Our early studies showed how a rapidly assembled, multicellular actin cable can function as a contractile purse-string to close wounds in simple epithelia including that of vertebrate embryos, and that assembly of this wound actin cable is dependent on the small GTPase switch, Rho. We subsequently established the Drosophila embryo as a model to image the wound re-epithelialisation process in vivo and showed that the actin cable, as well as dynamic, finger-like, zippering, filopodia that extend from leading edge cells, are required both for the repair of wounds and for the normal embryonic morphogenetic process of dorsal closure in Drosophila.  This finding gave rise to the now widely accepted dogma that “wound healing recapitulates morphogenesis”.

We have also demonstrated an active role for cells back from the leading edge during wound re-epithelialisation: live imaging of fly embryo wounds revealed that stochastic myosin flashes direct cell contractions that enable cell intercalation events that, in turn, release tension within the epithelium and allow it to advance forwards, and studies using transgenic mouse lines showed that Eph signalling drives junctional “loosening” to enable partial EMT for wound re-epithelialisation.

A “scribble video” highlighting a paper by Rob Nunan (also a keen surfer) where he showed how Eph signalling appears to mediate the loosening of epidermal “follower” cells to enable tension release and efficient wound re-epithelialisation

We are now utilising AI algorithms which can automatically quantify the contributions made by cell shape changes, cell movements, and cell divisions in large numbers of Drosophila pupal wounds to determine how these cell behaviours drive wound re-epithelialisation. Most recently, we have been knocking down each of the known conserved wound "damage" signals - the calcium flash, JNK signalling, and also inflammatory cells which deliver growth factor cues to the wound - in order to quantify how each of these signals influences each of the wound key re-epithelialisation cell behaviours.

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Razzell, W, Wood, W & Martin, P 2014, 'Recapitulation of morphogenetic cell shape changes enables wound re-epithelialisation', Development (Cambridge), vol. 141, no. 9, pp. 1814-20. https://doi.org/10.1242/dev.107045

Nunan, R, Campbell, J, Mori, R, Pitulescu, ME, Jiang, WG, Harding, KG, Adams, RH, Nobes, CD & Martin, PB 2015, 'Ephrin-Bs Drive Junctional Downregulation and Actin Stress Fiber Disassembly to Enable Wound Re-epithelialization', Cell Reports, vol. 13, no. 7, pp. 1380–1395. https://doi.org/10.1016/j.celrep.2015.09.085

Turley, J, Chenchiah, IV, Martin, P, Liverpool, TB, Weavers, H 2024, 'Deep learning for rapid analysis of cell divisions in vivo during epithelial morphogenesis and repair', eLife, vol. 12, RP87949. https://doi.org/10.7554/eLife.87949

Turley, J, Robertson, F, Chenchiah, IV, Liverpool, TB, Weavers, H, & Martin, P 2024, 'Deep learning reveals a damage signalling hierarchy that coordinates different cell behaviours driving wound re-epithelialisation', Development, vol. 151, no. 18, dev202943. https://doi.org/10.1242/dev.202943