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bioRxiv · 10.1101/2020.10.19.345082

Filopodia-based contact stimulated collective migration drives tissue morphogenesis

Bischoff, M.·Renkawitz-Pohl, R.·Bogdan, S.
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Abstract

Cells migrate collectively to form tissues and organs during morphogenesis. Contact inhibition of locomotion (CIL) drives collective migration by inhibiting lamellipodial protrusions at cell-cell contacts and promoting polarization at the leading edge. Here, we report on a CIL-related collective cell behavior of myotubes that lack lamellipodial protrusions, but instead use filopodia to move as a cohesive cluster in a formin-dependent manner. Genetic, pharmacological and mechanical perturbation analyses reveal essential roles of Rac2, Cdc42 and Rho1 in myotube migration. They differentially control not only protrusion dynamics but also cell-matrix adhesion formation. Here, active Rho1 GTPase localizes at retracting free edge filopodia. Rok-dependent actomyosin contractility does not mediate a contraction of protrusions at cell-cell contacts but likely plays an important role in the constriction of supracellular actin cables. We propose that contact-dependent asymmetry of cell-matrix adhesion drives directional movement, whereas contractile actin cables contribute to the integrity of the migrating cell cluster.

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Bischoff, M., Renkawitz-Pohl, R., Bogdan, S.. 2020-10-19. Filopodia-based contact stimulated collective migration drives tissue morphogenesis. https://doi.org/10.1101/2020.10.19.345082

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