Fig. 6. Embryonic CNS phenotypes found in 
3013 homozygotes are rescued by transgenic expression of Gliolectin. Forming commissures are visualized in black with mAb BP102 (A-D, mid-stage 13 embryos) and the pCC longitudinal pioneer is also stained black with mAb 1D4 (E-H, early stage 13 embryos). Compared with wild-type embryos (A,E), commissures and longitudinals are distorted (B, arrowhead and arrow, respectively) and pCC outgrowth is delayed (F, arrow indicates position of SP1 neuron) in 3013 homozygotes. rho-Gal4 driven expression of a single UAS-glec element (expression detected with mAb 1B7 in brown in C,D,G,H) partially rescues both the commissural (C, arrowhead) and longitudinal (G) phenotypes of 3013 homozygotes. In the rescued embryo, commissures are more clearly separated and organized than in the null. Likewise, pCC extension is comparable with wild type; the most severe abnormality observed in rescued embryos is indicated (G, arrow indicates a remaining gap between pCC and SP1 in a single segment). When rho-Gal4 drives expression from two copies of UAS-glec in a 3013/3013 background, commissures (D, arrowhead) and longitudinals are more completely rescued (arrow in D and H). Scale bar: 12 µm in all panels.
