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Updated: Apr 15, 2026

A Drosophila Model to Study Wound-induced Polyploidization
Published on: June 9, 2020
Rho family GTPase functions in Drosophila epithelial wound repair
Jeffrey M Verboon1, Susan M Parkhurst
1a Division of Basic Sciences; Fred Hutchinson Cancer Research Center ; Seattle , WA USA.
Abstract:
Epithelial repair in the Drosophila embryo is achieved through 2 dynamic cytoskeletal machineries: a contractile actomyosin cable and actin-based cellular protrusions. Rho family small GTPases (Rho, Rac, and Cdc42) are cytoskeletal regulators that control both of these wound repair mechanisms. Cdc42 is necessary for cellular protrusions and, when absent, wounds are slow to repair and never completely close. Rac proteins accumulate at specific regions in the wound leading edge cells and Rac-deficient embryos exhibit slower repair kinetics. Mutants for both Rho1 and its effector Rok impair the ability of wounds to close by disrupting the leading-edge actin cable. Our studies highlight the importance of these proteins in wound repair and identify a downstream effector of Rho1 signaling in this process.
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