

"...  Yet the underlying biology of aging remains a matter of uncertainty and debate.

Many lines of research align with the theory that aging is a direct result of decay — the inevitable degradation of molecules (including proteins or DNA), organelles, cells, or whole organs — from external assault or inexorable breakdown. When the body’s repair mechanisms fail to keep pace with these changes ...

Far from a random but linear process of wear and tear ... aging is a stepwise, programmed, orderly affair. “The destruction of the system is programmed at a very early stage,” ... Using technology that offers a systemwide view of the aging process in mice ... has outlined discrete stages of aging, akin to those of embryonic development, that are defined by changes in molecular signals and specific cell populations. In humans, the process likely begins before age 30. ...

In one series of experiments ... processed 21 million cells, sampled from 14 tissues or organs in about 50 male and female mice at five life stages, and built a data set of gene expression for each cell. “It’s extremely large-scale data,” ... “You know which organ it’s from and which age it’s from, and you also know extensive molecular information.” Each stage was marked by a dramatic decline in or expansion of specific cell types. ...

Two of his landmark papers, published in 2025 and 2026 in Science, point to a radical redistribution of the cells that make up the body as mammals age, and describe some of the epigenomic instructions that guide this process. “There are molecular changes and maybe some other changes in aging,” ... “but they all converge in the remodeling of the cell society.” ...

In one set of studies, we extracted more than 20 million cells from various organs from mice of different ages: 3, 6, 12, 16, and 23 months — roughly equivalent to 20, 30, 50, 60, and 75 years in humans. We analyzed the expression of 20,000 genes per cell and used this information to define the cell types. Then we tracked their population dynamics. ...

We found that not every cell type gets changed in aging. We identified 536 main cell types and 1,828 subtypes. Only about one-quarter of these subtypes show a strong shift in aging. Others remain stable across the lifespan.

It is surprising to find that changes in aging are not universal across all the cells, that there are specific cell populations that are more vulnerable. ...

We found that aging can be separated into distinct time windows. In each window, specific groups of cells show coordinated dynamics.

In the early phase, for example, we see that some cell types are rapidly depleted. This is followed by another phase, in which other cells are greatly expanded. ...

researchers have observed a phenomenon called “abrupt aging” in middle-aged humans that is consistent with the cell population dynamics we saw. When researchers analyze protein signatures in human blood, they see a significant change between the mid-40s and late 50s. People also tend to report an abrupt decline in function in middle age ...

What do your findings tell us about the nature of aging?

Previously, people saw aging as a linear accumulation of damage to molecules such as proteins and DNA.

But we found that aging is not a linear process. It’s more like a developmental process, in which there are distinct stages that involve coordinated changes in specific cell types across different organs. Our claim is that aging is not so much molecular damage as a remodeling of the entire cell society. ...

Our technology allows us to examine the genomic program that governs the function of each cell — which regions of the genome are active and which are silent. If it’s random molecular damage, we might see random changes across the genome. But we always see the same regions that are open [active] or closed [silent] at each stage. We identified 280,000 genomic regions that are reproducibly open or closed during the aging process in specific cell types. ...

So the body has a program for aging?

Yes, the abrupt changes in mammalian aging along with the coordinated cellular dynamics at each stage suggest there are upstream signals that control aging. It’s like a tree in autumn: Its leaves fall not in a linear way but in just two weeks during the transition between summer and autumn. ..."

From the editor's summary and abstract (1):

"Editor’s summary

Aging is a complex process that results in functional changes across tissues and cell types. These changes are beginning to be documented across organismal lifespans using single-nuclei RNA sequencing. Zhang et al. generated cell atlases across multiple time points in both a commonly used mouse strain and two immunodeficient strains and their wild-type counterparts, cataloging changes in cell populations and expression changes within cell types over these time points. Investigating the role of a diminished immune complement, the authors found that certain intestinal epithelial populations increased in the absence of these adult lymphocytes. This study provides a resource for researchers studying aging, particularly in the context of immunodeficiency. ...

Structured Abstract

INTRODUCTION

As we age, certain cell types within the diverse cellular landscape of various organs undergo substantial changes. These alterations not only affect the overall function of the organism but also play a critical role in the development of age-related diseases.

Cataloging these vulnerable cell types is essential for understanding the cellular basis of aging-related pathologies and for identifying potential interventions. However, the inherent heterogeneity and varying cell proportions within each organ make it challenging to identify rare but crucial aging-associated cell types. Although single-cell genomics studies have examined the effect of aging on various organs, conventional studies face challenges such as imbalanced sex representation, biased age sampling, and limited cell coverage. These limitations hinder a comprehensive and systematic dissection of the aging process at the cellular level.

RATIONALE

To establish a panoramic cellular characterization of organismal aging in mammals and identify cell types associated with the aging process, we optimized the low-cost, high-throughput EasySci method to establish a unified single-nuclei profiling platform for all major mammalian organs. We collected and profiled tissue and organ samples from mice across their life span using a sex-balanced cohort with multiple replicates, all processed by a single individual to minimize batch effects.

To dissect intercellular regulatory networks, we used a cell-knockdown strategy to selectively deplete mature lymphocytes in vivo in adult and aged mice, allowing us to investigate their role in regulating the population dynamics of other cell types during aging.

