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Fig. 5. Tws functions downstream of Dsh to inhibit Sgg activity. (A,B) vg-GAL4/UAS-Dsh (A) and vg-GAL4/+; UAS-Dsh/tws^P (B) wing blades. Inset in A shows expression pattern of vg-GAL4. Dsh-induced phenotype (ectopic bristles along the posterior margin) is suppressed by one copy of tws^P mutation. (C) vg-GAL4;UAS-Sgg fly showing underdeveloped wing blades owing to loss of Wg signaling. (D) vg-GAL4/+; UAS-Sgg/tws^P fly showing enhanced phenotype. Note total loss of wings and wing-to-notum transformation (shown at higher magnification in D'), a characteristic loss-of-wg phenotype. (E,F) vg-GAL4/+; UAS-Dsh tws^P/tws^P (E) and vg-GAL4/UASDNGSK-3ß; tws^P/tws^P (F) wing discs stained for Dll expression. Overexpression of dominant-negative Sgg/GSK3ß, but not Dsh, causes the rescue of tws^P/tws^P discs at the level of Dll expression (refer to Fig. 2F for Dll expression in tws^P/tws^P discs). (G) vg-GAL4/UAS-APC/CBD wing disc stained for Arm. Note very high levels of Arm in the DV boundary (compare with Fig. 4C) because of its sequestration by APC. In these cells, APC sequesters Arm, because Sgg (thereby the degradation machinery) is inhibited by Wg. (H) vg-GAL4/UAS-hAPC/CBD; tws^P/tws^P wing disc stained for Arm. In tws mutant background, APC fails to sequester Arm, suggesting that Sgg is active in all cells including the DV boundary.

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