Actin protrusions push at apical junctions to maintain E-cadherin adhesion

Significance All solid tissues rely on cadherin family cell–cell adhesion molecules for their cohesion and organization. Cadherin adhesive function depends on the actin cytoskeleton, but actin’s contribution to cell–cell adhesion is not fully understood. We demonstrate that actin polymerization-dependent protrusive activity operates continuously to push lateral membranes of neighboring cells together to keep cadherins in contact. Actin-dependent protrusive activity functions as a safety mechanism to quickly repair cadherin adhesive junctions whenever they fail and to prevent myosin-dependent contractile forces from tearing the junctions further apart. Since loss of cadherin adhesion is associated with a number of diseases including cancer progression, then misregulation of actin protrusive activity should be considered as a possible contributing factor to epithelial pathophysiology.