Abstract
An intracellular signaling pathway for activating plant defense genes against attacking herbivores and pathogens is mediated by a lipid-based signal transduction cascade. In this pathway, linolenic acid (18:3) is proposed to be liberated from cell membranes and is converted to cyclopentanones that are involved in transcriptional regulation of defense genes, analogously to prostaglandin synthesis and function in animals. Levels of 18:3 and linoleic acid in tomato (Lycopersicon esculentum) leaves increased within 1 h when the leaves were wounded with a hemostat across the main vein to simulate herbivore attacks. The increase correlated with the time course of accumulation of jasmonic acid, a cyclopentanone product of 18:3, that had previously been shown to increase in leaves in response both to wounding and to elicitors of plant defense genes. One hour after wounding, at least a 15-fold excess of 18:3 was found over that required to account for the levels of newly synthesized jasmonic acid. The free fatty acids in both control and wounded leaves accounted for less than 0.25% of the total fatty acids. However, the total lipid contents of the leaves remained relatively unchanged up to 8 h after wounding, indicating that extensive loss of lipids did not occur, although a gradual decrease in polar lipids was observed, mainly in monogalactosyl diacylglycerol of chloroplast lipids. The data support a role for lipid release as a key step in the signaling events that activate defense genes in tomato leaves in response to wounding by attacking herbivores.
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