RhoGEF2 is necessary for formation of ommatidia and remodeling of LCs and can rescue cellular defects caused by RhoGAP71E expression. (A) Snapshot of a WT fixed retina stained for E-cad. (B) GMR > RhoGEF2-expressing eye. Epithelial cells maintain normal shape and rearrangements. (C) GMR > RhoGAP71E induces intercalation defects (yellow arrows), cell loss (purple arrow), and expansion of apical cell area. (D) Co-expressing RhoGEF2 and RhoGAP71E partially rescued the GMR > RhoGAP71E phenotypes. (E) RhoGEF2 RNAi expression led to formation of rosettes (yellow arrows) and loss of LCs (purple arrow). (F) Quantification of lattice defects. One-way ANOVA with Tukey’s multiple comparisons comparing the mean of changes in formation of rosettes. RhoGEF2 versus RhoGAP71E, P = 0.0015. RhoGAP71E versus RhoGEF2/RhoGAP71E, P = 0.0056. RhoGEF2 versus RhoGEF2/RhoGAP71E, P = 0.3789. WT versus Ey-RhoGEF2 RNAi, P = 0.0017. N = 80–140 edges from three eyes. (G) Positively marked RhoGEF2 mutant cells in fixed tissue stained for E-cadherin. (G′ and G″) (G) Milder defects are found at the boundary of the clones with WT cells, while (G″) severe defects in the formation and structure of ommatidia are found inside the clones. Scale bar = 3 µm.