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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Mitochondrial CISD1/Cisd accumulation blocks mitophagy and genetic or pharmacological inhibition rescues neurodegenerative phenotypes in Pink1/parkin models

Fig. 1

Cisd accumulation disrupts mitochondria affecting locomotion and lifespan. A Representative immunoblot of whole fly lysates of the indicated genotypes from 2- and 30-day-old flies probed for Cisd (CISD2, Proteintech, 13318-1-AP) and Tubulin as loading control. B, C Quantification of Cisd monomer or dimer levels in 2- and 30-day-old flies analysed in A. D Confocal microscopy of flight muscle from 2-day-old wild-type control (WT ctrl) or Cisd overexpressing (OE) flies driven by da-GAL4, immunostained for ATP5A mitochondrial marker. E Climbing assay of 2- and 20-day-old WT and ubiquitous Cisd OE flies via the da-GAL4 driver. F Lifespan of WT and ubiquitous Cisd OE flies. N > 130 animals. G Confocal microscopy of neuronal soma from control (WT ctrl) or Cisd overexpressing (OE) larvae co-expressing the mito-GFP mitochondrial marker via the nSyb-GAL4 driver. H Climbing assay of 2- and 20-day-old WT and neuronal Cisd OE flies via the nSyb-GAL4 driver. I Lifespan of WT and neuronal Cisd OE flies. N > 90 animals. Statistical analyses: B RM one-way ANOVA with Geisser-Greenhouse correction; C paired t-test; E, H Mann-Whitney non-parametric test. *P < 0.05; **P < 0.01; ****P < 0.0001. Scale bars = 10 μm

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