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. 2012 Feb 29;7(2):e30958. doi: 10.1371/journal.pone.0030958

Figure 9. Inhibition of NO signal improves DG2-dFoxO-mediated DA neurodegeneration.

Figure 9

(A) Newly eclosed normal w- flies (Control) or transgenics harboring elav-GS>UAS-dFoxO/UAS-DG2 (n = 22 in each) were fed a yeast paste containing 50 µg/mL_ RU486 with or without 10 mM L-NAME or D-NAME every 4 days at 29°C. The graph presents the number of PPM 1/2 and PPL1 clusters of TH-positive neurons in 20-day-old adult flies. PPM1 and PPM2 clusters were counted together. Data are presented as the mean ± SE for three experiments (*, p<0.05 vs. Control). PPL, the protocerebral posterior lateral. Non; RU486 only. (B) A representative image of TH-positive PPL1, PPM1, PPM2 (upper circle) and PPM3 (lower circle) neurons of a wild-type w- adult fly. Arrowheads indicate a pair of PPM1 neurons. Bar = 50 µm. (C–E) Representative images of TH-positive neurons treated as in A. (F) Brain tissues of dFoxO transgenic flies treated with L-NAME or D-NAME were subjected to western blot analysis with anti-dFoxO. dFoxO SA mutant was also included as a non-phosphorylated control. Transgenes were expressed by the elav-GS driver. (G) Reduction of dNOS and DG2 activities confers stress resistance against 2 mM paraquat treatment. dNOS (−/−) vs. Control, p<0.0001; DG2 (+/−) vs. Control, p<0.01. The genotypes are: w- (Control), dNOSΔ15/dNOSΔ15 (dNOS (−/−)), DG2k04703/+ (DG2 (+/−)).