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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Uncoupling neuronal death and dysfunction in Drosophila models of neurodegenerative disease

Fig. 5

Compared to controls (a, Rh1-GAL4 / +), TEM reveals evidence of altered autophagy and endo-lysososomal flux in Rh1 > Tau b, Rh1 > Aß c and Rh1 > αSyn d flies at 10 days, but unchanged mitochondria. Autophagic vacuoles (arrowheads) and electron dense vacuoles (arrows) are indicated. Quantification e-g of ultrastructural features was based on electron micrographs from 3 distinct animals per genotype. e Number of mitochondria were quantified per ommatidium. Total number ommatidia counted (genotype, n): Rh1-Gal4/+, 18; Rh1 > Aß, 21; Rh1 > Tau, 20; and Rh1 > αSyn, 18. f Aß and αSyn induce autophagic vacuole formation in the Drosophila retina. Distinct vacuolar compartments representing autophagic flux were quantified per photoreceptor area (n / μm2), including autophagosomes, multi-vesicular bodies, multi-lamellar bodies, and lysosomes. g Increased frequency of electron dense vacuoles following expression of Tau, potentially consistent with the appearance of telolysosomes (also called lipofuscin granules). Total number photoreceptors quantified (genotype, n): Rh1-GAL4/+, 340; Rh1 > Aß, 269; Rh1 > Tau, 320; and Rh1 > αSyn, 257. Scale bar: 1 μm. All statistical comparisons were implemented using a two-tailed student’s t-test. *, p < 0.05; **, p < 0.01

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