Role of integrins in epithelial architecture in Drosophila ovary

Abstract

Tissue invasion could be caused by loss of proper epithelial architecture. When this happens, multi-layered epithelia are formed, increasing the invasive potential of a tissue and hyperplasia. Recently, mechanical properties of tumor cells have emerged as important factors during invasion. In our lab, we are interested in the processes that control epithelial formation and maintenance. We use the monolayer follicular epithelium (FE) of the Drosophila ovary as a model system. Integrins are main cell surface receptors connecting the extracellular matrix to the cell’s cytoskeleton. Elimination of integrins from the FE results in multi-layered epithelia. The aim of this study is to identify the mechanisms by which integrins maintain epithelial integrity. By laser-ablation experiments, STED and in vivo analysis, we show that integrin mutant cells exhibit an increase in cellular tension and F-actin levels. In addition, integrin mutant cells show ectopic localization of the myosin light chain (sqh) at their basal membrane. Furthermore, increasing one copy of sqh enhances the loss-of-integrin phenotype, creating malformations in the FE and invasion into the germline. The Hpo pathway has recently emerged as a novel mechanosensor and its elimination from the FE also causes multilayer. Interestingly, we find that in the FE loss of integrins or induced F-actin formation, by overactivation of actin nucleation factors, results in downregulation of the Hpo pathway. Our progress in trying to understand the concerted roles of F-actin regulators, Hippo and integrin signalling pathways in controlling cellular tension in the FE, critical to preserve its monolayered structure, will be discussed.