Fig. 7

Loss of Cisd rescues Pink1 and parkin mutant degenerative phenotypes. A Immunoblot of mitochondrial protein lysates from Cisd knockdown driven by da-GAL4 in WT versus Pink1 and parkin mutant backgrounds, alongside respective controls, probed for p62 and Atg8a (LC3) levels with ATP5a loading control. B Relative p62 levels quantified from blots in A, normalised to WT control. Statistical comparisons are against WT control unless indicated. C Immunoblots of whole fly lysates of genotypes as in A, probed for pUb, Ub, Cisd (CISD2, Proteintech, 13318-1-AP) and Tubulin as loading control. D Confocal micrographs of adult flight muscle from Cisd knockdown driven by da-GAL4 in WT versus Pink1 and parkin mutant backgrounds, alongside respective controls, immunostained for APT5a and p62. E Confocal microscopy analysis of mitophagy reporter mito-QC in flight muscle from Cisd knockdown driven by Mef2-GAL4 in 2-day-old WT and parkin mutant backgrounds, alongside WT control. F Quantification of the number of mitolysosomes shown in E. G Confocal microscopy analysis of mitophagy reporter mito-QC in flight muscle from Cisd knockdown driven by Mef2-GAL4 in 2-day-old WT and Pink1 mutant backgrounds, alongside WT control. H Quantification of the number of mitolysosomes shown in G. Data points indicate individual animals analysed. Statistical analysis: one-way ANOVA with Sidak’s post-hoc correction; *P < 0.05, **P < 0.01; ****P < 0.0001. Scale bars = 10 μm