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. 2017 Feb 9;13(2):e1006603. doi: 10.1371/journal.pgen.1006603

Fig 1. ApoD neuroprotection mechanism in polyglutamine-triggered neurodegeneration in Drosophila depends on lysosome-phagosome fusion in vivo.

Fig 1

A-H. Representative examples of adult eye external morphology by light microscopy of the central eye surface region. The expression of all transgenes is directed by the gmr:Gal4 driver to photoreceptor neurons. Polyglutaminated human Ataxin 1 (UAS:hATXN182Q) is combined with UAS:GLaz and/or UAS:Dor-RNAi transgenes. I. Quantification of photoreceptor degeneration by computing a regularity index (IREG) using FLEYE. No rescue is detected when Dor is knocked-down (confirmed with two independent recombinant lines, E and F). Data normalized to the control genotype (gmr/+) are shown. N = 20–30 flies/genotype. Statistical differences were assessed by ANOVA on Ranks and Tukey post-hoc correction. Genotypes C, E, F and H (degenerated) are significantly different from A, B, D, G (non-degenerated), p<0.001.