Leaf damage by herbivores in Nicotiana sylvestris Spegazzini and Comes (Solanaceae) produces a damage signal that dramatically increases de novo nicotine synthesis in the roots. The increased synthesis leads to increases in whole-plant nicotine pools, which in tum make plants more resistant to further herbivore attack. Because signal production and the response to the signal occur in widely separated tissues, the speed with which different damage signals exit a damaged leaf can be studied. We propose that electrical damage signals should exit a leaf faster (less than 60 min) than chemical damage signals. Excision of a leaf induces a smaller increase in nicotine production than does puncture damage, so we examined our proposition by excising previously punctured leaves at 1, 60, and 960 min after leaf puncture and quantifying the induced whole-plant nicotine pools six days later when the induced nicotine production had reached a maximum. Significant induced nicotine production occurred only if punctured leaves were excised more than 1 hr after puncture, which is consistent with the characteristics of a slow-moving chemical signal rather than a fast-moving electrical signal. We explore the nature of the chemical signal and demonstrate that additions of 90 mug or more of methyl jasmonate (MJ) in an aqueous solution to the roots of hydroponically grown plants induce de novo nicotine synthesis from (NO3)-N-15 in a manner similar to that induced by leaf damage. We examine the hypothesis that jasmonic acid (JA) functions in the transfer of the damage signal from shoot to root. Using GC-MS techniques to quantify whole-plant JA pools, we demonstrate that leaf damage rapidly (<0.5 hr) increases shoot JA pools and, more slowly (<2 hr), root JA pools. JA levels subsequently decay to levels found in undamaged plants within 24 hr and 10 hr for shoots and roots, respectively. The addition of sufficient quantities (186 mug) of MJ in a lanolin paste to leaves from hydroponically grown plants significantly increased endogenous root JA pools and increased de novo nicotine synthesis in these plants. However, the addition of 93 mug or less of MJ did not significantly increase endogenous root JA pools and did not significantly affect de novo nicotine synthesis. We propose that wounding increases shoot JA pools, which either directly through transport or indirectly through a systemin-like signal increase root JA pools, which, in tum, stimulate root nicotine synthesis and increase whole-plant nicotine pools.
