Suppression and enhancement of the Psn-induced apoptotic phenotype by alterations in Notch gene dosage. A and B, SEM images showing that the adult rough eye phenotype caused by increased cell death in GMR-GAL4, 2X UAS-Psn+14 (A) is strongly enhanced by removal of one dose of wild-type Notch in flies of genotype N54l9; GMR-GAL4, 2X UAS-Psn+14 (B). N54l9 is a deletion of Notch (Lindsley and Zimm 1992), which displays no dominant eye phenotype in heterozygotes. C and D, TUNEL assay showing that Psn-mediated programmed cell death seen in GMR-GAL4, 2X UAS-Psn+14 eye discs (C) is strongly reduced by coexpression of a constitutively activated form of Notch, termed sev-Notchact (Fortini et al. 1993; D). E and F, Overexpression of activated Notch using hs-Notch(intra) (Struhl et al. 1993) in homozygous PsnB3 mutant larvae (F) partially rescues the Psn loss-of-function phenotype, producing discs that are larger than tissues from equivalent PsnB3 mutant larvae (E). A, B, E, and F, Anterior at left; C and D, anterior at right.