Protein phosphatase 1 activity promotes cohesive collective cell migration by restricting actomyosin contractility to the periphery of the collective and maintaining proper cadherin–catenin complex protein levels at cell–cell junctions.

Epithelia exhibit size-dependent growth dynamics caused by a decoupling between boundary and bulk cellular dynamics that enable robust expansion and drive cell cycling, collective migration, and tissue-spanning vortices.

Notch signaling controls the collective migration of parapineal cells through its capacity to restrict FGF pathway activation to a few leading cells.

Neural crest cells differentiated from patient-derived cells with mutations in the chromatin remodeler CHD7 show defective delamination, migration and motility in vitro, and defective migration in chick embryos.

Computational and experimental studies show that different migration modes of eukaryotic cells are the result of the interplay between signaling waves and cell mechanics.

Uniform activation of Frizzled7 signaling is required and sufficient for directional mesendoderm cell migration during zebrafish gastrulation.

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

The ATM kinase has an unanticipated role in tumor progression through the regulation of cell migration by oxidative stress.

Genetic and biochemical approaches identify a new component of the cellular signaling machinery driving migration of limb muscle precursor cells during mouse embryogenesis and reveal the underlying molecular mechanism.

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.