Division of Horticulture and Processing, Department of Scientific and Industrial Research, Private Bag, Auckland, New Zealand.
Plant Physiol. 1985 Apr;77(4):969-73. doi: 10.1104/pp.77.4.969.
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.
冠菌素是一种由丁香假单胞菌 pv. 大豆产生的毒素,它在诱导豆叶出现黄化反应方面与细菌病原体的感染相同。虽然冠菌素的结构是已知的,但它的生物作用模式尚不清楚。其活性的一个可能线索是分子中环丙基侧链的乙基取代。该部分结构(1-氨基-2-乙基环丙烷-1-羧酸或 AEC)是乙烯前体 1-氨基环丙烷-1-羧酸(ACC)的类似物。当冠菌素以溶液形式应用于豆叶圆盘,或通过刺伤应用于完整叶片时,测量到乙烯产生的大量刺激。这种刺激伴随着组织中 ACC 含量的增加,并且与毒素引起的黄化反应的条件相同。ACC 合成的抑制剂氨基乙氧乙烯基甘氨酸抑制了乙烯的产生。这些结果,以及使用 l-[U-(14)C]蛋氨酸的实验结果表明,刺激涉及通过蛋氨酸途径产生新的乙烯。完整的、未水解的冠菌素分子可能是引起乙烯和黄化反应所必需的,因为水解产物(冠叶酸和冠氨酰基 AEC)单独使用都没有效果。冠菌素的一种天然类似物,冠酰缬氨酸,也刺激乙烯的产生并导致黄化。然而,不相关的假单胞菌植物毒素菜豆毒素,它也会导致黄化,但不会刺激乙烯的产生。因此,乙烯可能在冠菌素毒性综合征中具有特定的作用。