(a–e) Images of Drosophila adult eye. a′–e′ Adult eye imprints. a, c, e GMR-GAL4 was used to drive UAS-mahe or (b, c) UAS-hop(Tum-l) (d, e)UAS-hop-RNAi. a, a′ Ectopic mahe expression promotes eye roughening. b, b′ Overexpression of constitutive active form of hop results in slight ommatidial disorganization. c, c′ Coexpression of hop and mahe enhanced the rough eye phenotype compared to mahe alone. d, d′ Reduction of hop levels by RNAi mediated knockdown leads to no observable change in eye roughening phenotype. e, e′ RNAi mediated depletion of hop rescued the mahe induced eye roughness. f–j, k–o Acridine orange and caspase staining in eye antennal disc. f, k Acridine and caspase positive cells show cell death induced by mahe. g, l hopTum-l overexpression showed few dying cells. h, m Coexpession of hopTum-l and mahe enhanced cell death in comparison to mahe alone. i, n No dying cells were observed on downregulating the level of hop. j, o Downregulation of hop rescued the mahe induced cell death as depicted by acridine orange and cl-caspase staining. p Graph represents cl-caspase intensity per unit area which shows activated hopTum-l promotes mahe induced cell death, which was significantly reduced in combination with hop-RNAi. One-way ANOVA. Scale bar in 50 µm (f–j, k–o). Genotypes (a) w; +; GMR-GAL4,UAS-HA-mahe/+ (b) w; UAS-hopTum-l/+;GMR-GAL4/+ (c) w; UAS-hopTum-l/+;GMR-GAL4,UAS-HA-mahe/+ (d) w; UAS-hop-RNAi/+;GMR-GAL4/+ (e) w; UAS-hop - RNAi/+; GMR-GAL4,UAS-HA-mahe/+. One-way ANOVA * P < 0.05, ** P < 0.01, *** P < 0.001.