Fig. 7. Overexpression of p120^ctn or -catenin enhances the Rho1 phenotype. The graph shows percentage total embryos (y-axis) with segmental patterning in each phenotypic class (w,wild type; m, mild; s, severe) for the following genotypes: Rho1 homozygous mutants (¬Rho), Rho1 mutants with one copy of UAS-p120^ctn overexpressed with the actin-Gal4 driver (¬Rho + p120^ctn), Rho1 mutants with one copy of UAS--catenin overexpressed with the actin Gal4 driver (¬Rho + -ctn), and Rho1 mutants with one copy of UAS-actin-GFP overexpressed with the actin Gal4 driver (¬Rho + actinGFP). The number of embryos scored is indicated beneath each genotype. (B-D) Cuticles depicting representative examples of each phenotypic class: (B) homozygous Rho1 mutant phenotype exhibiting an anterior dorsal hole but relatively normal anterior-posterior (AP) segmentation, (C) mild disruption of AP segmentation resulting from overexpressed -catenin in the Rho1 mutant background, (D) severe disruption of AP segmentation resulting from overexpressed -catenin in the Rho1 mutant background. (E) Model depicting the relationship of Rho1 to components of adherens junctions. p120^ctn can cycle between the cytoplasm and AJs. In the cytoplasm p120^ctn inhibits Rho by preventing the exchange of GDP for GTP. At AJs it binds to the JMD of cadherin and can no longer inhibit Rho. p120ctn and/or -catenin may be involved in recruiting Rho1 to AJs, allowing it to be activated by GEFs and carry out its downstream functions. Rho1 could be anchored at the AJ through its interaction with -catenin or by insertion into the PM mediated by its isoprenylation modification. (PM: plasma membrane, CBD: catenin binding domain, JMD: juxtamembrane domain). For cuticles, anterior is left. Scale bar: 50 µm.