Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization
Year: 2026
Type: preprint
Abstract: Epithelial gap closure is essential for maintaining tissue integrity during development and wound healing. Previous studies have shown that closure of small gaps is driven by actomyosin purse-string contraction and traction forces generated at the gap edge. Here, we show that millimeter-scale circular gap closure in mouse epicardial (MEC1) monolayers is driven primarily by growth-mediated compressive stresses. Compared with MDCK monolayers, MEC1 cells close gaps more rapidly with reduced undulation near gap edge through coordinated tissue-wide extension-contraction. The collective closing dynamics can be modulated by partial epithelial-mesenchymal transition induction and Rho kinase inhibition. By integrating tissue and cell kinematic analyses, traction-force mapping, and a continuum framework that decomposes tissue strain rates into growth-, elastic-, and fluidity-related contributions, we reveal that growth-generated compression drives inward tissue flow, while elastic cell elongation and fluid-like tissue remodeling through cell-cell intercalation act synergistically to accommodate deformation and promote robust collective gap closure.
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: green
Awards: CAREER: Probing Multiscale Growth Dynamics in Filamentous Cell Walls, Intrasurgical tissue engineering of autologous grafts using irreversible electroporation for bladder reconstruction, Simulating Large-Scale Morphogenesis in Planar Tissues, Biophysics and Cell Biology of Meso-scale Gap Closure, Multiscale modeling of fluidity in partial EMT (pEMT) planar tissues
OpenAlex ID: W7168358524