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Fig. 7
Activity of non-muscle myosinII (NMII) is essential and sufficient for elongation of microridges. Immuno-colocalization using anti pNMII antibody and phalloidin in wild-type and has/apkc mutant at 48 hpf (a). Wild-type and has/apkc mutant treated with 10 µM Blebbistatin at 48 hpf and stained using phalloidin to visualize F-actin (b). Graphical representation of the distribution of ridge lengths and medians of Blebbistatin treated and control embryos at 48 hpf using bean plots (c). The same data is presented as percentage frequency distribution of ridges in short (0-5 µm), intermediate (5-20 µm), long (20-100 µm) and very long (>100 µm) categories (d). Distribution of means and variances of ridge lengths (e) for individual peridermal cells- in wild-type sibling and has/apkc mutant treated with DMSO and Blebbistatin at 48 hpf-presented in box-whisker plots. Immuno-colocalization using anti pNMII antibody and phalloidin staining in wild-type embryos and embryos over-expressing constitutively active MLCK at 48 hpf (f). In c and e the distributions sharing the same alphabet do not differ significantly (Dunn’s multiple comparisons test, P-value<0.05). In ((e) top) the distributions for apkc sib and apkc sib+Blebbistatin are considered statistically significantly different at P=0.058. Error bars in d are for the s.d. Scale bars in a,b and f are equivalent to 10 µm.