{
  "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.",
  "abstract_shown": true,
  "affiliations": [
    "University of Massachusetts Amherst"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 11,
  "authors": [
    {
      "name": "H. Jiang"
    },
    {
      "name": "C. Wei"
    },
    {
      "name": "P. Wang"
    },
    {
      "name": "J. Johnson"
    },
    {
      "name": "N. Olaranont"
    },
    {
      "name": "Y. Gu"
    },
    {
      "name": "F. Chen"
    },
    {
      "name": "J. Xu"
    },
    {
      "name": "Q. Wen"
    },
    {
      "name": "m. wu"
    },
    {
      "affs": [
        0
      ],
      "name": "Y. Sun"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/f6phmq80qvb25.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.07.09.737575",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.07.09.737575v2.full",
  "id": "f6phmq80qvb25",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.07.09.737575v2",
  "language": null,
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "biophysics"
    ],
    [
      "openalex",
      "1307|Cellular Mechanics and Interactions"
    ]
  ],
  "openalex": "W7168358524",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.07.09.737575v2.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-07-09",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/f6phmq80qvb25.ris",
  "sources": [
    {
      "first_seen": "2026-11-02T12:20:53Z",
      "native_id": "10.64898/2026.07.09.737575",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.07.09.737575v2"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "biorxiv:biophysics",
      "subfield": "biophysics"
    }
  ],
  "title": "Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization",
  "title_text": "Partial epithelial-to-mesenchymal transition mediates profound gap closure through growth and fluidization",
  "type": "preprint",
  "updated_at": "2026-11-03T00:20:34Z",
  "url": "https://research.draconitic.com/paper/f6phmq80qvb25",
  "venue": "bioRxiv",
  "versions": []
}