Fig. 3: Moesin and its regulators are required for hemocyte developmental dispersal.

a Imaging of Control and Moesin^Mut hemocytes on the ventral surface of the embryo revealing perturbation of hemocyte dispersal in the absence of Moesin. b Quantification of hemocyte speed in Control and Moesin^Mut hemocytes. **P  =  0.0047, Mann–Whitney two-tailed test. (n = 457 Control and 229 Moesin^Mut hemocytes from 6 and 7 embryos, respectively). c Nuclear tracks displayed normalized to a common starting point and quantification of hemocyte persistence in Control and Moesin^Mut hemocytes. ****P  <  0.0001, Mann–Whitney two-tailed test. (n = 537 Control and 844 Moesin^Mut samples from 12 and 14 hemocytes, respectively) d Quantification of the change in hemocyte acceleration upon contact inhibition of locomotion. Magenta arrow highlights the position of the colliding partner. **P  =  0.0015, ^nsP = 0.3203 Wilcoxon signed-rank test (hypothetical median value of 0, n = 23 Control and 11 Moesin^Mut collision events). e Schematic highlighting the classification of the degree of hemocyte developmental dispersal defects based on how far hemocytes have migrated along the ventral nerve cord (arrowheads). f Analysis of hemocyte migration in Moesin^Mut embryos revealing the four classes of dispersal defects. g Quantification of the degree of hemocyte dispersal defects in Moesin^Mut embryos, embryos expressing Moesin RNAi specifically in hemocytes, and embryos mutant for Moesin regulators, pten, sktl, slik, and embryos expressing slik RNAi specifically in hemocytes (n = 21 Control, 23 Moesin^Mut, 30 Moesin RNAi, 25 pten^Mut, 31 sktl^Mut, 21 slik^Mut and 26 slik RNAi embryos). Scale bars, 50 µm. All boxplots show medians, 25th and 75th percentiles as box limits, minimum and maximum values as whiskers; each datapoint is displayed as a marker. Scale bars, 10 µm.