Fig. 5. Genetic interactions between ed and genes of the Notch signaling pathway. Anti-HRP labeling of neurons in the embryos (A-H). (AD) Lateral views; (E-H) ventral views. Embryos in A-H were grown at 29°C. (A,E) Wild-type (WT) embryos. (B,F) Examples of the extent of hyperplasia of the CNS evident in ed^2B8/ed^ts embryos. Ectopic expression of N^act in the parasegments 4-6 mediated by the Kr-GAL4 driver, results in the suppression of neuronal cell fate in this region (C,G). ed^ts:UAS-N^act/ed^2B8; Kr-GAL4/+ embryos show strong suppression of the N^act overexpression phenotype, resulting in a near WT morphology (D,H). (I) Control wing of Dl^via1/+ fly. (J) ed^ts/ed^m1 flies grown at 25°C show a mild thickening of wing vein II. (K) ed^ts/ed^m1; Dl^via1/+ flies grown at 25°C show an enhancement of the thick wing vein II phenotype and show additional wing vein material (indicated by the arrowhead) in the posterior cell. (L) ed^ts/+heterozygous flies raised at 29°C show a WT wing morphology. (M) E(spl)^8D06/+ flies raised at 29°C show extra wing vein material (arrowhead) in the posterior cell with low penetrance. (N) ed^ts/+; E(spl)^8D06/+ flies at 29°C display more ectopic vein material (arrowhead) with full penetrance.