Fig. 4. cic acts downstream of the Ras/Raf pathway. (A) The differentiation of all the wing veins is prevented in rho^ve vn¹ homozygotes. (B) cic²/bwk¹¹ flies differentiate ectopic veins throughout the wing. (C) In the triple mutant rho^ve vn¹ cic²/ rho^ve vn¹ bwk¹¹, the loss of veins phenotype is completely suppressed and the extravein phenotype is completely epistatic. (D) Mutant clones Ras^c40b M⁺ autonomously prevent vein differentiation. (E) Two anterior clones cic² M⁺ cause ectopic veins (dorsal and ventral regions of the clone outlined in black and white, respectively). (F) Wing containing three M⁺ clones mutant for both cic² and Ras^c40b, differentiating extravein tissue. (G) Pupal wing staged 0-6 hours APF containing two large Ras^c40b M⁺ clones and stained with anti-Cic (red). Mutant clones are marked as patches free of GFP staining (green). (H) Red channel in G. Cic is autonomously expressed at high levels in all the Ras^c40b mutant cells. Cic is expressed at normal levels outside the mutant territories (white arrows) and is downregulated in the L3 vein (white line). (I) 0-6 hours APF pupal wing of a UASVn/Engrailed GAL4 fly stained with anti-Cic. Note the low levels of Cic present in the cells posterior to the L4 presumptive region (white line).