Fig. 6. GMR > egr induces Dronc-dependent necrosis when DrICE and Dcp-1 are inhibited.

a, a′ APF22h pupal eye disks labeled with cDcp1 (green in d and gray in d′) and ELAV (red in d). Loss of one copy of dronc does not or only slightly suppress GMR > egr-induced apoptosis. b–e Adult eye images. Although loss of one copy of dronc only slightly inhibits GMR > egr-induced small eye phenotype (compare 6b to 2b), it strongly suppresses the eye ablation phenotype induced by GMR > egr/GMR-p35 (compare 6c to 4d). This suppression is neutralized by expression of a wild-type form of Dronc (d), but not a catalytic site-mutated form of Dronc (e). f, g Adult eye images. Expression of Dronc and P35 in dronc heterozygous mutants does not reduce the eye size although it causes an eye pigmentation defect (f). Expression of a catalytic site-mutated form of Dronc does not result in any eye defects (g). h Quantification of the average adult eye size (mean ± SD) of various genetic backgrounds as indicated. One-way ANOVA with Bonferroni multiple comparison test was used to compute p-values. Asterisks indicate statistically significant changes (*P < 0.05 or ****P < 0.0001). Suppression of GMR > egr by expression of P35 is not statistically significant (n.s.). Heterozygous dronc mutants only weakly suppress GMR > egr-induced small eyes (GMR > egr/+, dronc^+/−). But they strongly suppress GMR > egr/GMR-p35-induced eye ablation phenotype (GMR > egr/GMR-p35, dronc^+/−). In this background, further expression of a wild-type form of Dronc (GMR > egr-dronc^wt/GMR-p35, dronc^+/−), but not a catalytic site-mutated form of Dronc (GMR > egr-dronc^C318A/GMR-p35, dronc^+/−), is sufficient to restore the eye ablation phenotype