Fig. 4.

Early induction of Prp8^S>F and Prp8^H>R expression causes adult eye defects. (A–F) Expression of Prp8^H>R (D) and Prp8^S>F (E) in the EADs using the early acting ey-Gal4 driver resulted in rough irregularly shaped adult eyes compared with control (A) and those expressing Prp8^wt (B) and Prp8^F>L RP variant (C). Outlines of adult eyes from the indicated genotypes highlight organ irregularities caused by ey-specific Prp8^H>R and Prp8^S>F expression (F). (G–L) The expressivity of the Prp8^H>R- and Prp8^S>F-induced phenotypes was markedly enhanced when overexpressed by the ey-Gal4 driver in prp8^del14/+ heterozygous flies carrying only one functional copy of endogenous prp8 gene. (M–X) Blocking apoptosis by expressing the pan-caspase inhibitor p35 restored adult eye size and mitigated the morphological defects caused by ey-specific overexpression of Prp8^S>F and Prp8^H>R in wild-type (M-R) or prp8^del14/+ heterozygous background (S–X). Outlines of adult eyes from the indicated genotypes are presented vertically aligned along their midline (F,L,R,X). (Y–Z′) ey-specific overexpression of Prp8^H>R and Prp8^S>F but not Prp8^wt or Prp8^F>L in prp8^del14/+ heterozygous background lead to smaller adult eyes relative to control (Y). The ommatidia loss could be prevented and eye size normalized by co-expression of p35 (Z, Z′). Data represent means±s.d., n≥8. Statistical significance was determined using ordinary one-way ANOVA with Tukey's multiple comparisons test; ***P<0.001, ****P<0.0001, n.s., non-significant. The exact number of adult eyes per genotype (n) and P-values are specified in Supplementary Dataset 2.