Iron Specifically Protects Corn Protoplasts from T-Toxin of Cochliobolus heterostrophus

Abstract

Ferric ion reduced the dmagin effects of T-toxin, a series of linear j-polyketols produced by the pathogenic fngus CocAliobolus heterostrophas, on leaf mesophylH protoplasts from susceptible T-cytoplasm corn.Of nine metals tested, only ferric and ferrous ions had this effect. Despite the presence of 12 available oxygen atoms in each T-toxin molecule, there was no evidence for the formation of an aqueous Fe2"-or Fe3-Ttoxin complex. The protective effect of iron was eliminated by a molar excess of EDTA. Iron had no effect on the sensitivity of T-cytoplasm mitochondria to T-toxin, even at a 1000-fold molar excess, nor did it protect roots of T-cytoplasm corn sings from inhibition by T-toxin. The mechanism by which iron specifically protects protoplasts from Ttoxin is not understood, but time lapse experiments suggest that iron acts on some intracellular site to modify T-toxin sensitivity and not on a transport system at the cell surface.The fungus Cochliobolus heterostrophus Drechsler (anamorph: Bipolaris maydis = Helminthosporium maydis) is the causal agent of southern corn leaf blight. Race T of this fungus differs from race 0 in its high virulence toward corn with T3 cytoplasm and its ability to synthesize a series of linear (chain length of 35-45 carbons) ,B-polyketopolyalcohols known as T-toxin (16). Each major member of this family of structurally related compounds strongly inhibits malate oxidation and stimulates NADH oxidation by mitochondria from susceptible corn shoots but has no equivalent effect on mitochondria, cells, or tissues from resistant (N-cytoplasm) corn or from other plants (24).The mitochondrion of T-cytoplasm corn is a major site of action of the toxin. Miller and Koeppe (22) first observed that low concentrations of T-toxin, within seconds after exposure, caused mitochondrial swelling, reduced the rate of oxidation of malate-pyruvate, increased rates of oxidation of succinate and NADH, and uncoupled oxidative phosphorylation. Succinate oxidation is either increased (25) or reduced (4, 30) by T-toxin treatment, apparently depending upon the KCI concentration in the assay medium. Stimulation of ATPase activity (4,25), activation of cytochrome oxidase and succinate cytochrome c re-

Prevention of stress in iron metabolism of plants

“…Radical formation by iron is not necessarily a harmful event; in ribonucleotide reductase a free radical, stabilized by iron, is essential for enzyme activity (Harder & Follman 1987); iron specifically protects corn protoplasts from T-toxin of a pathogenic mould (Macrae & Yoder 1987), probably by producing 02' Recent reviews on the role of iron as an inducer of radical formation are by Halliwell & Gutteridge (1988) and Dunford (1987); about the effects of radicals by Halliwell (1987), Leshem (1988) and Thompson et al (1987).…”