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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: PARIS induced defects in mitochondrial biogenesis drive dopamine neuron loss under conditions of parkin or PINK1 deficiency

Fig. 3

Rescue of PARIS induced dopaminergic neurodegeneration and climbing defect by PINK1 or parkin. a Representative confocal images of DA neuron clusters visualized by GFP immunofluorescence in 50-day old flies in the genotypes indicated. Scale = 50 μM. b TH-Gal4 driven PARIS, but not C571A causes significant loss of neurons in all DA neuron clusters on day 50, compared to age-matched control flies (TH > GFP). Knock-down of parkin or PINK1 in the PARIS flies phenocopies this effect and also exacerbates DA neuron loss in PARIS flies. PARIS induced neurodegenerative effects are ameliorated by overexpression of PINK1, parkin or PGC-1α. Overexpression of PGC-1α also rescues neuron loss in PINK1 or parkin knockdown flies. Quantitative data = mean ± SEM, One-way ANOVA *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. c Total number of DA neurons in the four major DA for the indicated time points. N = 10 flies per genotype for each time point. Quantitative data = mean ± SD, Two-way ANOVA. See also Tables S4 and S5 (d) Comparison of climbing performance in the different genotypes at the indicated time points. TH > GFP flies served as control. N = 80 flies per genotype for time points indicated. Quantitative data = mean ± SEM, Two-way ANOVA. See also Tables S6 and S7. TH-Gal4 mediated EGFP shRNA induction served as non-target control for shRNA response. See also Additional file 9, Figure S2 and Additional file 13, Figure S3

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