ReviewTension (re)builds: Biophysical mechanisms of embryonic wound repair

- Rapid wound repair in embryonic epithelia is driven by collective cell movements.
- Cell movements around wounds are coordinated by junctional and cytoskeletal rearrangements.
- A calcium-dependent, heterogeneous actomyosin cable contracts and pulls neighbouring cells into the wounded region.
- Contractile forces are transmitted around the wound through cell junctions assembled at discrete points at the wound edge.
- Actin-based protrusions promote cell migration and sheet fusion during tissue repair.

Embryonic tissues display an outstanding ability to rapidly repair wounds. Epithelia, in particular, serve as protective layers that line internal organs and form the skin. Thus, maintenance of epithelial integrity is of utmost importance for animal survival, particularly at embryonic stages, when an immune system has not yet fully developed. Rapid embryonic repair of epithelial tissues is conserved across species, and involves the collective migration of the cells around the wound. The migratory cell behaviours associated with wound repair require the generation and transmission of mechanical forces, not only for the cells to move, but also to coordinate their movements. Here, we review the forces involved in embryonic wound repair. We discuss how different force-generating structures are assembled at the molecular level, and the mechanisms that maintain the balance between force-generating structures as wounds close. Finally, we describe the mechanisms that cells use to coordinate the generation of mechanical forces around the wound. Collective cell movements and their misregulation have been associated with defective tissue repair, developmental abnormalities and cancer metastasis. Thus, we propose that understanding the role of mechanical forces during embryonic wound closure will be crucial to develop therapeutic interventions that promote or prevent collective cell movements under pathological conditions.