Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization
- 1University of Massachusetts Amherst
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.
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BibTeX
@misc{jiang2026partial,
title = {{Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization}},
author = {H. Jiang and C. Wei and P. Wang and J. Johnson and N. Olaranont and Y. Gu and F. Chen and J. Xu and Q. Wen and m. wu and Y. Sun},
howpublished = {bioRxiv},
year = {2026},
month = jul,
doi = {10.64898/2026.07.09.737575},
url = {https://www.biorxiv.org/content/10.64898/2026.07.09.737575v2},
note = {CC BY},
}
RIS
TY - UNPB
TI - Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization
AU - H. Jiang
AU - C. Wei
AU - P. Wang
AU - J. Johnson
AU - N. Olaranont
AU - Y. Gu
AU - F. Chen
AU - J. Xu
AU - Q. Wen
AU - m. wu
AU - Y. Sun
PY - 2026
DA - 2026/07/09
PB - bioRxiv
DO - 10.64898/2026.07.09.737575
UR - https://www.biorxiv.org/content/10.64898/2026.07.09.737575v2
AB - 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.
ER -