Induction of cyanide-insensitive respiration in Neurospora crassa

• Published in: The Journal of biological chemistry 1974-06, Vol.249 (11), p.3551-3556
• Main Authors: Edwards, D.L, Rosenberg, E, Maroney, P.A
• Format: Article
• Language: English
• Subjects: Antimycin A - pharmacology; Cell Nucleus - metabolism; Chloramphenicol - pharmacology; Cyanides - pharmacology; Cycloheximide - pharmacology; Cytochromes - metabolism; Drug Synergism; Enzyme Induction; Enzyme Repression; Hydroxamic Acids - pharmacology; Kinetics; Mitochondria - drug effects; Mitochondria - enzymology; Models, Chemical; Neurospora - metabolism; Neurospora crassa - cytology; Neurospora crassa - drug effects; Neurospora crassa - enzymology; Neurospora crassa - metabolism; Oxidoreductases - biosynthesis; Oxygen Consumption - drug effects; plant biochemistry; plant physiology; Potassium - pharmacology; Ribosomes - metabolism; Salicylates - pharmacology
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/S0021-9258(19)42607-0

Treatment of cultures of Neurospora crassa with chloramphenicol results in the appearance of a mitochondrial respiratory pathway that is insensitive to cyanide and antimycin A but is inhibited by salicylhydroxamic acid. Under the experimental conditions employed, protein(s) required for the expression of the alternate pathway is synthesized on cytoplasmic ribosomes at a constant rate for 2.5 hours after an initial 0.5-hour lag. Titration of chloramphenicol-treated cultures with salicylhydroxamic acid and cyanide shows that the flux of reducing equivalents through the cytochrome chain proceeds at the maximum possible rate, while the flux of reducing equivalents through the alternate respiratory pathway proceeds at a variable rate. The flux through the cytochrome chain decreases with a half-life of 4.6 hours upon addition of chloramphenicol and the flux through the alternate oxidase pathway increases as the flux through the cytochrome chain decreases. The alternate pathway is synthesized and assembled during a time period when only small changes occur in the flux through the cytochrome chain and oxidative phosphorylation is not affected. The data are consistent with a model for induction of the pathway that proposes a mitochondrially synthesized repressor protein to repress the nuclear genes that code for the alternate oxidase.