Autonomous patterns of cell contraction in the context of localized apical extracellular matrix constraints specify tissue stresses that reshape the wing epithelium.

Overexpression of PLK1 triggers oncogenic transformation and transcriptional reprogramming of prostate epithelial cells, which stimulates cell migration and invasion.

In chick skeletal muscle, an incoming signal leads to two interdependent outcomes: a cell fate change and an epithelial-mesenchymal transition.

Cell movement toward and away from the midline of an epithelium over tens of hours are caused by spontaneous or externally-applied shear forces to eliminate force imbalances within the tissue.

The process of cytokinesis can allow cell lineages to intermix in mammalian epithelia, and cellular aspect ratio is a critical modulator of this behavior.

Quantitative analysis in quasi-3D reveals apically driven cell behaviours that are closely coordinated across the tissue to allow ordered tube invagination through a focal point.

During Kupffer's vesicle morphogenesis, cell volume anisotropy impacts cell shape changes.

The pathogenic bacterium Listeria monocytogenes spreads infection using a two-tiered strategy, where most bacteria spread locally but a few 'pioneers' move further, increasing the likelihood of a persistent infection.

The control of local cell properties such as epithelial cell number and mechanical force production by Hippo signaling is a major determinant of lung branching.

The transcription factor PROP1 controls a genetic network that drives pituitary stem cells to undergo an epithelial-to-mesenchymal-like transition and differentiate.