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Abstract
Adherens junction (AJ) assembly under force is essential for many biological processes like epithelial monolayer bending, collective cell migration, cell extrusion and wound healing. The acto-myosin cytoskeleton acts as a major force-generator during the de novo formation and remodeling of AJ. Here, we investigated the role of non-muscle myosin II isoforms (NMIIA and NMIIB) in epithelial junction assembly. NMIIA and NMIIB differentially regulate biogenesis of AJ through association with distinct actin networks. Analysis of junction dynamics, actin organization, and mechanical forces of control and knockdown cells for myosins revealed that NMIIA provides the mechanical tugging force necessary for cell-cell junction reinforcement and maintenance. NMIIB is involved in E-cadherin clustering, maintenance of a branched actin layer connecting E-cadherin complexes and perijunctional actin fibres leading to the building-up of anisotropic stress. These data reveal unanticipated complementary functions of NMIIA and NMIIB in the biogenesis and integrity of AJ.
Highlights
Tissue integrity and plasticity rely on cell-cell adhesion and cell contractility
NMIIB KD cells presented a strongly enlarged area of junctional F-actin meshwork colocalizing with bÀcatenin that corresponded to overlapping membrane extensions stained with cortactin (Figure 5a,e,f and Figure 5—figure supplement 1a,b). While they retained some of the perijunctional actin bundles, we could observe numerous oblique actin bundles directed toward the junction (Figure 5a and Figure 5—figure supplement 1a,b). These results show that NMIIA supports the organization of perijunctional actin bundles while NMIIB contributes to restrain the extent of the juxtamembrane F-actin meshwork that couples perijunctional bundles to the plasma membrane, restraining lamellipodial activity at the junction
We explore for the first time the involvement of Non-muscle Myosin II (NMII) isoforms during early steps of epithelial junction formation
Summary
Tissue integrity and plasticity rely on cell-cell adhesion and cell contractility. The formation, remodeling and disassembly of cell-cell adhesions are fundamental events accompanying all stages of morphogenesis, tissue homeostasis and healing. AJ mediated by E-cadherin/catenin complexes are key elements of epithelial cell-cell adhesions and the first ones to assemble upon contact initiation (Adams et al, 1998; Green et al, 2010; Takeichi, 2014) They provide strong mechanical coupling between neighboring cells through association with the acto-myosin cytoskeleton (Mege and Ishiyama, 2017). Subsequent signaling events involving Rho GTPases trigger local remodeling of the actin cytoskeleton through Arp2/3- or formin-mediated actin polarization in the vicinity of AJs (Grikscheit et al, 2015; Kovacs et al, 2002; Yamada and Nelson, 2007) These cytoskeletal rearrangements drive the expansion of cellcell contacts and inter-cellular adhesion strengthening (Green et al, 2010; Krendel and Bonder, 1999; Chu et al, 2004)
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