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Oxidation processes and ubiquinone localization in the branched respiratory system of mi-1 mutant of Neurospora crassa.

1. Stimulation of succinate oxidation in mi-1 mitochondria by Mg2+ and Pi is abolished on uncoupling, which points to the energy-linked activation of succinate oxidation. 2. Mitochondria exhibited respiratory control with succinate and NADH when the cyanide-insensitive oxidation was inhibited by salicylhydroxamic acid (SHAM). SHAM lowered the oxidation rate with NADH and succinate to the same level, though the NADH oxidation rate was 2.5 times as high as with succinate. 3. Despite the high stimulation of succinate oxidation via the SHAM-sensitive pathway in the active and controlled state of mitochondria, the redox state of UQ in all metabolic states remains unchanged. On inhibition of the cyanide-insensitive pathway, UQ reduction is greatly increased only in the controlled and active state. With NADH as a substrate, UQ does not respond to the metabolic states of mitochondria. 4. The redox changes of cytochrome c parallel those of UQ. 5. Branching of the respiratory chain in mi-1 mitochondria is discussed.