Figure 8. PCP function is required for polarization of actomyosin contractility during junction shrinking.
(A–B). Confocal images of Xenopus neural epithelia labeled evenly with Myl9-GFP and membraneBFP and mosaically with H2B-RFP serving as a tracer for either Xdd1 (A) or Pk2-ΔPΔL (B) expression. Scale = 10 µm (C) Graph plotting Myl9-GFP intensity along V-junctions (0–45° relative to mediolateral axis) and T-junctions (46–90° relative to mediolateral axis) normalized as a ratio to the mean cytoplasmic intensity of the cells sharing the junction. Control cells (n = 91 V, 91T) and cells expressing Xdd1 (n = 44 V, 53 T) and Pk2-ΔPΔL (n = 45 V, 45 T). Ctrl V vs. T, p<0.0001****; Pk2-ΔPΔL V vs. T, p=0.2304; Xdd1 V vs. T, p=0.0022**; Control V vs. Xdd1 V, p=0.5826; Control T vs. Xdd1 T, p<0.0001****; Control T vs. Pk2-ΔPΔL T, p<0.0001**** (Mann-Whitney Test for significance). Error bars represent standard deviation. (D) Distributions of normalized Myl9-GFP intensity plotted against the angle of the junction at which intensity was measured in control cells and cells expressing Xdd1 or Pk2-ΔPΔL. Correlation coefficients for Xdd1 and Pk2-ΔPΔL were shown to be significantly different from controls using the Fischer R-to-Z transformation. n = 498 junctions (Control), n = 263 junctions (Xdd1) and n = 245 junctions (Pk2-ΔPΔL) from four experiments, five embryos (Xdd1); three experiments, seven embryos (Pk2-ΔPΔL).