We use cookies to improve your experience of our website. Privacy Policy

Skip to main content

Materials Research Institute



Cell-ECM interactions regulate epithelial morphogenesis by controlling the architecture and mechancial properties of actomyosin networks, with Maria Dolores Martin Bermudo, Andaluz de Biología del Desarrollo, Seville, Spain

Image: Maria Dolores Martin Bermudo
Maria Dolores Martin Bermudo

Date: 24 October 2019   Time: 13:00 - 14:00

Maria Dolores Martin Bermudo is visiting Queen Mary to give a seminar this Thursday 24th Oct at 1pm in the Fogg lecture theatre. The talk is entitled "Cell-ECM interactions regulate epithelial morphogenesis by controlling the architecture and mechancial properties of actomyosin networks” and an abstract is below.

All are welcome and we look forward to seeing you there.

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.

Location:  Fogg lecture theatre, G.E. Fogg Building, Mile End Campus, Queen Mary