A Cdc42-mediated supracellular network drives polarized forces and Drosophila egg chamber extension

Anna Popkova, Orrin J. Stone, Lin Chen, Xiang Qin, Chang Liu, Jiaying Liu, Karine Belguise, Denise J. Montell, Klaus M. Hahn, Matteo Rauzi () and Xiaobo Wang ()
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Anna Popkova: Université de Toulouse, CNRS, UPS
Orrin J. Stone: University of North Carolina at Chapel Hill
Lin Chen: Université de Toulouse, CNRS, UPS
Xiang Qin: Université de Toulouse, CNRS, UPS
Chang Liu: Université de Toulouse, CNRS, UPS
Jiaying Liu: Université de Toulouse, CNRS, UPS
Karine Belguise: Université de Toulouse, CNRS, UPS
Denise J. Montell: University of California
Klaus M. Hahn: University of North Carolina at Chapel Hill
Matteo Rauzi: Université Côte d’Azur, CNRS, Inserm, iBV
Xiaobo Wang: Université de Toulouse, CNRS, UPS

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Actomyosin supracellular networks emerge during development and tissue repair. These cytoskeletal structures are able to generate large scale forces that can extensively remodel epithelia driving tissue buckling, closure and extension. How supracellular networks emerge, are controlled and mechanically work still remain elusive. During Drosophila oogenesis, the egg chamber elongates along the anterior-posterior axis. Here we show that a dorsal-ventral polarized supracellular F-actin network, running around the egg chamber on the basal side of follicle cells, emerges from polarized intercellular filopodia that radiate from basal stress fibers and extend penetrating neighboring cell cortexes. Filopodia can be mechanosensitive and function as cell-cell anchoring sites. The small GTPase Cdc42 governs the formation and distribution of intercellular filopodia and stress fibers in follicle cells. Finally, our study shows that a Cdc42-dependent supracellular cytoskeletal network provides a scaffold integrating local oscillatory actomyosin contractions at the tissue scale to drive global polarized forces and tissue elongation.

Date: 2020
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DOI: 10.1038/s41467-020-15593-2

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