Abstract

Tobacco necrosis virus (TNV) producing necrotic local lesions in soybean primary leaves, stimulated ethylene production, ethylene-forming activity (EFA) and 1-aminocyclopropane-1-carboxylic acid (ACC) accumulation. The inhibitors of ethylene biosynthesis, aminoethoxyvinylglycine and Co 2+, completely prevented ethylene production by the infected leaves, while a free-radical scavenger, propyl gallate, drastically inhibited it. These results indicate that the biosynthesis of stress ethylene during the hypersensitive reaction (HR) of soybean to TNV proceeds through the methionine cycle. Ethylene inhibitors did not prevent necrosis, suggesting that ethylene does not act as a phytotoxin. Ethylene production does not appear to be involved in localizing TNV infection, because its complete inhibition did not affect lesion growth or accumulation of TNV antigen. Ethylene production, EFA and free ACC were not affected in uninoculated leaves of inoculated soybean plants, indicating that there is no systemic effect on ethylene biosynthesis during HR. In contrast, EFA was activated in analogous uninoculated leaves of inoculated cowpea and asparagus bean plants, a finding that illustrates that care must be taken in interpreting results from single models.

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