Fig. 3. So binds to the pros enhancer and activates transcription. (A) The three putative So-binding motifs are highlighted in red within the core-enhancer. These are also present in the mini-enhancer. (B) Alignment of a consensus So-binding site and the three putative So-binding sites. Essential residues are colored red; conserved residues are colored blue. (C) A mobility-shift gel showing a complex that contains So protein and labeled SoAE DNA. SoAE is a So-binding site identified in the so gene autoregulatory element. Each reaction also contained a 50-fold molar excess of an unlabeled competitor DNA as indicated, except for the reaction loaded into the leftmost lane, which did not contain competitor. The SoAE(mut) competitor has a mutated So-binding site; the Lozenge competitor contains a So-target sequence identified in the lz enhancer. The Pros competitors contain the three putative So-binding sites from the pros enhancer. (D,E) Transgenic core-enhancer-β-gal reporter expression (green) in eye discs counterstained for Pros (purple). (D-D'') The wild-type core-enhancer induces β-gal expression in the same cells that express Pros. (E-E'') The core-enhancer with mutant So sites does not induce β-gal expression. (F) Schematic of the approach to make so(ey) and eya(ey) mutant eye discs. The expression patterns of So/Eya in wild-type (left), so/eya mutant (middle) and so(ey)/eya(ey) (right) mutant eye discs are shown in red. In so(ey) or eya(ey) eye discs, So/Eya expression is limited to cells anterior to the MF (black line). (G-J) Expression of neural-specific Elav (purple) and Pros protein (green) in a wild-type eye disc (G-G''), an eya(ey) disc (H-H''), a so(ey) disc (I-I''), and an Lz-GAL4/+; UAS-so^DN/+ disc (J-J'').