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. 2020 Jan 16;29(4):649–661. doi: 10.1093/hmg/ddz277

Figure 7.

Figure 7

Dysfunction of mitochondrial complexes in Slc25a46−/− mice mitigated by AAV–Slc25a46 vector treatment. (A) Complex I activities in the brain, heart, liver and muscle of P50 mice. AAV–Slc25a46-treated mutants showed a significantly improved function of complex I in heart and muscle tissues (P = 0.0104 and 0.0110, respectively). (B) Complex II + III activities in the brain, heart, liver and muscle of P50 mice. AAV–Slc25a46-treated mutants showed a restored function of complex II + III in brain tissue (P = 0.0110). (C) Complex IVactivities in various tissues. Upper right panel: the activity of complex IV in the heart of AAV-treated mutants was significantly higher than the activity levels observed in untreated mutants (P = 0.016). As expected, WT mice also showed significantly higher activity than untreated mutants (P = 0.0040). Lower right panel: both AAV–Slc25a46-treated mutants and WT mice showed significantly higher complex IV activity in muscle tissue than the activity levels observed in mutants (P < 0.0001 for both comparisons). The dataset of mitochondrial activity assays was generated from three mice of each group. (*P < 0.05, **P < 0.01, ****P < 0.0001).