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Fig. 5. Genetic interactions with Notch, Su(H) and Hairless. (A) Overexpression of GFP in the gmr-pattern results in normal eyes and was used as control (GMR>GFP). Upper panel, side view with posterior at the right; lower panel, top view. (B) RNAi to Pros26.4 causes a posterior to anterior degeneration of the retina visible by glossy appearance and adhering necrotic tissue in the posterior half of the eye (arrow) (GMR>dsS4). (C) Overexpression of Hairless results in smaller eyes with irregular ommatidia (GMR>H). (D) This phenotype is strongly enhanced by reduction of Pros26.4 activity: eyes are much smaller and have an overall glossy appearance due to ommatidial fusion (arrow) (GMR>H, dsS4). (E) Overexpression of Su(H) causes hypertrophy of the eye, which is apparent in the top view [white arrow; GMR>Su(H)]. (F) The overgrowth phenotype remains unchanged by knock-down of Pros26.4, whereas retina degeneration and necrosis, which happens only later in development, is clearly visible [arrow; GMR>Su(H), dsS4]. (G) Overgrowth is even more pronounced when N^ICD is overexpressed (white arrow; GMR>N). (H) Again, this phenotype remains unchanged by reduction of Pros26.4 activity. Genotypes are (A) gmr-Gal4 / UAS-GFP; (B) gmr-Gal4 / +, UAS-dsS4 / +; (C) gmr-Gal4 UAS-H / UAS-GFP; (D) gmr-Gal4 UAS-H / +, UAS-dsS4 / +; (E) gmr-Gal4 / +, UAS-Su(H) / +; (F) gmr-Gal4 / +, UAS-dsS4 UAS-Su(H) / +; (G) gmr-Gal4 / +, UAS-N^ICD / TM3 Sb; (H) gmr-Gal4 / +, UAS-dsS4 UAS-N^ICD / +. Crosses were maintained at 25°C (A-D) and 18°C (E-H).

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