Abstract
BackgroundTissue morphogenesis and organogenesis require that cells retain stable cell-cell adhesion while changing shape and moving. One mechanism to accommodate this plasticity in cell adhesion involves regulated trafficking of junctional proteins.Methodology/Principal FindingsHere we explored trafficking of junctional proteins in two well-characterized model epithelia, the Drosophila embryonic ectoderm and amnioserosa. We find that DE-cadherin, the transmembrane protein of adherens junctions, is actively trafficked through putative vesicles, and appears to travel through both Rab5-positive and Rab11-positive structures. We manipulated the functions of Rab11 and Rab5 to examine the effects on junctional stability and morphogenesis. Reducing Rab11 function, either using a dominant negative construct or loss of function alleles, disrupts integrity of the ectoderm and leads to loss of adherens junctions. Strikingly, the apical junctional regulator Crumbs is lost before AJs are destabilized, while the basolateral protein Dlg remains cortical. Altering Rab5 function had less dramatic effects, not disrupting adherens junction integrity but affecting dorsal closure.Conclusions/SignificanceWe contrast our results with what others saw when disrupting other trafficking regulators, and when disrupting Rab function in other tissues; together these data suggest distinct mechanisms regulate junctional stability and plasticity in different tissues.
Highlights
Cell-cell adhesion is critical both for development and disease
In epithelial tissues cadherin-catenin complexes preferentially localize at the apical end of the lateral cell membranes, forming an adhesive belt connecting a cell to its epithelial neighbors
One postulated contributor to junctional plasticity is traffic of junctional proteins, including both targeting after initial synthesis and endocytosis for recycling or destruction
Summary
Cell-cell adhesion is critical both for development and disease (reviewed in [1,2,3,4]). Polarized mammalian cell culture systems (predominantly MDCK cells) have been used to examine regulation of AJ trafficking (reviewed in [9]) In this system, E-Cadherin is targeted to basolateral membranes, where it forms cell-cell adhesive contacts within a monolayer. In the Drosophila imaginal disc epithelium, inactivation of either Rab or the syntaxin Avalanche lead to failure to endocytose the apical junctional protein Crumbs (Crb), disrupting epithelial architecture [31] In this tissue DEcadherin (DEcad) accumulation at the membrane is unaltered [31], in the embryo Crb is essential for AJ maintenance [32]. In the developing wing imaginal disc epithelium, DEcad is trafficked through both Rab5-positive early endosomes and Rab11-positive recycling endosomes, in a process that is dynamin, Rab, and exocyst dependent [33] This regulated cadherin recycling appears to be required for junctional remodeling during planar polarization in this tissue.
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