Fig. 7. Inhibiting apoptosis partially rescues pcm¹⁴ phenotypes.

(A) A diagrammatic representation of the apoptosis pathway in Drosophila, indicating the main proteins involved in triggering apoptosis in response to an apoptotic stimuli. (B–D) Inhibiting apoptosis in pcm¹⁴ wing imaginal discs was achieved by crossing in the Df(3L)H99 deletion (which deletes pro-apoptotic genes hid, grim and reaper) as a heterozygote. The presence of Df(3L)H99 reduced the amount of Caspase 3 staining and increased the size of the pcm¹⁴ wing discs (compare C with D) (n = 13). (E) Inhibiting apoptosis partially rescues the size of pcm¹⁴ wing imaginal discs. Reducing the copy number of reaper, hid and grim from 2 to 1 using the Df(3L)H99 deletion as a heterozygote (pcm¹⁴;;Df(3L)H99/+) rescues the wing disc size from 45% to 81% (n≥31). Use of the Ark⁸² allele as a homozygote rescues wing disc size from 45% to 85% that of wild type, showing that the adaptor protein Ark is required for much of the pcm¹⁴ induced apoptosis (n≥19). Overexpression of the Inhibitor of apoptosis protein DIAP1 using the 69B-GAL4 driver (pcm¹⁴;GAL80_ts/+;69B-GAL4/UAS-DIAP1) rescues the size of pcm¹⁴ discs from 45% to 67% that of wild type, confirming that Pacman is acting through the pathway in A (n≥19) ****p<0.0001. Inhibiting apoptosis in the pcm^WT background increases wing disc size to 105% using the Df(3L)H99 deletion (p<0.05), 112% using the Ark⁸² homozygous mutation (p<0.0001) and 115% using the UAS-DIAP1 (p<0.0001). Error bars represent 95% confidence limits. (F–H) Inhibiting apoptosis rescues the delay in wing imaginal disc development as determined by Wingless staining at 120 hours (compare G with H) (n = 13). Scale bars represent 100 µm.