Fig. 2: Mitochondrial defects in Mrps5 mutant hearts. | Nature Communications

Fig. 2: Mitochondrial defects in Mrps5 mutant hearts.

From: A defect in mitochondrial protein translation influences mitonuclear communication in the heart

Fig. 2

a Transmission electronic microscopic (TEM) images of Mrps5fl/fl and Mrps5cKO hearts at 8 to 18 weeks after tamoxifen injection showing mitochondria (M) and sarcomeres (S). Scale bar as indicated in the bottom of the figure panels. b Quantification of mitochondrial cristae length of Mrps5fl/fl and Mrps5cKO cardiomyocytes from 8 to 18 weeks after tamoxifen injection. c Quantification of ATP content in heart tissue samples from Mrps5fl/fl and Mrps5cKO mice, 8 to 18 weeks after tamoxifen injection. d Oxygen consumption rate of Mrps5fl/fl and Mrps5cKO hearts at 8 to 18 weeks after tamoxifen injection. e Quantification of activities of the ETC complexes of Mrps5fl/fl and Mrps5cKO hearts at 8 to 18 weeks after tamoxifen injection. f Immunoblot of mitochondrial electron transport chain protein complexes isolated from Mrps5fl/fl and Mrps5cKO mouse heart mitochondria at 12 weeks after tamoxifen injection. g Quantification of mitochondrial genome encoded protein expression level from Mrps5fl/fl and Mrps5cKO mouse heart mitochondria via parallel reaction monitoring (PRM) mass spectrometry at 10 weeks after tamoxifen injection. h Representative immunoblot and quantification of mitochondrial genome encoded proteins from lysates of Mrps5fl/fl and Mrps5cKO mouse hearts at 12 weeks after tamoxifen injection. VDAC serves as a loading control. N numbers are indicated in each panel. All data were presented as mean ± SEM. P values were determined by a two-tailed unpaired Students’ t-test.

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