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Chiral Porous Sheet Assembly for Multiple Chirality Induction in Macrocycle Formation
Aqueous asymmetric pseudocapacitor featuring high areal energy and power using conjugated polyelectrolytes and Ti3C2Tx MXene
Evaluation of synergistic factors on BTEX urinary biomarkers in motorcycle riders exposed to heavy traffic in a megacity
Chlorocobaltate-Enabled Selective Separation of CoCl<sub>2</sub> from Mixed Chloride and Nitrate Salts of Mn, Co, and Ni
Neural Network Nodal Ambient Noise Tomography of a transient plumbing system under unrest, Vulcano, Italy
Numerical simulation of transcranial static magnetic fields for the treatment of global epilepsy in children
Surface Fe<sup>IV</sup>═O Induced Highly Selective Phenol Polymerization via Proton-Coupled Electron Transfer
Vibrio cholerae motility is associated with inter-animal transmission
Abstract Outbreaks of cholera are caused by the highly transmissive pathogen Vibrio cholerae. Infant mouse studies have elucidated many aspects of V. cholerae pathogenesis; however, the components of pathogenesis that feed-forward to promote transmission have remained enigmatic because animal models routinely bypass the mechanisms of inter-animal transmission by directly inoculating cultured bacteria into the stomach. Here, a transposon screen reveals that inactivation of the V. cholerae motility-linked gene motV increases infant mouse intestinal colonization. Compared to wild-type V. cholerae, a ΔmotV mutant, which exhibits heightened motility in the form of constitutive straight swimming, localizes to the crypts earlier in infection and over a larger area of the small intestine. Aberrant localization of the mutant is associated with an increased number of V. cholerae initiating infection, and elevated pathogen burden, diarrhea, and lethality. Moreover, the deletion of motV causes V. cholerae to transmit from infected suckling mice to naïve littermates more efficiently. Even in the absence of cholera toxin, the ΔmotV mutant continues to transmit between animals, although less than in the presence of toxin, indicating that phenotypes other than cholera toxin-driven diarrhea contribute to transmission. Collectively, this work provides experimental evidence linking intra-animal bottlenecks, colonization, and disease to inter-animal transmission.
Insights into the interaction of Fibrinogen with Timolol Maleate and elucidation of binding sites via. spectroscopic and molecular docking study
Unraveling the Relaxation Dynamics of Uracil: Insights from Time-Resolved X-ray Photoelectron Spectroscopy
A cis-natural antisense RNA regulates alternative polyadenylation of SlSPX5 under Pi starvation in tomato
Improving perceptions of cultivated meat and plant-based proteins in Singapore
Mapping Excited-State Decay Mechanisms in Acetylacetone by Sub-20 fs Time-Resolved Photoelectron Spectroscopy
Author Correction: Cycloparaazine, a full-azine carbon nanoring
Hybrid optimization-based deep learning for energy efficiency resource allocation in MIMO-enabled wireless networks
An abiding mystery of the French Revolution is solved — by epidemiology
Structure–Function Relationships in Sequence-Controlled Copolymers for Rare Earth Element Chelation
The balance between B55α and Greatwall expression levels predicts sensitivity to Greatwall inhibition in cancer cells
Abstract The Greatwall kinase inhibits PP2A-B55 phosphatase activity during mitosis to stabilise critical Cdk1-driven mitotic phosphorylation. Although Greatwall represents a potential oncogene and prospective therapeutic target, our understanding of the cellular and molecular consequences of chemical Greatwall inactivation remains limited. To address this, we introduce C-604, a highly selective Greatwall inhibitor, and characterise both immediate and long-term cellular responses to the chemical attenuation of Greatwall activity. We demonstrate that Greatwall inhibition causes systemic destabilisation of the mitotic phosphoproteome, premature mitotic exit and pleiotropic cellular pathologies. Importantly, we show that the cellular and molecular abnormalities associated with reduced Greatwall activity are specifically dependent on the B55α isoform, rather than other B55 variants, underscoring PP2A-B55α phosphatases as key mediators of the cytotoxic effects of Greatwall-targeting agents in human cells. Additionally, we establish that sensitivity to Greatwall inhibition varies in different cell line models and that dependency on Greatwall activity reflects the balance between Greatwall and B55α expression levels. Our findings highlight Greatwall dependency as a cell-specific vulnerability and propose the B55α-to-Greatwall expression ratio as a predictive biomarker of cellular responses to Greatwall-targeted therapeutics.