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. 2019 Oct 17;31(16):1213–1234. doi: 10.1089/ars.2018.7718

FIG. 7.

FIG. 7.

Mutations in Miro1 lead to increased LC3-independent autophagy and impaired energy metabolism. (A) Crude mitochondrial fractions were obtained from immortalized fibroblasts. Rab9 levels were analyzed by Western blot. (B) Quantification of Rab9 protein levels in mitochondrial fractions from (A) (n = 3). (C) Representative Western blot image of Rab9 in whole cell lysates of immortalized fibroblasts treated with 10 nM bafilomycinA1 for 4 h. (D) Quantification of Rab9 protein levels from (C). Significance determined using the Wilcoxon test (n = 6–11). (E) Measurement of steady-state ATP level under baseline conditions in immortalized fibroblasts. Significance assessed with the Mann–Whitney test (n = 6). (F) Schematic overview of the mechanism of impaired ER–mitochondria contact sites and increased mitophagy in Miro1 mutant background. *p < 0.05; **p < 0.01; ***p < 0.001. Color images are available online.