Fig. 2. Reduction of Kul levels leads to loss of wing veins. (A) Wild-type wing. (B) Expression of ds-kul in the central part of the wing by sal-GAL4 led to loss of veins (arrow). This phenotype suggests that Kul may normally be required for proper signaling by the Notch pathway. (C) Overexpression of Kul by sal-GAL4 led to an expansion of veins (arrow). (D) kul RNA is broadly distributed in the wing imaginal disc. (E) Expression of ds-kul at the anterior-posterior boundary of the wing disc by ptc-GAL4 led to elimination of endogenous kul RNA within this domain (arrowhead). (F) Expression of kul by the ptc-GAL4 driver exhibited a marked elevation in kul RNA. (G) Overexpression of Kuz by sd-GAL4 led to an expansion of veins (arrow), similar to Kul. (H) Expression of dskuz by MS1096-GAL4 led to thickening of the veins, similar to a kuz loss-of function phenotype. (I) The specificity of ds-kul was monitored in S2 cells. HA-tagged Kul (Kul-HA) is detected as a high molecular precursor, and as a mature protein lacking the pro-domain. Co-expression of ds-kul eliminated expression of the protein. By contrast, ds-kuz had no effect on the expression of Kul-HA. However, ds-kul had no effect on the expression of Kuz-HA, while ds-kuz eliminated the expression of the Kuz-HA protein. We conclude that ds-kul is specific. Expression of UAS-GFP was used to demonstrate similar transfection levels.