Wounds cause an increase of intracellular calcium. (Ai) Movie stills of a pupal notum expressing the calcium probe G-CaMP3-GFP driven by pnr-GAL4 in the early seconds of wound healing. After an initial rise in intracellular calcium in the vicinity of the wound, which spreads throughout the injured tissue, a wave of high calcium levels can be observed progressing toward the wound center. (Aii) Graphic representation of the calcium wave color coded as Fig. 2 Aii. Bar, 10 µm. (B) Movie stills showing that TRPM down-regulation impairs the actin flow. (Bii) Graphic representation of the actin flow, color coded as Fig. 2 Aii. An impairment of the actin flow can be seen when TRPM is down-regulated. Bar, 10 µm. (Ci and Cii) Graphs representing the variation of actin and myosin flow intensity in WT and TRPM RNAi showing that TRPM down-regulation affects both actin and myosin flows. Shadows represent the SEM for each curve. (Ciii) Quantification of myosin cable intensity in WT and TRPM RNAi shows that this structure is weaker when TRPM expression is reduced (P = 0.007, Mann-Whitney test). (D) Graph representing GCaMP3-GFP (calcium probe) intensity in wild-type, Dia RNAi, ROCK RNAi, and TRPM RNAi. Calcium levels in Dia knockdown are similar to wild-type, whereas ROCK RNAi initially shows low levels of intracellular calcium that decay very slowly. In TRPM down-regulation the initial increase of calcium levels is impaired and it decreases faster to basal levels.