Fig. 5: Diminished MCU degradation is responsible for enhanced uniporter activity in Tfam KO hearts, and prolongs survival. | Nature Communications

Fig. 5: Diminished MCU degradation is responsible for enhanced uniporter activity in Tfam KO hearts, and prolongs survival.

From: Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment

Fig. 5: Diminished MCU degradation is responsible for enhanced uniporter activity in Tfam KO hearts, and prolongs survival.

a Immunoblotting for the specified proteins in P10-P14 mouse heart lysates. Samples from 3 mice shown per genotype. b Analysis of Tfam and Mcu transcripts in mouse hearts. c Ca2+ uptake in isolated cardiac mitochondria incubated in Oregon Green BAPTA 6F (OGB6F). Arrow indicates 10 µM Ca2+ pulse. d Summary of the normalized rate of Ca2+ uptake after a 10 µM Ca2+ pulse. e Heart weight to body weight ratios of P10-P14 mice of the indicated genotypes. f Kaplan–Meier survival analysis of the Tfam KO mice compared to Tfam-Mcu DKO mice. Comparison via a log rank test. Summary data are presented as mean values ± SEM. Statistics: (b) Kruskal–Wallis followed by Dunn’s test with Bonferroni correction; (d, e) 1-way ANOVA followed by Bonferroni-corrected means comparisons; (f) Log-rank test. Source data are provided as a Source Data file.

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