Cell-ECM interactions regulate epithelial morphogenesis by controlling the architecture and mechancial properties of actomyosin networks, by Maria Dolores Martin-Bermudo of Andaluz de Biología del Desarrollo, Seville, Spain
Date: Thu 24 Oct 2019, 13:00 - 14:00
Location: Fogg Lecture Theatre
Forces generated by the actomyosin cytoskeleton are key contributors to many morphogenetic processes. The actomyosin cytoskeleton organizes in different types of networks depending on intracellular signals and on the way cells interact with each other and with the extracellular matrix (ECM). However, actomyosin networks are not static and transitions between them have been proposed to drive morphogenesis. Still, little is known about the mechanisms that regulate the dynamics of actomyosin networks during morphogenesis. This work uses the Drosophila follicular epithelium, real-time imaging, laser ablation and quantitative analysis to study the role of cell-ECM interactions mediated by integrins in the architecture and maintenance of basal actomyosin networks and its contribution to epithelia morphogenesis. We find distinct integrin requirements for the three types of networks found on the basal surface of follicle cells. Elimination of integrins from follicle cells impairs F-actin recruitment to basal stress fibres and their maintenance. We propose that available F-actin is then incorporated into the cortical cytoskeleton, as we find increased F-actin levels in these basal networks. This reorganization has important consequences for the morphogenesis and homeostasis of this epithelium. Cell autonomously, the rise in cortical F-actin results in increased cortical tension, which restricts growth of the basal surface of mutant cells. Non-cell autonomously, wild type cells contacting mutant ones suffer a dramatic change in their morphology, which includes reorientation of their stress fibres and acquisition of spreading capacity. Altogether, we propose that cell-ECM interactions mediated by integrins regulate epithelia morphogenesis and maintenance by controlling the dynamics and architecture and mechanical properties of the different types of basal actin networks.