Imp-L2 overexpression suppresses dInR-induced growth. (a-e) Scanning electron micrographs of compound eyes. All flies (females) carry the GMR-Gal4 and UAS-dInRwttransgenes. The dInr-dependent big eye phenotype (a) is suppressed by EP5.66 (b). UAS-Imp-L2 (c) and the stronger UAS-s.Imp-L2 (d) also suppress, but EP5.66 driving the mutant Imp-L2MG2 allele can no longer suppress the dInR overexpression phenotype (e). (f) Genomic organization of the Imp-L2 locus. The mutant alleles and P-element insertions used in this study are indicated. MG2 marks the point mutation in the EMS allele Imp-L2MG2 that generates a premature stop codon. (g) Alignment of Imp-L2, its orthologs in invertebrates and the putative human ortholog IGFBP-7. Black and gray boxes indicate amino acid identity and similarity, respectively. The triangle marks the premature stop codon in Imp-L2MG2. Asterisks mark the cysteines forming the two disulfide bridges. The gray bars indicate the Ig domains. Dm, Drosophila melanogaster Imp-L2; Ag, Anopheles gambiae CP2953; Sf, Spodoptera frugiperda IBP; Ce, Caenorhabditis elegans zig-4; Hs, Homo sapiens IGFBP-7.