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.
Highlights
Actomyosin supracellular networks emerge during development and tissue repair
While actin bundles extend from medial stress fibers to the sub-basal cell–cell contact zone forming filopodia, myosin II (Myo-II) is not enriched at this zone and concentrates instead in the medial region (Fig. 1j)
Previous studies have shown that subcellular actomyosin oscillations play a key role in egg chamber elongation. We extend this by directly probing subcellular mechanics and by showing how cellular forces are integrated at the tissue scale to drive tissue extension
Summary
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. Supracellular actomyosin networks are commonly reported in developmental processes and tissue repair during wound healing These cytoskeletal structures provide large scale mechanical forces and can function as segregating barriers[1,2] or as mechanical actuators responsible for tissue remodeling as for example epithelial buckling[3], closure[4,5], and extension[6,7]. Filopodia are involved in many biological processes, such as growth cone guidance, cell migration, wound closure, and macrophage-induced cell invasion[12,13,14] These thin membrane protrusions are 60–200 nm in diameter and contain parallel bundles of 10–30 actin filaments held together by actin-binding proteins[15,16]. The formation of parallel actin bundles and filopodia is initiated by the IRSp53-mediated plasma membrane bending and the recruitment of the small
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