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Fig. 4 | Skeletal Muscle

Fig. 4

From: RETRACTED ARTICLE:Exercise-induced mitochondrial p53 repairs mtDNA mutations in mutator mice

Fig. 4

Endurance exercise-mediated repair of mtDNA mutations is mitochondrial p53-dependent. a A fluorescence-based in vitro DNA primer extension-mutation repair assay in muscle mitochondrial extracts from WT, PolG-SED, and PolG-END (n = 6–8/group) to assess the excision of the unpaired artificial point mutations. b p53 immunodepletion prevents mutation repair in muscle mitochondrial extracts from PolG-END (n = 5/group). A non-specific IgG antibody was used as negative control antibody. c Endurance stress test time to exhaustion in four independent trials in WT, PolG-SED, PolG-END, PolG-p53 MKO-SED, and PolG-p53 MKO-END mice (n = 5–6/group). d Representative electron micrographs of myofibers (quadriceps femoris) from WT, PolG-SED, PolG-END, PolG-p53 MKO-SED, and PolG-p53 MKO-END (n = 4/group). e Random mtDNA somatic mutation rate (per 1000 nucleotides of mtDNA) in muscle (quadriceps femoris) WT, PolG-SED, PolG-END, PolG-p53 MKO-SED, and PolG-p53 MKO-END mice (n = 3–4/group). f mtDNA copy number in muscle mitochondria from PolG-SED, PolG-END, PolG-p53 MKO-SED, and PolG-p53 MKO-END mice (n = 4–5/group) relative to WT mice (horizontal line). g Cytochrome c oxidase (COX) activity in muscle from WT, PolG-SED, PolG-END, PolG-p53 MKO-SED, and PolG-p53 MKO-END mice (n = 4–5/group). Asterisk (PolG-SED vs. both WT and PolG-END): *P < 0.05, **P < 0.01, ***P < 0.001; dagger (PolG-p53 MKO-SED vs. PolG-SED OR PolG-p53 MKO-END vs. PolG-END): P < 0.05; closed circle (PolG-END vs. PolG-SED): P < 0.05, P < 0.01, P < 0.001. Error bars represent SEM. AU arbitrary units

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