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Lariat RNA debranching prevents harmful siRNA burst in plants
Lariat RNAs are formed from introns during pre–messenger RNA splicing, after which they are degraded by the debranching enzyme DBR1. Impairment of DBR1 leads to developmental arrest, yet the mechanism remains unclear. In this study, we found that debranching of lariat RNA prevents production of 21- and 22-nucleotide lariat-derived small interfering RNAs (lasiRNAs), which causes a burst of exonic siRNAs, thereby safeguarding development and defense response. LasiRNA biogenesis relied on RNA-dependent RNA polymerases and Dicer-like proteins (DCLs). Upon pathogen infection and dysfunction of DBR1, many lariat RNAs were hijacked by DCL4 and DCL2 and processed into siRNAs that particularly target immunity genes, ultimately disrupting plant defense responses. Collectively, DBR1-mediated lariat RNA removal serves as a protective mechanism to prevent the activation of a small RNA–based defense system in plants.
Sodium crotonate alleviates diabetic cardiomyopathy in association with enhanced histone H3K18 crotonylation
Why heritage sites are at risk in a warming world — and how to save them
Nodeless superconducting gap and electron-boson coupling in (La,Pr,Sm) <sub>3</sub> Ni <sub>2</sub> O <sub>7</sub> films
The discovery of superconductivity in Ruddlesden-Popper bilayer nickelate films under ambient pressure provides an opportunity to directly investigate electronic energy scales of the superconducting state and the pairing mechanism. We report angle-resolved photoemission spectroscopy measurements of superconducting (La,Pr,Sm) 3 Ni 2 O 7 thin films by developing an ultrahigh-vacuum cryogenic sample quenching and transfer technique. A superconducting gap of ~18 milli–electron volts with coherence peaks is observed along the Brillouin zone diagonal. The finite gap persists across the entire Brillouin zone, revealing the absence of gap nodes. A kink is observed in the energy-momentum dispersion at ~70 milli–electron volts below the Fermi level, indicating an electron-boson coupling. The simultaneous observation of a nodeless superconducting gap and electron-boson coupling provides insight into the pairing symmetry and gluing mechanism in Ruddlesden-Popper bilayer nickelates.
A prediction model based on tumor immune microenvironment for immunotherapy response in gastric cancer
Reversible suppression of autophagy in a mouse model reveals neuronal resilience
Impairments in intracellular quality-control mechanisms, including autophagy, affect neuronal integrity and function. Despite numerous studies aimed at slowing neuronal deterioration, it remains unclear whether neuronal function and intracellular quality can be restored once impaired. We developed a mouse model in which autophagy could be rapidly and reversibly regulated to investigate the reversibility of such defects. Suppressing autophagy led to proteome and transcriptome changes, inclusion body accumulation, and axonal swelling, all of which were largely ameliorated after autophagy restoration. Consistent with these cellular abnormalities, autophagy suppression induced motor and cognitive dysfunction, which was also reversed on autophagy restoration. Our findings elucidate the potential resilience of neuronal function and quality enabled by intracellular clearance.
Quantified LIME explainability and class-specific dual-branch trust calibration for safety-critical road-scene perception in autonomous navigation
Words vs. worlds
As building bigger and better chatbots gets harder, AI researchers turn to agents that learn in simulated worlds
Effect of ignition timing on combustion characteristic of the elliptical rotary engine under different rotary speeds
Will AI spark a scientific renaissance — or a diffuse monoculture?
An ancient mystery: missing males
Fossil proteins show 20 members of an extinct human species found in a South African cave were female
Model architecture dominates nutritional estimation accuracy in vision-language systems
Forty years of high-temperature superconductivity
EU Omnibus proposal increases pesticide risks
More efficient environmental risk assessment and stronger protection are achievable
Dorothy Hodgkin: A Life <b>Dorothy Hodgkin: A Life</b> <i>Georgina Ferry</i> Granta Books, 1998. 423 pp.
Antibiotics stimulate protein transfer to persister cells
The exchange of biological matter between bacterial cells drives adaptation and evolution. However, whether bacteria can exchange functional proteins remains unclear. In this work, we found that antibiotic treatment can induce vesicle-mediated horizontal protein transfer within and between bacterial species. We developed a genetic system in Escherichia coli to track transfer events and performed single-cell transcriptomic profiling on an isogenic population of bacteria. Antibiotics stimulated the differentiation of this isogenic population into distinct cell states: donor cells that activated a membrane stress response to release protein-containing vesicles and recipient cells that suppressed this response to acquire protein from their neighbors. Protein uptake enhanced the antibiotic persistence of recipient cells, revealing that vesicle exchange promotes bacterial survival during antibiotic treatment.
Cryo–electron microscopy structures of human cone visual pigments
Human trichromatic color vision relies on three cone opsins [long-, middle-, and short-wavelength-sensitive opsins (LWS-, MWS-, and SWS-opsins, respectively)], whereas scotopic rod vision is mediated by rhodopsin. Although the structure of rhodopsin was solved more than 20 years ago, cone opsin structures have been lacking. Here, we present cryo–electron microscopy structures of the three human cone opsins, each bound to a G protein and all- trans retinal in the presumed active state. All three cone opsins differ markedly from rhodopsin. Within the retinal binding pocket, we identified a distinct counterion site (LWS- and MWS-opsins) and a ring of serines around the retinal (SWS-opsin). The active cone opsin structures explain how amino acid substitutions fine-tune spectral sensitivity and help clarify the molecular basis of color vision deficiencies and key differences in rod versus cone activation.