Quantitative proof that persistent cell migration in the timescale of hours relies on a feedback between polarized trafficking and protrusive activity stabilizing cell front.

Stochastic cell migration modulates exposure to signals that regulate commitment in the nephron progenitor niche.

Functional analysis of filopodia by specific interference with their formation and distribution reveals a critical role in conferring intracellular polarity and in controlling the dynamic properties of chemokine-guided cell migration in vivo.

β- and γ-cytoplasmic actins have different translation rates in cells and exert different nucleotide coding sequence-dependent effects on cell migration.

Fat2 signals from the trailing edge of each cell to localize WAVE activity to the leading edge of the cell behind, polarizing protrusive regions within cells and across the epithelium.

Data-driven mathematical modeling suggests that leading neural crest cells in a moving stream can robustly communicate with trailing cells by remodeling their extracellular matrix, thereby enabling long-distance collective migration.

The p75 neurotrophin receptor prevents the migration of the granule cell precursors away from its mitogenic niche in the external granule layer of the cerebellum, by maintaining a pool of undifferentiated cells capable of responding to mitogenic signals.

Expression of Pitx2c at the onset of gastrulation drives convergence and extension movements in the zebrafish embryo by promoting downstream pathways affecting chemokine signaling, integrin-ECM interactions, and planar cell polarity components.

Analysis of axial polarity distributions shows that Wnt5a regulates collective cell migration in vivo by stabilizing vinculin at adherens junctions and fine-tuning mechanocoupling between neighbouring cells.

Computational modelling and experimental manipulation show that Notch signalling regulates collective cell migration by allocating distinct migratory identities through the control of cell cycle progression.