Fig. 3: Mitochondria in OPA1-KO liver have disrupted cristae, but maintain normal respiratory capacity. | Nature Communications

Fig. 3: Mitochondria in OPA1-KO liver have disrupted cristae, but maintain normal respiratory capacity.

From: The mitochondrial fusion protein OPA1 is dispensable in the liver and its absence induces mitohormesis to protect liver from drug-induced injury

Fig. 3

Electron micrographs of thin sections from floxed (a) and OPA1-KO livers (b–f). Many OPA1-KO mitochondria lack normal cristae, but maintain their electron density (b). A number of mitochondria in OPA1-KO liver have primordial cristae or junction-less cristae (c–f). LD: lipid droplet. Scale bars in (a) and (b) are 2 μm and (c–f) are 1 μm. One liver from a floxed animal and two livers from KO animals were processed. The results were consistent. g Respiration analyses. Basal (in glutamate/malate), state 3, leak, and maximum OCRs were measured by sequential additions of ADP, oligomycin, and FCCP, respectively. n = 6 animals per group. Data are presented as mean values +/- SEM. Unpaired t test. h–k No significant differences in ATP-linked ( = Basal–Leak), reserve capacity ( = Max–Basal) and respiratory control ratio (state 3/state 4o) as well as liver ATP content. n = 6 animals per group. Data are presented as mean values +/- SEM. Unpaired t test. Source data are provided as a Source Data file. l EM of isolated mitochondria from control (floxed) liver. Note wider cristae compared with those in mitochondria in situ. m–o EM of isolated mitochondria from OPA1-KO liver. Cristae ballooning is evident. These cristae are mostly attached to the inner boundary membrane by junctions (arrows and arrowheads). One mitochondrial preparation each from floxed and KO animals were processed.

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