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

Abstract

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.

Coronin 1B supports RhoA signaling at cell-cell junctions through Myosin II

“…1A), as we had previously demonstrated in Caco-2 colon epithelial cells. 20 RNAi-mediated depletion of Coronin 1B in MCF-7 cells (Fig. 1B) perturbed F-actin organization and resulted in the fragmented distribution of the E-cadherin ring at junctions (Fig.…”

“…We recently identified an important role for the actin regulator, Coronin 1B, in the assembly of the actomyosin apparatus at the ZA. 20 We found Coronin 1B was necessary for the architecture of non-aligned F-actin filaments generated by Arp2/3 to be reorganized into aligned bundles, and thereby promote the effective incorporation of NMII to generate contractility and maintain junctional tension. 20 Thus, depletion of Coronin 1B, while dramatically altering F-actin architecture, also reduced junctional NMII localization at the ZA.…”

“…20 We found Coronin 1B was necessary for the architecture of non-aligned F-actin filaments generated by Arp2/3 to be reorganized into aligned bundles, and thereby promote the effective incorporation of NMII to generate contractility and maintain junctional tension. 20 Thus, depletion of Coronin 1B, while dramatically altering F-actin architecture, also reduced junctional NMII localization at the ZA. Given the capacity for NMII to feedback to regulate RhoA, 20 we then wondered if this capacity for Coronin 1B to influence NMII recruitment at the junction, might translate to affect RhoA signaling itself.…”

“…20 Thus, depletion of Coronin 1B, while dramatically altering F-actin architecture, also reduced junctional NMII localization at the ZA. Given the capacity for NMII to feedback to regulate RhoA, 20 we then wondered if this capacity for Coronin 1B to influence NMII recruitment at the junction, might translate to affect RhoA signaling itself.…”

“…7 In addition to activation by RhoA-ROCK signaling 2,19 , the junctional localization of NMIIA can also be influenced by the F-actin networks with which it associates. 20,21 Actin regulators comprise actin polymerization factors as well as regulators of F-actin architecture. Both these groups of proteins can modulate NMII localization and cortical stability by either altering cellular F-actin content or through reorganization of filament networks to facilitate the incorporation of NMII.…”