Stress fibers with multiple adhesions along their lengths and treadmilling dynamics may help migrating epithelial cells maintain a linear trajectory and thereby reinforce their collective motility.

Cellular and tissue level analysis reveals how different cell behaviors involving dynamics of the basal domain cooperate in space and time to shape an epithelial organ.

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

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

Nuclear export inhibition reveals concurrent epithelial and mesenchymal phenotypes that cause mechanosensitive disorder in collectively migrating epithelia.

Eph receptor signaling commonly excludes migrating embryonic cells from regions of high ligand density; however, in sea urchin embryos pigmented immunocytes are attracted to regions expressing high levels of Ephrin.

Neuronal progenitor cells autonomously inhibit polarization via the transcription factor Zeb1.

Epithelial cells utilize a covering sheath of motile cells to migrate in confinement.

Skin cells in zebrafish use sodium chloride-dependent electrical gradients to sense tissue injury and guide migration in the appropriate direction to close the wound.

A key Ras-driven signaling pathway stimulates the preferential translation of an effector, EPSTI1, that is both necessary and sufficient for the epithelial-to-mesenchymal transition-like phenotype in colorectal cancer cells.