R.-M. Mege

This study investigates how α-catenin, vinculin, and VASP work together in a complex to regulate actin assembly during adherens junction formation.

The paper shows that substrate stiffness drives mechanical switches in epithelial monolayers, leading to stochastic failure through topological defects.

This study shows cells retain memory of their path through physicochemical footprints, leading to self-interacting random walks and altered space exploration.

The paper investigates how epithelial cell monolayers switch from extensile to contractile behavior as intercellular contacts weaken, revealing mechanotransductive responses and implications for cell sorting and tissue dynamics.

This study identifies a dual-mode actin mechanism involving lamellipodia protrusions and purse-string contractility that drives apoptotic cell extrusion in epithelia.

This study shows that collective cell migration in epithelial monolayers arises from single-cell polarity signals rather than cell-cell junctions.

This study shows FGFR1 stabilizes N-cadherin at cell-cell contacts, enhancing adhesion and reducing cell migration through Src and p120 pathways.

This study identifies distinct roles of myosin II isoforms in adherens junction biogenesis, showing NMIIA provides mechanical force for junction maintenance while NMIIB facilitates E-cadherin clustering and anisotropic stress.

This study identifies a novel mode of collective oscillations in epithelial cell sheets under confinement, showing that oscillatory motion drives cellular movements and is regulated by confinement dimensions and force transmission.

This study shows that force-dependent vinculin binding to α-catenin stabilizes adherens junctions and regulates cell-cell contact dynamics and collective cell behavior.