Coronin 1B Reorganizes the Architecture of F-Actin Networks for Contractility at Steady-State and Apoptotic Adherens Junctions

In this study we sought to identify how contractility at adherens junctions influences apoptotic cell extrusion. We first found that the generation of effective contractility at steady-state junctions entails a process of architectural reorganization whereby filaments that are initially generated as poorly organized networks of short bundles are then converted into co-aligned perijunctional bundles. Reorganization requires coronin 1B, which is recruited to junctions by E-cadherin adhesion and is necessary to establish contractile tension at the zonula adherens. When cells undergo apoptosis within an epithelial monolayer, coronin 1B is also recruited to the junctional cortex at the apoptotic/neighbor cell interface in an E-cadherin-dependent fashion to support actin architectural reorganization, contractility, and extrusion. We propose that contractile stress transmitted from the apoptotic cell through E-cadherin adhesions elicits a mechanosensitive response in neighbor cells that is necessary for the morphogenetic event of apoptotic extrusion to occur. [Display omitted] •Actomyosin network reorganization is necessary for effective junctional contractility•Coronin 1B recruits to E-cadherin contacts, where it regulates F-actin architecture•Actomyosin network reorganization supports apoptotic contractility•E-cadherin recruits coronin 1B for effective apoptotic contractility Michael et al. show that coronin 1B regulates F-actin network architecture reorganization at cell-cell junctions. This not only maintains junctional tension in epithelia at steady state but is also required for apoptotic cell extrusion, suggesting that extrusion requires a mechanosensitive response in neighboring cells elicited by contractile stress in the apoptotic cell.