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How one RNA nucleotide switch activates fluorescent dyes

RhoBAST is a tiny RNA molecule that activates fluorescent dyes, enabling researchers to track RNA molecules in living cells with super-resolution. An international collaboration, which includes Ronald Micura and his team from the Institute of Organic Chemistry, has now shown that a small, local “nucleotide flip” within the RNA controls this fluorescence activation.

Fluorescent light-up aptamers (FLAPs) are short RNA sequences that bind and activate small dye molecules that otherwise exhibit only weak fluorescence. This enables genetic tagging of RNAs for live-cell imaging without the need for protein fusion markers. Because the dye is only “switched on” upon binding to the RNA, background fluorescence remains low.

Systems such as Spinach, Broccoli, Mango and Pepper have continuously advanced this principle over the past years. RhoBAST additionally enables high-resolution imaging of individual RNA molecules in living cells.

Cancer Is Quantum — and That Could Change How We Treat It

Beneath cancer’s genetic chaos, tumor cells may be confined to just a handful of recurring states, revealing a simpler path to treatment.

Cancer is often defined by its complexity: countless mutations, shifting cell populations, and tumors that evolve under pressure. But Andrea Califano’s research points to a surprising possibility: that beneath all that variation, cancer cells may be confined to only a handful of stable states.

It is this hidden order that led Califano, a physicist by training and now a cancer researcher, to describe cancer as a “quantum disease.” The comparison is not literal; rather, it reflects the idea that tumor cells may occupy discrete biological states, much as electrons are limited to specific energy levels in an atom.

Chemotherapy alters ‘Darwinian battleground’ in our bodies

Cancer treatments, including chemotherapy and radiation therapy, give a growth advantage to cells with particular genetic changes in healthy tissue, new research finds.

Researchers from the Wellcome Sanger Institute, University of Cambridge, University College London and their collaborators used DNA sequencing to map mutations in normal esophageal tissue from esophageal cancer patients who had received either chemotherapy, chemotherapy and radiation therapy, or no treatment before surgery.

The results, published in Nature Genetics, show that different cancer treatments changed the landscape of mutations in normal tissue. In particular, combined chemotherapy and radiation therapy led to significantly more normal cells with cancer-related mutations in these patients.

Cacao genetics could help breeders reduce heavy metal levels in cocoa beans

Cadmium is a naturally occurring, toxic heavy metal found in many soils across Latin America and the Caribbean, where cacao trees are widely cultivated. It makes its way into cocoa seeds, called beans, that are roasted and made into chocolate, according to the Food and Agriculture Organization of the United Nations (FAO)—but some cacao varieties take up less of the toxic element than others. An international team of researchers, including Penn State scientists, found genetic differences in how two varieties managed cadmium uptake and facilitated the metal’s movement throughout the plant.

The findings—published this week (Sept. 8) in Plant and Soil—may be an early step toward breeding cacao that accumulates less cadmium, according to the collaborators from Penn State and Corporación Colombiana de Investigación Agropecuaria–AGROSAVIA (the Colombian Agricultural Research Corporation).

While trace amounts of cadmium in chocolate don’t present a serious risk to public health, long-term exposure to too much cadmium can lead to bone fragility as well as kidney and lung damage, explained one of the study’s two senior authors, Siela Maximova, research professor of plant biotechnology in Penn State’s College of Agricultural Sciences.

AI reveals new class of cellular ‘off switch’ linked to cancer pathways

Cornell researchers have used artificial intelligence to uncover a previously unknown way cells control how proteins move inside them, a process essential for growth, communication and movement, and one that is often disrupted in cancer.

The study, published Sept.9 in the Journal of Cell Biology, shows that a little-understood protein called Avl9 acts as an “off switch” for another protein, Arf1, which helps direct where materials go inside cells. Turning Arf1 off at the right time is critical as it regulates cellular transport, otherwise cells become disorganized which leads to negative effects. The researchers also found that Avl9 is part of a broader group of proteins that may perform the same function, pointing to a previously unrecognized system cells use to keep this process in balance.

Led by Chris Fromme, professor of molecular biology and genetics at the College of Agriculture and Life Sciences and faculty in the Weill Institute for Cell and Molecular Biology, the team used AlphaFold, an artificial intelligence software that predicts the structures of proteins and how they might interact, to search for previously unknown partners of Arf1.

Google DeepMind publishes AIpowered predictions for the effect of all 9 billion possible singlepoint mutations to human DNA

DeepMind’s catalogue of predicted DNA mutation effects, could help scientists unlock the cause of rare genetic diseases and help them find cures.

Scientists engineer ready-to-use cancer-fighting T cells for solid tumors

T-cell receptor, or TCR, therapy is a cancer treatment that genetically reprograms immune cells, called T cells, to hunt down cancer with precision. It’s similar to another treatment, CAR T-cell therapy, but with one key difference: CAR T-cell therapy can only spot proteins that naturally appear outside a cancer cell. TCR therapy, however, can also catch small protein fragments from inside the cell that are carried to the surface and displayed like little name tags.

Scientists Uncover New Clues Behind the “Suicide Headache” Mystery

Cluster headache causes extreme pain, but its origins remain unclear. New research links the disorder to genetics, inflammation, and tobacco smoke exposure.

Unlike an ordinary headache, a cluster attack typically erupts without warning and causes excruciating pain around one eye. Episodes can last from 15 minutes to three hours and often return at similar times each day. The severity of the condition has led to its troubling nickname, the “suicide headache.”

Scientists have long suspected that both genes and environmental exposures contribute to cluster headaches. Two studies from Karolinska Institutet in Sweden have now examined those influences from different angles, revealing signs of inflammation, altered gene regulation, and increased exposure to toxic substances.