Effects of toxin from Helminthosporium maydis T on respiration and associated activities in maize tissue

Abstract Earlier work proved that toxin from Helminthosporium maydis race T uncouples oxidative phosphorylation by mitochondria isolated from susceptible but not from resistant plants. However, an effect on the mitochondrial site in vivo was never demonstrated. In our experiments, toxin-treated leaves and coleoptiles from susceptible plants had 20 to 60% greater oxygen uptake than did control tissues; resistant tissues were not affected. Toxin inhibited glycolysis in susceptible tissue; the inhibition was slow to develop and was not alleviated by intermediates of the glycolytic pathway. In contrast, 2,4-dinitrophenol (50 μm) stimulated glycolysis. Toxin did not affect glycolysis in resistant tissue and in cell-free preparations from susceptible or resistant plants; thus, the effect on glycolysis in vivo appears to be secondary or indirect. Levels of acid-labile organic phosphates were decreased in susceptible but not in resistant tissues after exposure to toxin for 1 h. Toxin did not affect phosphatase activities associated with microsomal fractions and with cell walls. These data, plus data from other sources, support the hypothesis that toxin affects a mitochondrial site in intact tissue; indeed, the mitochondrial site may be the only important site for direct action of the toxin.