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. 2015 Nov 26;6:8966. doi: 10.1038/ncomms9966

Figure 5. Oxidative stress is regulated by Nos activity in GFAPR79H transgenic flies.

Figure 5

(a) Double-label immunofluorescence shows activation of the oxidative stress reporter GstD1-lacZ in glial cells (top panel, arrows) but not in neurons (bottom panel, arrowheads). Repo marks glial cells; elav marks neuronal cells. 4,6-Diamidino-2-phenylindole (DAPI) labels nuclei. Scale bar, 5 μm. Genotype: repo-GAL4, UAS-GFAPR79H/+. Flies were 20 days old. (b) Overexpression of Nos in GFAPR79H transgenic flies (GFAP Nos OE) increases the number of β-gal-positive cells, while Nos knockdown (GFAP Nos RNAi) decreases the number of β-gal-positive cells in GFAPR79H transgenic flies. No GstD-lacZ activation is detected in Ctrl and Nos OE alone. *P<0.01, **P<0.001 compared with GFAP transgenic flies (GFAP), F=82.35, df=29; one-way ANOVA with Tukey's multiple comparison test, n=6 per genotype. Flies were 20 days old. Ctrl is GstD1-lacZ/+; repo-GAL4/+. GFAP is GstD1-lacZ/+; repo-GAL4, UAS-GFAPR79H/+. Nos OE is GstD1-lacZ, UAS-Nos/+; repo-GAL4/+. GFAP Nos OE is GstD1-lacZ, UAS-Nos/+; repo-GAL4, UAS-GFAPR79H/+. GFAP Nos RNAi is GstD1-lacZ/+; repo-GAL4, UAS-GFAPR79H/UAS-Nos RNAi.