Tension transmission across a supracellular network drives increased tissue rigidity in the Drosophila retina.

Organ morphologies generated in development must be maintained in dynamic growth environments over long physical distances and timescales. How complex tissues like the Drosophila retina execute specialized cellular morphogenetic programs while maintaining their larger, tissue-scale morphology is not well understood. Here, we show that the developing retina acquires an organ scale curvature early in pupal development. Concurrently, uniform, sustained Rok-mediated actomyosin contractility organized through apical cellular adhesions in interommatidial pigment cells (IOPCs) increases junctional tension across the ommatidial network to drive a ∼5-fold increase in tissue rigidity. Induction of mosaic defects in IOPC junctional tension coupled with in silico modeling of the IOPC network revealed that tension transmission within the IOPC network bridges the cell and tissue scales, providing structural integrity to the retina without changing ommatidial geometry. We propose that tension transmission across tissue-spanning supracellular networks, by uniformly modulating epithelial rigidity, can stabilize three-dimensional organ morphology.