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Fig. 3
Vangl2 asymmetry is not affected in hair cells of MZwnt11 (wnt11f1) mutants. a–d&nbs ;Double β-II-Spectrin (labeling the cuticular plates) a nd Vangl2 immunodetection in primI neuromasts of 5 dpf wild type (a), MZscrib mutants (b), scrib siblings (c) and MZwnt11 (wnt11f1) mutants (d). e– b>h Double β-II-Spectrin (labeling the cuticular plates) a nd Vangl2 immunodetection in primII neuromasts of 5 dpf wild type (e), MZscrib mutants (f), scrib siblings (g) and MZwnt11 (wnt11f1) mutants (h). i Quantification of the percentage of hair cells that show asymmetric Vangl2 for each of the conditions in both primordia-derived neuromasts. j–n Clonal localiza ion of GFP-XVangl2 in hair cells of neuromasts that show primI and primII polarity in wild type (j, k) and MZwnt11 (wnt11f1) mutants (m, n) neuromasts. The majority of the clones were localized in neuromasts in the head, which show the same hair cell orientation as in primI and primII-derived neuromasts in each of the cases. l, o Quantification of GFP-XVangl2 fluorescence around the cuticular plates (360°) of hair cells in neuromast that show primI and primII polarity of wild type (l) and MZwnt11f mutants (o). p GFP fluorescence and Phalloidin enrichment (polarity ratio, calculated from the cap of max value to the lowest value) in the different conditions analyzed in (l, o). Error bars in l, o, and p represent S.E.M. ***Fisher’s exact test p < 0.01. Scale bar sp;a equals 5 μm, j b> equals 2 μm