Even though the ctenophore Mnemiopsis leidyi develops polarized epithelial tissues, polarization is not mediated by the conserved mechanisms polarizing bilaterian and cnidarian epithelial 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.

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.

Myosin isoforms exhibit different functions in the formation of adherens junctions and the transmission of mechanical forces.

Novel modelling strategies can integrate the dynamics of processes regulating the intestinal epithelium at multiple scales in homeostasis and following perturbations to provide unprecedented insights into the biology of the epithelium and support the development of safer novel drug candidates.

Isotonic treatment limits keratinocyte movement, spatially restricts reactive oxygen species production, and rescues sensory neuron function after thermal injury.

Active and passive contributions to cell shape change and rearrangements can be distinguished from observed cell geometry, revealing the self-organization mechanisms underlying internally-driven epithelial convergent extension.

Loss of polarity in epithelial cells leads to mitogenic cytokine upregulation, via coincident activation by JNK and atypical protein kinase C (aPKC), and Polycomb derepression.

Loss of the transcription factor Rreb1 results perturbs epithelial architecture during mouse development resulting in invasive cell behaviors, severe cardiovascular defects, and embryonic lethality.