Inhibition of negative feedback for persistent epithelial cell–cell junction contraction by p21-activated kinase 3

Abstract

Actin and myosin operate at cell–cell junctions during junctional shortening. Here the authors show that prolonged actomyosin contractility can compromise junctional shortening, and that Pak3 is required for attenuation of abnormal active protrusive structure and thus keeps junction contraction, appropriate E-cadherin distribution, and junction shortening in Drosophila.