Fig. 8: Proposed model.

a Comparison between filopodia-based and lamellipodia-based cell migration. Lamellipodia-based migration requires the Arp2/3 complex generating branched actin filament networks that serve as the major engine to push the leading edge forward, whereas filopodia support mesenchymal migration by promoting cell–matrix adhesiveness at the leading edge stabilizing the advancing lamellipodium or by sensing the environment. In filopodia-based migration, it seems that filopodia replace the lamellipodium as the motor of motility. We assume that polymerization of bundled actin filaments through formins pushes parts of the membrane. Arp2/3 complex contributes to filopodia branching and thereby provides new barbed ends generating new filopodia. b Key features and cell behavior in testis myotube migration compared to c migrating mesenchymal neural crest cells undergoing CIL. Different from neural crest cells, myotubes did not migrate as loose cohorts, but maintain cohesiveness. Unlike neural crest cells, migrating myotubes are not simply polarized along a front-rear axis and do not form a contact-dependent intracellular Rho gradient that initiates cell polarization driving directed cell migration. In myotube migration, a contact-dependent asymmetry of cell–matrix adhesion rather acts as a major switch to drive locomotion toward the free space. Individually or loosely connected migrating cells, like neural crests cells are able to migrate persistently due to classical front-rear polarity. By contrast, testis myotubes rely on constant cohesion to break symmetry. Supracellular contractile actin cables contribute to the integrity of the migrating cell cluster and thereby to cohesion.