Fig. 3. Ectopic veins produced by sax clones depend on gbb function. In a wild-type background (A-C), sax-null clones produce an ectopic vein, while in a gbb⁴/gbb⁴ mutant background (D) sax-null clones fail to produce vein duplications. Higher magnification of clones: A`-D', bright field; A"-D", dark field). sax clones are marked with sha^IN. Elimination of trichomes on both surfaces of the wing (i.e. a double-sided clone) appears black in dark field. (A,B,D) Anterior border of each double-sided clone (white arrowhead), ectopic vein (black arrowhead). (C) Posterior border of clone (white arrowhead). (A) sax clone with anterior border between L2 and L3 produces an ectopic vein at the anterior border of the clone. (B) sax clone with its anterior border between L1 and L2 produces an ectopic vein anterior to L2. (C) A sax clone in the posterior compartment that generated an ectopic L5 outside the clone boundary. (D) sax clone in a genetic background reduced for gbb function is very similar in position and shape to that shown in B but it lacks an ectopic vein. (E-H) Schematics depicting effect of sax clone (white box) on graded pMad (purple) in the anterior compartment of wing discs. x-axis indicates distance from Bmp source near the AP boundary. y-axis indicates level of pMad or Bmp signaling activity. (E) Relative domains of kni, sal, omb and brk expression and the position of L2 primordia (thick blue line). (F-H) Interpretation of clone in A,B,D, respectively. (F,G) Loss of Sax results in a reduction in Bmp signaling (gray arrows) within the clone and an increase in Gbb (blue), which influences the level of Bmp signaling in surrounding cells (black arrows). (H) Increased availability of mutant Gbb protein (pale blue) is not sufficient to raise pMad levels to the point necessary for ectopic L2 specification.