Fig. 5: Calmodulin regulates MCC apical emergence.

A Representative MIP image of the apical surface area of a MCC expressing calmodulin-GFP. Calmodulin displays colocalization with the basal bodies and the apical actin network. B Schematic depicting the localization of calmodulin in a MCC in relation to the basal bodies and the apical actin network. C Representative images of the skin epithelium from stage 24 control and calmodulin inhibitor-treated embryos. MCC fail to fully integrate into the superficial skin epithelium when calmodulin activity is blocked, as evident by their small apical surface area. D Quantification of the apical surface area of MCCs from control (n = 100 MCCs) and calmodulin inhibitor-treated embryos (n = 100 MCCs), 5 different embryos. Two-sided unpaired student’s t test; ****p  <  0.0001; mean ± SEM. E Representative images of the skin neuroepithelium from embryos expressing wild-type calmodulin or Ca²⁺ binding deficient calmodulin mutant (CALM1234). Expression of CALM1234 results in defective MCC apical emergence (green arrows) while expression of WT calmodulin does not affect MCC apical emergence (white arrows). F Quantification of MCC apical emergence upon expression of WT and Ca²⁺ binding deficient mutant calmodulin. Two-sided χ² test; ****p  <  0.0001. G Quantification of the apical surface area of MCCs expressing WT and Ca²⁺binding deficient mutant calmodulin. N = 80 control MCCs, 46 MCCs expressing WT calmodulin and 20 MCCs expressing mutant calmodulin from 4 embryos injected with WT calmodulin DNA and 4 embryos injected with mutant CALM1234 DNA. Two-sided unpaired student’s t test; ****p  <  0.0001; mean ± SEM. Scale bars: A: 2 μm, D, F: 20 μm. Source data are provided as a Source data file.