A Comparison of Purified Host Specific Toxin from Helminthosporium maydis, Race T, and Its Acetate Derivative on Oxidation by Mitochondria from Susceptible and Resistant Plants.

NADH or succinate oxidation and malate oxidation were differentially affected in mitochondria from both susceptible and resistant corn by a purified and chemically characterized preparation of host-specific toxin from Bipolaris (Helminthosporium) maydis, race T. NADH and succinate oxidation by susceptible T corn mitochondria were stimulated 50 to 200% with apparent uncoupling from the cytochrome chain at approximately 10(-9)m toxin (5 to 20 ng/ml). Significant inhibition of malate oxidation was observed at slightly higher toxin concentrations, but oxidation was still coupled to ADP utilization. Inhibition of malate oxidation also was observed in N corn (resistant) and soybean mitochondria at approximately 1,000-fold greater concentrations, but stimulation of NADH and succinate oxidation was not found at any toxin concentration tested.A fully acetylated toxin derivative at approximately 1 microgram per milliliter also caused stimulation of NADH or succinate oxidation in T corn mitochondria, but not those of N corn or soybean mitochondria at 100 micrograms per milliliter. Malate oxidation was inhibited to the same extent by toxin acetate with mitochondria from T corn, N corn, and soybean. The blocking of hydroxyl groups in race T toxin by acetyl functions eliminated selectivity toward malate oxidation only. The data suggest that inhibition of malate oxidation is either a separate or secondary effect of selective action of toxin on T corn mitochondria, perhaps by interference with transport in or out of the matrix. Sensitivity of T, but not N, corn mitochondria to purified toxin decays within minutes after pellets are suspended in aqueous osmotica, with no obvious change in mitochondrial integrity. The action of race T toxin seems to involve a labile process, such as ion gradient(s), or an unstable structural conformation of T corn mitochondria.

[1]  J. Daly,et al.  Biological activity of purified host-specific pathotoxin produced by Bipolaris (Helminthosporium) maydis, race T , 1980 .

[2]  J. Daly,et al.  Characterization of the host-specific pathotoxin produced by Helminthosporium maydis, race T, affecting corn with Texas male sterile cytoplasm , 1979 .

[3]  D. Matthews,et al.  Helminthosporium maydis Race T Toxin Induces Leakage of NAD from T Cytoplasm Corn Mitochondria. , 1979, Plant physiology.

[4]  R. M. Spanswick,et al.  Reduction of Adenosine Triphosphate Levels in Susceptible Maize Mesophyll Protoplasts by Helminthosporium maydis Race T Toxin. , 1979, Plant physiology.

[5]  D. E. Koeppe,et al.  Mitochondrial Heredity: A Determinant in the Toxic Response of Maize to the Insecticide Methomyl , 1978, Science.

[6]  E. Earle,et al.  Cytoplasm-specific Effects of Helminthosporium maydis Race T Toxin on Survival of Corn Mesophyll Protoplasts. , 1978, Plant physiology.

[7]  M. Bednarski,et al.  Effects of toxin from Helminthosporium maydis T on respiration and associated activities in maize tissue , 1977 .

[8]  M. Bednarski,et al.  Reversible Effects of Toxin from Helminthosporium maydis Race T on Oxidative Phosphorylation by Mitochondria from Maize. , 1977, Plant physiology.

[9]  C. Arntzen.  Selective Inhibition ofK+,Na+,Cl-, andPO43-UptakeinZea mays L.byBipolaris (Helminthosporium) maydisRaceT Pathotoxin , 1977 .

[10]  G. Brierley,et al.  Energy-dependence exchange of K+ in heart mitochondria. K+ efflux. , 1977, Archives of biochemistry and biophysics.

[11]  R. Flavell.  Inhibition of electron transport in maize mitochondria by Helminthosporium maydis race T pathotoxin , 1975 .

[12]  J. Daly,et al.  Inhibition of Dark CO(2) Fixation and Photosynthesis in Leaf Discs of Corn Susceptible to the Host-specific Toxin Produced by Helminthosporium maydis, Race T. , 1975, Plant physiology.

[13]  G. Strobel,et al.  Isolation and Partial Characterization of Four Host-specific Toxins of Helminthosporium maydis (Race T). , 1974, Plant physiology.

[14]  C. Arntzen,et al.  Induction of Stomatal Closure by Helminthosporium maydis Pathotoxin. , 1973, Plant physiology.

[15]  D. E. Koeppe,et al.  The effect of toxin from Helminthosporium maydis (race T) on isolated corn mitochondria: swelling , 1973 .

[16]  D. E. Koeppe,et al.  A Comparison of Mitochondria Isolated from Male‐Sterile and Nonserile Cytoplasm Etiolated Corn Seedlings , 1973 .

[17]  J. Comstock.  Host Specificity of a Toxin from Phyllosticta maydis for Texas Cytoplasmically Male-Sterile Maize , 1973 .

[18]  J. H. Peverly,et al.  The effect of pathotoxin from Helminthosporium maydis (race T) on energy-linked processes of corn seedlings , 1973 .

[19]  D. E. Koeppe,et al.  Southern Corn Leaf Blight: Susceptible and Resistant Mitochondria , 1971, Science.

[20]  D. Smith,et al.  Reaction of corn seedlings with male-sterile cytoplasm to Helminthosporium maydis. , 1970 .

[21]  B CHANCE,et al.  Respiratory enzymes in oxidative phosphorylation. III. The steady state. , 1955, The Journal of biological chemistry.

[22]  O. H. Lowry,et al.  Protein measurement with the Folin phenol reagent. , 1951, The Journal of biological chemistry.