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BoNT intoxication of neurons is revisited using a genome-wide siRNA screen and organelle-specific reporters, suggesting a mechanism of translocation to the cytosol fundamentally different than previously proposed.

The cell cycle phosphatase CDC25B controls cell cycle progression and neurogenesis through independent pathways.

Computations based on detailed atomic models explain how the ATP-driven sodium-potassium pump avoids transporting the wrong type of ions in order to maintain the physiological concentration of sodium and potassium ions across the cell membrane.

Embryonic fate-mapping approaches in zebrafish, Xenopus and lamprey illuminate the evolutionary origins of carotid body glomus cells and pulmonary neuroendocrine cells.

Independent osmotic, genetic and biochemical perturbations modulate neurotransmitter release in a multiplicative manner.

Enzyme evolution is reversible on a structural and functional (phenotypic) level, but through a different mutational pathway that leads to genotypic incompatibility with the ancestor.

Quantitative statistical modelling reveals local coordination of stochastic gene transcription dynamics in pituitary tissue, which is relevant for integrated tissue responses to physiological stimuli.

Ezrin controls endo-lysosomal signaling by maintaining TSC inhibition through EGFR signaling, activating mTORC1, and inhibiting lysosomal function, unveiling a critical endosome–lysosome network essential for autophagy and cellular homeostasis.

Systems analysis of antibody repertoires reveals that strong humoral responses lead to extensive B-cell overlap across multiple lymphoid organs, indicating physiological axes of B-cell migration and a direct correlation with antigen specificity.

The most vulnerable motor units lose a fundamental firing property before the denervation of their muscle fibers in ALS mice, changing our view of the role of excitability in neurodegeneration.