Skip to main content
. 2019 Aug 14;10(8):613. doi: 10.1038/s41419-019-1862-0

Fig. 2. GMR > egr induces apoptosis via hid in the Drosophila eye.

Fig. 2

ad Adult eye images. Compared with wild type (a), expression of egr under the control of GMR (GMR-GAL4 UAS-egr, GMR > egr) induces a strong eye ablation phenotype (b). This phenotype is completely suppressed by an RNAi knockdown of egr (egrRNAi, c) or expression of puckered (puc, d), a negative regulator of JNK. Late 3rd instar larval eye disks labeled with cDcp1 (eh, j) or cDcp1 and GFP (ii′′). Compared with wild type (e), GMR > egr induces massive apoptosis indicated by cDcp1 labeling (f). This apoptosis is suppressed in dronc null mutants (g) or by expression of a GMR-p35 transgene (h). In GMR>egr disks with hid mutant clones marked by lack of GFP (i), apoptosis is blocked in the clones (highlighted by yellow dotted lines in i′ and i′′ which are enlarged images of the outlined area in i). In contrast, rpr mutants (rpr87/XR38a, combination of a deletion and a null mutant of rpr) do not suppress GMR > egr-induced apoptosis (j). kn Adult eye images. hid mutant clones (k), expression of a RING domain-deleted, therefore stabilized, form of Diap1 (GMR-BIR, l) or dronc null mutants (pharate adults were dissected out of the pupal cases, m) strongly suppress GMR > egr-induced eye ablation phenotype. In contrast, rpr mutants (rpr87/XR38a) do not suppress the small eyes induced by GMR > egr (n)