Coronatine is a toxin produced by Pseudomonas syringae pv. 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 discs 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-(14)C]
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. However, the unrelated pseudomonad phytotoxin
phaseolotoxin, which also causes
chlorosis, did not stimulate
ethylene production.
Ethylene thus may have a specific role in the
coronatine toxic syndrome.