Altered mitochondrial membrane activities associated with cytoplasmically-inherited disease sensitivity in maize.

The effect of Helminthosporium maydis, race T, pathotoxin on mitochondria isolated from etiolated maize seedlings with different cytoplasmic genomes was investigated. Mitochondria isolated from plants with the Texas cytoplasm, which confers male sterility and field susceptibility to Helminthosporium maydis race T, were sensitive to the pathotoxin while mitochondria from male fertile plants with normal cytoplasm, which are resistant to race T of the fungus, were resistant to the pathotoxin. The pathotoxin induced uncoupling of oxidative phosphorylation, activation of cytochrome oxidase and succinate cytochrome c reductase, inhibited electron transport at an early site in the electron transport chain and overcame the malate and succinate inhibition of ATPase in sensitive mitochondria. All of the pathotoxin-induced abnormalities are consistent with the hypothesis that the pathotoxin has a binding site on the inner membrane of sensitive but not resistant mitochondria and this site is controlled by cytoplasmic DNA. It is concluded that a component of susceptibility of maize lines to Helminthosporium maydis, race T, is the uncoupling and inhibition of mitochondrial electron transport by race T pathotoxin.