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Updated: Aug 14, 2026

Optogenetic Inhibition of Rho1-Mediated Actomyosin Contractility Coupled with Measurement of Epithelial Tension in Drosophila Embryos
Published on: April 14, 2023
TGF-β signaling modulates adhesion and actomyosin contractility to pattern epithelial permeability in Drosophila
Harshath Amal1, Thea Jacobs1, Max Lohrberg1
1Institute of Integrative Cell Biology and Physiology, Cells in Motion (CiM) Interfaculty Centre, University of Münster, 48149 Münster, Germany.
Abstract:
Epithelial morphogenesis and homeostasis depend on dynamic remodeling of cell-cell junctions. Tricellular junctions (TCJs) control epithelial permeability and plasticity, yet how TCJs are remodeled remains unclear. In the Drosophila ovarian follicular epithelium, TCJs open transiently in a process called patency to allow passage of yolk proteins for uptake by the oocyte. Here we investigated how a TGF-β signaling gradient represses patency along the follicular epithelium. We show that TGF-β signaling blocks patency cell-autonomously by strengthening E-Cadherin (E-Cad)-based adhesion through inducing E-Cad transcription and preventing E-Cad removal from vertices. Elevated E-Cad levels alone are not sufficient to block patency, implying that additional TGF-β-dependent mechanisms stabilize E-Cad at vertices. We identify p120-catenin upregulation as a mechanism that may contribute to strengthened adhesion. In parallel, TGF-β signaling activates myosin II through Rho-Rok signaling. However, myosin II activity is dispensable for TGF-β-mediated patency suppression. Thus, our findings suggest that TGF-β signaling controls TCJ remodeling in follicle cells primarily by reinforcing E-Cad-based adhesion, disentangling the roles of adhesion and actomyosin contractility in maintaining TCJ integrity and revealing how a morphogen gradient spatially patterns epithelial permeability.
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