Stimulation of Ethylene Production in Bean Leaf Discs by the Pseudomonad Phytotoxin Coronatine

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Abstract
Coronatine is a toxin produced by Pseudomonas syringae pathovar glycinea which induces the same chlorotic response in bean leaves as does infection by the bacterial pathogen. Although the structure of coronatine is known, the biological mode of action is not. One possible clue to its activity is the ethyl-substituted cyclopropane side chain of the molecule. This part structure (1-amino-2-ethycyclopropane-1-carboxylic acid or AEC) is an analog of the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC). When coronatine was applied to bean leaf disks in solution, or to intact leaves through prick application, a substantial stimulation of ethylene production was measured. This stimulation was concomitant with an increase in ACC content of the tissue, and occurred under the same conditions as did the chlorotic response to the toxin. The stimulation of ethylene production was inhibited by aminoethoxyvinylglycine, an inhibitor of ACC synthesis. These results, along with those of experiments using L-[U-14C]methionine, indicated that the stimulation involved de novo production of ethylene via the methionine pathway. The whole, unhydrolyzed coronatine molecule is probably necessary to elicit both the ethylene and chlorosis responses since neither hydrolysis product (coronafacic acid and coronamic acid [AEC]) is effective alone. A naturally occurring analog of coronatine, coronafacoylvaline, also stimulated ethylene production and caused chlorosis. The unrelated pseudomonad phytotoxin, which also causes chlorosis, did not stimulate ethylene production. Ethylene thus may have a specific role in the coronatine toxic syndrome.