The SJ component Nrx-IV is mislocalized at the wound edge in kune mutants. (A–F) Confocal images of the epidermis during wound closure in control (A–C) and kune strong mutant embryos (D–F) expressing Cherry::Moesin labeling F-actin (A, A′, A′′, D, D′, and D′′) and Nrx-IV–GFP (B, B′, B′′, E, E′, E′′) before and upon laser wounding. (C, C′, F, F′) Merged images. (A, A′, B, B′, D, D′, E, and E′) Maximum Z projections of 61 slices (22-µm-thick stack). (A′′, B′′, C′, D′′, E′′, and F′) YZ sections marked by dashed lines shown in 30-mpw panels. Arrowheads in A′′, B′′, C′, D′′, E′′, and F′ mark the wound edge. Dashed squares mark zoomed regions shown in A′, B′, D′, and E′. Bars: 20 µm (A, B, D, and E); 10 µm (A′, A′′, B′, B′′, C, and C′). Upon wounding, Nrx-IV decreases at the wound edge compared with cells away from the edge, mostly not colocalizing with the actin cable (arrowheads in A′, B′, C, D′, E′, and F). In kune mutants, Nrx-IV–rich accumulations are visible at the wound edge at 30 mpw, colocalizing with the actin cable (asterisks in D′, E′, and F). (G) Graph of average Nrx-IV–GFP intensity levels before wounding in control (40 junctions from four embryos) and kune mutants (50 junctions from five embryos). (H) Graph of fold change decrease in Nrx-IV–GFP intensity in wound edge junctions at 10 and 30 mpw (compared with before wounding), in control (15 junctions from four embryos), and kune embryos (14 junctions from three embryos). (I) Graph showing Nrx-IV intensity at the apical side of cells before wounding in control (30 junctions from six embryos) and kune embryos (30 junctions from six embryos). An unpaired t test (G and I) and a two-way ANOVA and multiple comparisons Sidak test (H) were performed to test for significant differences between groups. *, P < 0.05; ***, P < 0.0001. Error bars represent SEM.