The force-sensitive protein Ajuba regulates cell adhesion during epithelial morphogenesis.

The reorganization of cells in response to mechanical forces converts simple epithelial sheets into complex tissues of various shapes and dimensions. Epithelial integrity is maintained throughout tissue remodeling, but the mechanisms that regulate dynamic changes in cell adhesion under tension are not well understood. In , planar polarized actomyosin forces direct spatially organized cell rearrangements that elongate the body axis.

Recapitulation of morphogenetic cell shape changes enables wound re-epithelialisation.

Wound repair is a fundamental, conserved mechanism for maintaining tissue homeostasis and shares many parallels with embryonic morphogenesis. Small wounds in simple epithelia rapidly assemble a contractile actomyosin cable at their leading edge, as well as dynamic filopodia that finally knit the wound edges together. Most studies of wound re-epithelialisation have focused on the actin machineries that assemble in the leading edge of front row cells and that resemble the contractile mechanisms that drive morphogenetic episodes, including Drosophila dorsal closure, but, clearly, multiple cell rows back must also contribute for efficient repair of the wound.

Calcium flashes orchestrate the wound inflammatory response through DUOX activation and hydrogen peroxide release.

A crucial early wound response is the recruitment of inflammatory cells drawn by danger cues released by the damaged tissue. Hydrogen peroxide (H2O2) has recently been identified as the earliest wound attractant in Drosophila embryos and zebrafish larvae. The H2O2 signal is generated by activation of an NADPH oxidase, DUOX, and as a consequence, the first inflammatory cells are recruited to the wound within minutes.

Swatting flies: modelling wound healing and inflammation in Drosophila.

Aberrant wound healing can lead to a variety of human pathologies, from non-healing chronic wounds that can become dangerously infected, to exuberant fibrotic healing in which repair is accompanied by excessive inflammation. To guide therapeutic intervention, we need a better understanding of the fundamental mechanisms driving tissue repair; this will require complementary wound-healing studies in several model organisms. Drosophila has been used to model genetic aspects of numerous human pathologies, and is being used increasingly to gain insight into the molecular and genetic aspects of tissue repair and inflammation, which have classically been modelled in mice or cultured cells.

'White wave' analysis of epithelial scratch wound healing reveals how cells mobilise back from the leading edge in a myosin-II-dependent fashion.

Collective cell migration is absolutely essential for a wide variety of physiological episodes including the re-epithelialisation component of tissue repair. However, the investigation of such processes has been frustrated by difficulties in quantitatively analysing the behaviours of a large body of cells within a migrating epithelial sheet, which previously required manually tracking a large number of individual cells, or using advanced computational techniques. Here, we describe a novel and simpler image subtraction method with which we can visualise and quantify collective cell mobilisation as a 'white wave' that propagates back from the leading edge of a scratch-wounded monolayer of cultured epithelial cells.