EFFECTS OF OCTADECANOID METABOLITES AND INHIBITORS ON INDUCED NICOTINE ACCUMULATION IN NICOTIANA-SYLVESTRIS

We examined the effects of inhibitors of the octadecanoid pathway (n-p ropyl gallate, acetosalicylic acid, salicylhydroxamic acid, methyl sal icylate, and antipyrine) on wound- and jasmonate-induced nicotine accu mulation and compared the nicotine-inducing ability of exogeneous addi tions of linolenic acid (18:3) and its methyl ester, linoleic acid (18 :2), abscisic acid, traumatic acid, and methyl dihydrojasmonate to the nicotine-inducing ability of exogenous additions of methyl jasmonate (MJ). The first four of these inhibitors significantly reduced wound-i nduced nicotine accumulation when applied in a lanolin paste to wounde d tissues immediately after wounding at concentrations of 89-90 mu g/p lant. When methyl salicylate and propyl gallate were mixed individuall y with MJ, neither inhibited MJ-induced nicotine synthesis, which sugg ests that the inhibitors block jasmonate synthesis or release from sto red pools and not its effects. Linolenic acid or its methyl ester appl ied to undamaged plants or damaged plants (to either damaged or undama ged leaves) or to the roots of hydroponically growing plants did not i nduce nicotine accumulation or increase nicotine accumulation above le vels found in damaged plants. Similarly, traumatic acid, linoleic acid , and abscisic acid did not induce nicotine accumulations. Methyl dihy drojasmonate, which is biosynthetically derived from linoleic acid, ha d 12-56% of the nicotine-inducing activity of MJ when added to the roo ts of hydroponically grown plants. The signal transduction pathway med iating wound-induced nicotine production therefore shares many feature s of the pathway eliciting wound-induced proteinase inhibitor producti on but differs in not being regulated at the lipase step in jasmonic a cid production and not being responsive to abscisic acid.