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Fig. 1
has/apkc function is important for restricting the length of microridges by preventing their precocious elongation. Immuno-colocalization using anti-aPKC antibody and phalloidin, which labels F-actin, in wild type and has/apkc mutant at 48 hpf (a) followed by colocalization coefficient analysis by Pearson’s (PC) method and Manders’ overlap for aPKC with F-actin (M1) and F-actin with aPKC (M2) at 48 hpf in wild-type embryos (b). Graphical representation (c) of apical surface area and total cell surface area in wild type and has/apkc mutant at 48 hpf. Visualization of the distribution of ridge lengths and medians in wild-type and aPKC-deficient embryos at various developmental time points using bean plots (d). The frequency distribution of ridges (e) in short (0-5 µm), intermediate (5-20 µm), long (20-100 µm) and very long (>100 µm) categories during development. Quantification in d and e are based on phalloidin stainings performed in wild-type and apkc morphants (f). Time-lapse imaging of microridges in clones expressing lifeActRFP under CMV promoter in wild-type and apkc morphants during 19-22 hpf and in has/apkc siblings (wild type) and mutants during 27-30 hpf (g). Error bars in c and e indicate s.d., whereas square brackets represent comparison. Probability values ‘P’ are for the Student’s t-test. Asterisks in the bean plot (d) represent significant difference in median values at P<0.05 as calculated by pairwise multiple comparison procedures using Dunn’s Method. Scale bars in a,f and g correspond to 10 µm.