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. 2013 Mar 18;110(16):6400–6405. doi: 10.1073/pnas.1221132110

Fig. 1.

Fig. 1.

Parkin promotes mitophagy in vivo. (A) Experimental workflow. (B) parkin and Atg7 mutations prolong mitochondrial protein half-life. Box-and-whisker plots of fold change in half-life show median, quartiles, and extreme values. parkin mean and SD = 1.30 ± 0.22; Atg7 = 1.47 ± 0.30. *P < 0.005, mutant vs. control, by nested ANOVA. (C and D) The effects of parkin and Atg7 mutations on half-life correlate significantly for (C) individual mitochondrial proteins but not for (D) proteins from other organellar targets of autophagy (ribosomes, endoplasmic reticulum, and peroxisomes). n = 147 mitochondrial proteins; n = 58 other organellar proteins. All correlations reported as Pearson r. (E) The effects of parkin mutation on mitochondrial protein half-life do not correlate significantly with the effects of SOD2 deficiency (n = 103).