Fig. 7. Lack of role for diap1 in the vCrz PCD. (A) Control (UAS-mCD8-GFP/+;;Crz-gal4/+). (B) Targeted expression of the diap1^RNAi in Crz neurons (UAS-mCD8-GFP/+; symUAS-diap1^RNAi/+; Crz-gal4/+) (cf. Huh et al., 2004). Intact GFP signals (vCrz) at 1 hour APF suggest that knockdown of endogenous diap1 does not cause premature cell death. (C) Effect of diap1^RNAi on premature death of the salivary glands. The symUAS-diap1^RNAi or y w (control) was crossed to the 34B-gal4; UAS-GFP, and then white prepupal progeny were examined for GFP. In the control, intense GFP signals are seen in a pair of the salivary glands (left, arrow), whereas the signals are significantly weakened by diap1^RNAi (right, arrow). (D) Crz-IRy in homozygous th^SL at 6.5 hours APF. (E) X-gal histochemistry of UAS-lacZ/+; Crz-gal4/UAS-diap1 at 6 hours APF. Both genetic and transgenic diap1 gain of function do not prevent vCrz death. (F) Rescue of the salivary gland degeneration by diap1. In a control pupa (34B-gal4/+; UAS-GFP/+, n=5) at 18 hours APF, faint GFP signals (left, arrow) reflect the PCD in this tissue. By contrast, strong GFP signals (right, arrow) are maintained by diap1 expression (34B-gal4/+; UAS-GFP/UAS-diap1, n=8). (G,H) Delayed PCD of vCrz neurons (G) in a dronc-null mutant (dronc⁵¹/dronc^I24) or (H) in a homozygous dark-null mutant (dark^CD4). Arrows indicate Crz-IR neurons that still survive at stages indicated in each panel. Scale bars: in A, 100 µm for A,B,D,E; in G, 50 µm for G,H.