Fig. 6. RhoGAP Cv-c is localised basolaterally and controls Rho1 activity. (A) Cuticles and distribution of GFP-Actin (green) in the spiracles of wild-type and cv-c⁷ mutant embryos. Notice the partially uninvaginated Filzkörpers in cv-c⁷ mutants (arrows) accompanied by disruption of the apical Actin (inset). (B) Expression of Venus-Cv-c (green) in spiracle cells using the ems-GAL4 driver, co-stained with the basolateral marker -Spectrin (red) (i-iii) and with RhoGEF2 (red) (i'-iii'). (C) Cv-c gain of function (using emsGAL4 and UAS-Cv-c) leads to invagination failure of the most distal cells of the spiracular chamber (arrowheads) correlating with a disruption of their apical Actin (arrow). Green, GFP-Actin; red, Armadillo. (D) PKNG58AeGFP (i) and mRFP-Actin (i') profiles in spiracles overexpressing RhoGAP Cv-c. The cell cluster on the right (bracket) failed invagination and shows weaker apical Rho1 activity (yellow arrowhead) than the remaining invaginated cells (white arrowhead). (E) PKNG58AeGFP expression in a cv-c⁷ mutant spiracle with a severe phenotype. Apical and basal sections (dorsal view) and probe distribution along the xz axis. Notice the apical restriction of active Rho1, non-uniformly associated with the apical junctions. Scale bars: 10 µm.