Abstract

The metabolic fate of arachidonic acid (AA) applied to potato tuber was investigated. Arachidonic acid was stable compared to exogenously-supplied linoleic acid, which is native to potato. More than 50% of the AA was recovered unmodified 24 h after treatment, while less than 30% of applied linoleic acid remained by 4 h. Metabolism of [ 14 C]AA occurred at a low level (2–5%) immediately upon treatment and continued through 30 h, with accumulation of radiolabel in the oxidized fatty acid fractions. Arachidonic acid which remained intact in tissue was incorporated rapidly into acyl lipids, primarily phosphatidyl choline and phosphatidyl ethanolamine, in a similar pattern to incorporation of exogenously-supplied linoleic acid. The AA released from esterification in phosphatidyl choline by potato tissue followed the fate of free AA. Glucans from Phytophthora infestans and CaCl 2 —both enhancers of hypersensitive resistance—enhanced metabolism of AA to compounds comigrating with oxidized fatty acids. Salicylhydroxamic acid, an inhibitor of hypersensitive resistance, inhibited oxidative metabolism of AA. No effect of these factors on incorporation of AA into phospholipids was observed. These results are consistent with the hypothesis that AA is oxidized by potato as an initial step in triggering hypersensitive resistance, although elicitor activity that could be ascribed to AA metabolites was not found.

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