Data from: ESCRT-III-dependent adhesive and mechanical changes are triggered by a mechanism detecting alteration of Septate Junction integrity in Drosophila epithelial cells

Barrier functions of proliferative epithelia are constantly challenged by
mechanical and chemical constraints. How epithelia respond to and cope
with disturbances of barrier functions to allow tissue integrity
maintenance is poorly characterized. Cellular junctions play an important
role in this process and intracellular traffic contribute to their
homeostasis. Here, we reveal that, in Drosophila pupal notum, alteration
of the bi- or tricellular septate junctions (SJs) triggers a mechanism
with two prominent outcomes. On one hand, there is an increase in the
levels of E-cadherin, F-Actin and non-muscle Myosin II in the plane of
adherens junctions. On the other hand, β-integrin/Vinculin-positive cell
contacts are reinforced along the lateral and basal membranes. We found
that the weakening of SJ integrity, caused by the depletion of bi- or
tricellular SJ components, alters ESCRT-III/Vps32/Shrub distribution,
reduces degradation, and instead favours recycling of SJ components, an
effect that extends to other recycled transmembrane protein cargoes
including Crumbs, its effector β-Heavy Spectrin Karst, and β-integrin. We
propose a mechanism by which epithelial cells, upon sensing alterations of
the septate junction, reroute the function of Shrub to adjust the balance
of degradation/recycling of junctional cargoes and thereby compensate for
barrier junction defects to maintain epithelial integrity.