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. 2005 Sep 9;102(38):13670–13675. doi: 10.1073/pnas.0504610102

Fig. 1.

Fig. 1.

Inhibition of DJ-1A expression by RNAi leads to photoreceptor neuron loss and eye degeneration. (A) Quantitative RT/PCR analysis of DJ-1A mRNA level after RNAi. DJ-1B and RP49 serve as controls. (B) Western blot analysis of DJ-1A protein level after RNAi. DJ-1B and actin serve as controls. (C-H) SEM images of GMR-GAL4/+ (C), GMR-GAL4>UAS-DJ-1A-RNAi (D), GMR-GAL4/Df(2R)CX1 (E), and GMR-GAL4>UAS-DJ-1A-RNAi/Df(2R)CX1 (F) eyes. Df(2R)CX1 is a chromosomal deficiency that deletes DJ-1A. G and H are magnified views of C and D, respectively. (I and J) Staining of photoreceptor neurons in GMR-GAL4/+ (I), and GMR-GAL4>UAS-DJ-1A-RNAi (J) eyes. Arrows in J mark ommatidia with photoreceptor loss. (K-N) Rescue of DJ-1A RNAi phenotypes by overexpressing DJ-1A or human DJ-1. All flies are homozygous for a recombinant GMR-GAL4;UAS-DJ-1A-RNAi chromosome and thus have a stronger phenotype than the one shown in B. In addition, the flies coexpress UAS-GFP (L), UAS-DJ-1A (M), UAS-hDJ-1 (N), or no other transgene (K).