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Embryonic and mechanical manipulations of Xenopus multiciliated epithelium reveals that cell non-autonomous tensile forces generated by embryonic elongation calibrate cilia number in multiciliated cells via a mechanosensitive ion channel, Piezo1.

Genetic analyses reveal the importance of dynamic protein processing at the apical cell membrane in response to forces damaging cell membranes during tube expansion in tubular organs.

Biological shapes and morphological transitions can emerge from combining directed interactions between cells with apical-basal and planar cell polarity.

ICAM-1 engagement controls hepatic cell polarity, but this receptor can also signal without prior leukocyte interaction, thanks to its confinement into apical, microvilli-enriched, bile-canalicular domains and its actin connector EBP50.

A new morphological structure evolved through extreme changes in cell height requires novel connections to an extracellular matrix network, which predates the origin of structure.

Genetically engineered mouse models show that PLK4 protein and kinase activity are essential for multiciliogenesis, demonstrating that the early steps of centriole assembly are conserved between cycling and multiciliated cells.

Cell-cell junctions and the actin cytoskeleton are key players in the organisation and patterning of the extracellular matrix (ECM) on the apical side of tracheal cells.

Proteins pivotal to epithelial polarization organize in separated clusters, simplifying the current view by showing that a small fraction of the many protein–protein interactions proposed are prominent in mature epithelia.

Neural stem cells in the dentate gyrus have unique cytoplasmic processes that promote privileged access to circulating factors by a unique contact point with an endothelial cell.

The 3D shape and dynamic organization of epithelial cells are far more complex than previously believed, but can be explained with simple physical principles based on lateral surface energy minimisation.