RESULTS

We generated PanSci, an atlas comprising single-nucleus transcriptome profiles of 21,786,931 cells from >600 samples, covering 14 different tissues or organs across five life stages in both male and female mice.

This extensive dataset enabled us to construct a unified cellular map of organismal aging, identifying >300 distinct cell types and >3000 cellular states. Using this dataset, we characterized sex-dimorphic gene expression patterns shared across organs and cell types as well as cell types with sex-specific molecular programs. Additionally, by clustering >200 cell subtypes undergoing marked aging-associated population changes, we uncovered nonlinear temporal dynamics of aging at the cellular level.

Moreover, we mapped the cross-organ immune landscape of aging, revealing both widespread and organ-specific alterations in immune cells. We further explored the regulatory roles of the immune system on aging and pinpointed specific age-related cell population expansions that are lymphocyte dependent.

CONCLUSION

PanSci provides a comprehensive catalog of aging-related cell population changes, featuring a balanced representation of replicates across sexes, a broader age range, and substantially larger cell numbers compared with existing studies. Our data suggest that aging, at the cellular level, progresses through dynamic changes rather than a simple linear trajectory.

By identifying >200 distinct cellular states with marked aging-related changes, we demonstrate the potential of scalable single-cell genomic techniques to uncover key cellular targets for therapeutic innovations aimed at restoring cellular functions and rejuvenating systemic biological processes in aging and diseases. ..."

From the editor's summary and abstract (2):

"Editor’s summary

Aging atlases have been generated for multiple organisms, but they are often restricted to capturing the transcriptional landscape across cells.

Lu et al. created a single-cell chromatin accessibility atlas in mice for 21 tissues over three age time points ... They combined this atlas with a previous gene expression atlas of aging and found many changes in cellular composition and chromatin accessibility with aging.

Changes occurred across cell types, but immune cells in particular showed diverging patterns with aging, and the authors were able to trace these patterns to particular transcription factor motifs within the peaks. Many of these changes were sex specific, reinforcing the importance of using diverse samples in such endeavors. ...

Structured Abstract

INTRODUCTION

Aging is the leading risk factor for many diseases. This association underscores the potential of therapies targeting the aging process itself to delay or prevent age-related diseases. Substantial advances in single-cell genomics have enabled the profiling of alterations in aging. However, these analyses typically focus on transcriptomics and overlook the impact of chromatin landscapes.

RATIONALE

Single-cell assay for transposase-accessible chromatin using sequencing (ATAC-seq), which analyzes genome-wide chromatin accessibility at the single-cell level, has enabled the mapping of the cell type–specific chromatin landscape in a range of mammalian tissues.

With a further optimized version of single-cell ATAC-seq by combinatorial indexing (EasySci-ATAC), we investigated aging-associated changes in cell populations and chromatin changes across the entire organism, aiming to identify aging-associated noncoding regions and their corresponding cell types.

RESULTS

In this study, we applied EasySci-ATAC to profile chromatin accessibility in more than 10 million nuclei across 21 tissue types from mice spanning three age groups (1 month, 5 months, and 21 months). We detected a total of 1.3 million cis-regulatory elements and identified cell type–specific usages of them.

We reported aging-associated population dynamics of 536 tissue-level main cell types and 1828 finer-grained subtypes. In broadly distributed cell types, we observed coordinated expansion or depletion of the same subtype in multiple organs.

At the molecular level, we identified extensive chromatin reprogramming with aging, including changes in the accessibility of individual peaks and certain transcription factor motifs, and linked them to expression changes of putative target genes.

Moreover, we detected extensive sexual dimorphism, including age-conserved, sex-specific chromatin states for the same cell types and age-sex interaction effects at both proportional and molecular levels.

CONCLUSION

Our organism-level single-cell chromatin accessibility atlas illuminates how aging remodels cellular composition and regulatory regions of multiple tissues.

In addition to many highly tissue-specific changes, we uncovered coordinated cellular and molecular dynamics that are shared across different organs, including immune remodeling, broad depletion of functional cell types, the emergence of inflammation-related states, and sex-dependent trajectories.

By cataloging these changes, we offer a resource for understanding the molecular logic of aging and for guiding therapeutic strategies aimed at preserving or restoring youthful tissue states. ..."

Why Aging May Be a Program, Not a Breakdown | Quanta Magazine "By deciphering the molecular signatures of millions of mouse cells, Junyue Cao has found that aging is not haphazard wear and tear but rather a “remodeling of the cell society.”"

A panoramic view of cell population dynamics in mammalian aging (1, no public access, only cited 94 times which is low for a paper that was first published March 2024 as preprint)

A Panoramic View of Cell Population Dynamics in Mammalian Aging (1, preprint, open access)

Organism-wide cellular dynamics and epigenomic remodeling in mammalian aging (2, no public access, cite 14 times)

Organism-wide cellular dynamics and epigenomic remodeling in mammalian aging (2, preprint, open access)

Cellular architecture of organismal aging.

An organism-wide single-cell atlas of chromatin accessibility reveals cellular dynamics and epigenomic remodeling during aging.