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Integrin-based adhesions promote cell-cell junction and cytoskeletal remodelling to drive embryonic wound healing
Journal article   Peer reviewed

Integrin-based adhesions promote cell-cell junction and cytoskeletal remodelling to drive embryonic wound healing

Michelle Ly, Clara Schimmer, Raymond Hawkins, Katheryn E Rothenberg and Rodrigo Fernandez-Gonzalez
Journal of cell science, Vol.137(5), 261138
03/01/2024
DOI: 10.1242/jcs.261138
PMID: 37970744

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Abstract

Embryos repair wounds rapidly, with no inflammation or scarring. Embryonic wound healing is driven by the collective movement of the cells around the lesion. The cells adjacent to the wound polarize the cytoskeletal protein actin and the molecular motor non-muscle myosin II, which accumulate at the wound edge forming a supracellular cable around the wound. Adherens junction proteins, including E-cadherin, are internalized from the wound edge and localize to former tricellular junctions at the wound margin, in a process necessary for cytoskeletal polarity. We found that the cells adjacent to wounds in the Drosophila embryonic epidermis polarized Talin, a core component of cell-extracellular matrix (ECM) adhesions, which preferentially accumulated at the wound edge. Integrin knockdown and inhibition of integrin binding delayed wound closure and reduced actin polarization and dynamics around the wound. Additionally, disrupting integrins caused a defect in E-cadherin reinforcement at tricellular junctions along the wound edge, suggesting crosstalk between integrin-based and cadherin-based adhesions. Our results show that cell-ECM adhesion contributes to embryonic wound repair and reveal an interplay between cell-cell and cell-ECM adhesion in the collective cell movements that drive rapid wound healing.
Actins - metabolism Animals Cadherins - metabolism Cell Adhesion Cell Movement - physiology Drosophila - metabolism Integrins - metabolism Intercellular Junctions - metabolism Wound Healing - physiology

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