Effects of Helminthosporium maydis race T toxin on electron transport in susceptible corn mitochondria and prevention of toxin actions by dicyclohexylcarbodiimide

Journal Article · Fri Dec 01 00:00:00 EST 1989 · Plant Physiology; (USA)

DOI:https://doi.org/10.1104/pp.91.4.1296· OSTI ID:5837303

Holden, M J; Sze, H ^[1]

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1. Univ. of Maryland, College Park (USA)

The effect of Helminthosporium maydis race T toxin on electron transport in susceptible cytoplasmic male-sterile Texas corn (Zea mays L.) mitochondria was investigated, using dichlorophenol indophenol and ferricyanide as electron acceptors. Succinate-dependent electron transport was stimulated by the toxin, consistent with the well described increase in membrane permeability induced by the toxin. Malate-dependent electron transport was inhibited. This inhibition of electron transport increased as a function of time of exposure to the toxin. Mitochondria from normal-fertile (N) corn were not affected by the toxin. Both the inhibition of electron transport and the increase in ion permeability, such as dissipation of membrane potential and Ca{sup 2+} gradients, induced by the toxin in T corn was prevented by N,N{prime}-dicyclohexylcarbodiimide, a hydrophobic carbodiimide. A water-soluble carbodiimide, 1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide, was ineffective in preventing dissipation of membrane potential by the toxin. These results suggest that the various toxin actions are mediated via interaction of the toxin with one target site, most probably a 13 kilodalton polypeptide unique to T mitochondria. N,N{prime}-dicyclohexylcarbodiimide may confer protection by modifying an amino acid residue in a hydrophobic portion of the target site.

• OSTI ID: 5837303
• Journal Information: Plant Physiology; (USA), Vol. 91:4; ISSN 0032-0889
• Country of Publication: United States
• Language: English

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