Methyl jasmonate and cis-jasmone do not dispose of the herbivore-induced jasmonate burst in Nicotiana attenuata.

The oxylipin pathway mediates wound- and herbivore-induced defense reactions in Nicotiana attenuata as evidenced by a transient jasmonic acid (JA)-burst that precedes these defense responses. The fate of this induced JA-burst remains unknown. Two derivatives of JA, its methylester, methyl jasmonate (MeJA) and cis-jasmone (cisJ), are thought to be a means of disposing of JA through volatilization at the plant surface. In N. attenuata, the headspace quantities of these compounds did not change over 3 days, although levels of MeJA and cisJ increased 100- and 70-fold, respectively, in surface extracts of attacked leaves after feeding of Manduca sexta larvae or application of larval regurgitant to mechanical wounds. Inhibition of the wound-induced increase in JA with indole-3-acetic acid (IAA) revealed an association between the JA accumulation and subsequent increases in MeJA and cisJ. Induced systemic increases of MeJA were not of local origin and therefore do not contribute to the inactivation of the JA-burst in the wounded leaf. The total amount of MeJA and cisJ produced could only account for 9% of the JA-burst elicited by herbivore attack and therefore their production do not represent major disposal pathways of JA in N. attenuata.