Cno supports Ecad stability in a parallel pathway to the α-Cat M region. (A) Quantification of cuticle defects from cno-RNAi α-Cat-RNAi α-CatX and gfp-RNAi α-Cat-RNAi α-CatX embryos. Phenotypic categories are color-coded and examples are given in Fig. S5. (B) Overexpression of Cno improves epithelial integrity in α-Cat-RNAi embryos. (C) Denticle belt count for α-Cat-RNAi α-CatX embryos overexpressing Cno or GFP-RNAi as control. gfp-RNAi controls same as in Fig. 5 E. (D) Ectoderm at stage 8/9 of α-Cat-RNAi α-CatX embryos immunostained for Ecad, expressing either UAS-cno, cno-RNAi or UAS-gfp-RNAi as control. Ecad levels are enhanced by Cno overexpression, ameliorating defects found in α-Cat-ΔM23 embryos, whereas Cno knockdown causes an enhancement of AJ fragmentation in α-CatR-ΔM1 embryos compared to control. Scale bar, 10 μm. (E)Rap1-RNAi enhances defects in α-Cat-RNAi α-CatR and α-Cat-RNAi α-Cat-ΔM embryos. gFP-RNAi controls same as in C. Chi-square test, **** = P < 0.0001. (F)Vinc null mutant enhances defects caused by cno-RNAi. Chi-square test, **** = P < 0.0001. (G)jub-RNAi enhances defects caused by cno-RNAi. Chi-square test, *** = P < 0.001. For A–C and E–G, n = number of embryos analyzed. (H) Schematic summary: Redundancy between the M region interactors Jub, Vinc, and Cno support epithelial integrity. Cno supports adhesion in part through M2/3-dependent recruitment to TCJs and an α-Cat independent pathway involving Rap1. Arrows denote functional relationships.