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Cell sizedependent mRNA transcription drives proteome remodeling

You et al. show that size-dependent proteomic remodeling originates at the transcriptomic level. Protein and mRNA turnover contribute minimally to the proteomes of large cells, implicating transcription as the primary driver of size-dependent gene expression. Moreover, mRNA synthesis scales with size through a proportional increase in burst length.

Complex suicidal somersault behavior in male redback spiders may be explained by surprisingly simple genetics

The Australian redback spider (Latrodectus hasselti), a cousin of the North American black widow spider, is known to practice sexual cannibalism, which is somewhat common among spider species. However, the male Australian redback has also been observed facilitating the process with strange moves. Despite the complexity of these behaviors, a new study, published in Biology Letters, indicates that one of these behaviors arises from simple genetics, while another may be more complex.

Australian redback males perform an extraordinary mating somersault that places their abdomen near the female’s fangs while mating. Although this results in a form of self-sacrifice, the behavior can help males mate longer and father more offspring. This means that even if the female eats them, they were successful from an evolutionary point of view. Some redback spiders also exhibit abdominal narrowing, which makes it more difficult for the female to bite them during mating, delaying death long enough for the male to complete a second mating.

A close New Zealand relative of the Australian redback, the katipo spider, lacks both male self-sacrifice traits and does not exhibit cannibalistic mating behavior. Yet, the two species are capable of mating, producing hybrids. This, however, is only possible with a katipo female and redback male, since the redback female displays only aggressive behavior toward the katipo male.

CRISPR roadblocks: Scientists identify genes blocking gene therapy success

Like a delivery driver navigating crowded city streets, a gene-therapy-toting lipid nanoparticle faces a gauntlet of potential detours on its journey toward a cell’s nucleus. First, there’s entering the cell’s plasma membrane; then navigating around organelles like the Golgi apparatus, mitochondria and endoplasmic reticulum—all destinations that can errantly absorb the particle’s payload, rendering it ineffective at best or harmful at worst. And that’s all before the particle even enters the nucleus and successfully makes a genetic change.

Sleep could help identify people at risk of developing Alzheimer’s disease at an earlier stage

What if certain signs of the disease were to manifest subtly during sleep, long before the first memory problems appear? This is the line of inquiry being explored by a team of researchers at ULiège.

A team of scientists from the University of Liège (GIGA Neurosciences), supported by the Stop Alzheimer’s Foundation, has analyzed the sleep patterns of more than 500 healthy people. Among middle-aged participants, a higher frequency of nocturnal micro-awakenings was found to be associated with a greater genetic risk of developing Alzheimer’s disease, whereas this link was not observed in young adults. This research, published in the journal Sleep, suggests that the study of sleep could, in the long term, contribute to the early identification of vulnerable individuals.

Glioblastoma isoform diversity mapping

Researchers have achieved a major breakthrough in brain cancer research by developing the most comprehensive map to date of isoform diversity in glioblastoma, the most common and aggressive form of brain cancer in adults. Using advanced long-read single-cell sequencing, the team uncovered thousands of previously unknown tumor-specific genetic isoforms that had remained invisible to conventional approaches. The discovery reveals a new source of potential therapeutic targets, including candidates that could be harnessed for future personalised cancer vaccines and immunotherapies. The findings were published in Nature Communications.

Glioblastoma is notoriously difficult to treat because tumor cells within the same patient can behave, grow and respond to treatment differently. Understanding this cellular diversity is essential for developing more effective therapies.

Every gene in the human body can produce slightly different versions of its genetic instructions, known as isoforms. These variations can profoundly influence cellular function and in cancer, may determine whether tumour cells are recognised by the immune system or evade detection. Until now, the technology used to study individual cancer cells could read only short fragments of genetic information, limiting researchers’ ability to study full-length isoforms in individual cells.

In vivo CRISPR screen identifies gene edits that strengthen CAR-T therapy against solid tumors

For patients with blood cancers like leukemia and lymphoma, the immunotherapy known as CAR-T cell therapy can be lifesaving. Doctors remove a patient’s immune cells, called T cells, engineer them in the lab to better recognize and attack cancer, and infuse them back into the bloodstream. But for solid tumors—which include lung, pancreatic, ovarian, colon, breast and other cancer types—these engineered immune cells still face too much resistance to effectively treat the disease.

Now, scientists at Gladstone Institutes and UC San Francisco (UCSF) have discovered a pair of genetic edits that make CAR-T cells more effective at infiltrating and fighting solid tumors. In mice, T cells with these edits dramatically outperformed standard CAR-T cells, clearing tumors in many cases where unedited CAR-T cells had little or no effect.

The discovery, published in Nature, was made using the world’s first in vivo genome-wide CRISPR screen in human T cells. Developed by the same team, this platform enabled researchers to study the effects of gene edits on CAR-T cells inside living mice across the entire genome, rather than only in isolated cell cultures in a dish.

Genetic switch could help tomatoes produce fruit in cold weather

Every tomato begins with a flower. But before a fruit can grow, an intricate sequence of events must happen in perfect order. The flower’s male and female organs must develop together, pollen must be released at exactly the right time, and fertilization must occur.

Many things can disrupt this delicate process, including genetic changes and environmental stress. Temperature extremes are a major challenge: Cold can reduce pollen viability and prevent fertilization, while previous research has shown that heat can also interfere with fruit set.

Now, researchers have uncovered a genetic system that keeps this process synchronized. Their findings could eventually help scientists develop tomato varieties that produce fruit more reliably during challenging growing conditions, including colder seasons.

Did Cellular Life Begin Twice? New Study Points to Two Independent Origins

Early metabolism may have begun as a mix of metal and enzyme catalysis before bacteria and archaea independently evolved into free-living cells.

Four billion years ago, the chemistry that eventually became life may have been unfolding around hydrothermal vents, where naturally occurring metals helped drive reactions before cells possessed the full machinery they use today. Researchers at Heinrich Heine University Düsseldorf (HHU) and collaborating institutions have reconstructed part of that transition, tracing how metabolism and enzymes changed as the ancestors of bacteria and archaea began to diverge.

The study, published in Science Advances, examined the chemical network early cells used to produce essential components of life and investigated how those reactions could have been powered. The researchers conclude that the transition to free-living bacteria and archaea may have occurred independently, even though both lineages share the same underlying genetic code.

Genome study reveals centromeres as one of the fastest-changing regions in human DNA

A centromere is a specific region on a chromosome that ensures that, when a cell divides, the chromosome separates accurately so each new cell receives the correct amount of genetic material. Despite their essential role, centromeres remain one of the last major blind spots in the human genome.

A recent study published in Nature set out to reveal what had been hidden inside human centromeres, using advanced long-read sequencing and custom-built computational tools to piece together 2,110 complete centromeres. The researchers sampled individuals from 28 population groups across five continents, then compared their centromeres with 5,747 assembled by the Human Pangenome Reference Consortium to trace how these regions differ and evolve.

They discovered 226 major centromere haplotypes—distinct genetic patterns—and 1,870 new genetic variants. By studying a four-generation family, they were able to follow centromeres as they changed from parent to child, tracking genetic changes across generations.

For 15,000 years, humans and dogs have been changing each other

Dogs have been shaping—and being shaped by—humans for about 15,000 years, evolving from early partners of hunter-gatherers into an astonishing range of specialized companions. Across the globe, they adapted alongside people to wildly different environments and needs, from powerful Arctic sled dogs and agile rainforest hunters to high-altitude dogs with genetic traits for surviving thin air. Some were even bred for wool, while others played important spiritual or ceremonial roles.

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