Journal
NATURE PHYSICS
Volume 15, Issue 11, Pages 1195-1203Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41567-019-0618-1
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Funding
- Medical Research Council Skills Development Fellowship [MR/N014529/1]
- EPSRC
- Swiss National Science Foundation [31003A-160095]
- Royal Society University Research Fellowship [URF/R1/180187]
- UCL Institute for the Physics of Living Systems
- Medical Research Council Fellowship [MR/L009056/1]
- UCL Excellence Fellowship
- NSFC International Young Scientist Fellowship [31650110472]
- Lister Institute Research Prize Fellowship
- MRC [MC_U12266B]
- Swiss National Science Foundation (SNF) [31003A_160095] Funding Source: Swiss National Science Foundation (SNF)
- MRC [MR/L009056/1, MR/N014529/1] Funding Source: UKRI
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The collective behaviour of cells in epithelial tissues is dependent on their mechanical properties. However, the contribution of tissue mechanics to wound healing in vivo remains poorly understood. Here, we investigate the relationship between tissue mechanics and wound healing in live Drosophila wing imaginal discs and show that by tuning epithelial cell junctional tension, we can systematically alter the rate of wound healing. Coincident with the contraction of an actomyosin purse string, we observe cells flowing past each other at the wound edge by intercalating, reminiscent of molecules in a fluid, resulting in seamless wound closure. Using a cell-based physical model, we predict that a reduction in junctional tension fluidizes the tissue through an increase in intercalation rate and corresponding reduction in bulk viscosity, in the manner of an unjamming transition. The resultant fluidization of the tissue accelerates wound healing. Accordingly, when we experimentally reduce tissue tension in wing discs, the intercalation rate increases and wounds repair in less time.
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