In plants, herbivore attack elicits the rapid accumulation of
jasmonic acid (JA) which results from the activation of constitutively expressed biosynthetic
enzymes. The molecular mechanisms controlling the activation of JA biosynthesis remain largely unknown however new research has elucidated some of the early regulatory components involved in this process. Nicotiana attenuata plants, a wild tobacco species, responds to
fatty acid amino acid conjuguates (FAC) elicitors in the oral secretion of its natural herbivore, Manduca sexta, by triggering specific defense and tolerance responses against it; all of the defense responses known to date require the amplification of the
wound-induced JA increase. We recently demonstrated that this FAC-elicited JA burst requires an increased flux of free
linolenic acid (18:3) likely originating from the activation of a plastidial glycerolipase (GLA1) which is activated by an abundant FAC found in insect oral secretions, N-linolenoyl-
glutamate (18:3-Glu). The lack of accumulation of free 18:3 after elicitation suggests a tight physical association between GLA1 and LOX3 in N. attenuata leaves. In addition, the
salicylate-induced
protein kinase (SIPK) and the nonexpressor of PR-1 (NPR1) participate in this activation mechanism that controls the supply of 18:3. In contrast, the
wound-induced
protein kinase (WIPK) does not but instead regulates the conversion of 13(S)-hydroperoxy-18:3 into
12-oxo-phytodienoic acid (
OPDA). These results open new perspectives on the complex network of signals and regulatory components inducing the JA biosynthetic pathway.