Fig. 7

Reducing levels of ROS, JNK, or SREBP in circbabo(5,6,7,8S)-depleted flies rescues the LD accumulation and neurodegeneration phenotypes. A–C Fat bodies carrying the GstD1-GFP reporter and expressing the indicated transgenes under the control of cg-Gal4 were imaged to visualize GFP (green). circbabo(5,6,7,8S) depletion led to increased levels of GstD1-GFP. This phenotype can be rescued by introducing the hSOD1 transgene. Scale bar, 20 μm. D Quantification of GFP fluorescence intensity in A, B, and C (one-way ANOVA with Turkey post hoc test, n = 3–4, ** p < 0.01; *** p < 0.001). E–H Various combinations of the indicated transgenes were expressed under the control of cg-Gal4. Nile red and DAPI were employed to label lipid droplets and nuclei, respectively. Overexpression of hSOD1 or knockdown of bsk rescued the LD accumulation phenotype in cg > shcircbabo(5,6,7,8S) flies. (I) Quantification of LD size in E, F, G, and H (one-way ANOVA with Turkey post hoc test, n = 5, * p < 0.05; *** p < 0.001; ns, non-significant). J TG levels in a similar set of samples as in E, F, G, and H were measured and normalized (one-way ANOVA with Turkey post hoc test, n = 3, * p < 0.05; ** p < 0.01). K–N The eyes of 30-day-old flies carrying the indicated combinations of transgenes driven by GMR-Gal4 were analyzed with TEM. The photoreceptor cell loss phenotype elicited by the depletion of circbabo(5,6,7,8S) was rescued by hSOD1 overexpression or bsk depletion. Scale bar, 5 μm. O Quantification of the number of intact photoreceptors in each ommatidium from flies with the indicated genotypes of K–N. Different number of (K = 19, L = 32, M = 11, N = 11) ommatidiawere counted. P Lifespan of flies carrying the indicated combinations of transgenes driven by the pan neuronal nSyb-Gal4 driver is shown (n represents number of groups for each genotype, 15–20 flies for each group. shGFP, vector = 10; shcircbabo(5,6,7,8S)-A, vector = 10; shcircbabo(5,6,7,8S), hSOD1 = 9; shcircbabo(5,6,7,8S), shbsk = 8)