Fig. 4. sal acts upstream of svp during R3/R4 specification. All panels represent third instar eye discs where svp^– clones (A-C, svp^e22 – transcript null allele) or sal^– clones (D,E) were induced by Flipase-mediated mitotic recombination and are labeled by the absence of ubi-GFP staining (green). Anterior is to the left and the equator is at the top. The blue channel shows ELAV. (A) Salm (red) expression in R3/R4 is not repressed after row seven in the svp^– area. In wild-type ommatidia, Salm expression is progressively repressed in R3/R4 after row seven (arrows). In svp^– ommatidia, Salm expression persists in R3/R4 in more posterior rows (arrowheads). (B) In svp^– clones, Fmi (red) is present in all sides of the apical membrane of R3/R4 (arrowheads). In wild-type ommatidia, Fmi is localized in the equatorial side of R3 and R4 (arrows). High magnification of svp^– (top, right) and wild-type (bottom, right) ommatidia (asterisk) show the localization of Fmi in the R3 and R4 apical membrane (dashed line). (C) In svp^– clones, the expression of m0.5-lacZ (red) is lost in R4. (D) In sal^– ommatidia, sev-svp rescues m0.5-lacZ (red) expression in one cell of the pair, in many cases the one in the R4 position. In the wild-type ommatidia, sev-svp leads to m0.5-lacZ expression in both R3 and R4. (E) sev-N^act induces m0.5-lacZ (red) in R3 and R4, both in sal^– and non-mutant ommatidia. Scale bars: 10 µm.