Jasmonic acid (JA) and its biologically active derivatives (bioactive JAs) perform a critical role in regulating plant responses to
wound stress. The perception of bioactive JAs by the
F-box protein COI1 triggers the SCF(COI1)/
ubiquitin-dependent degradation of
JASMONATE ZIM-DOMAIN (JAZ)
proteins that repress the expression of JA-response genes. JA is required for many
wound-inducible systemic defense responses, but little is known about the role of the
hormone in long-distance signal relay between damaged and undamaged leaves. Here, we show that the wounding of Arabidopsis thaliana leaves results in the rapid (<5 min) accumulation of jasmonoyl-
l-isoleucine (
JA-Ile), the bioactive form of JA, in leaves distal to the
wound site. The rapid systemic increase in
JA-Ile preceded the onset of early transcriptional responses, and was associated with JAZ degradation.
Wound-induced systemic production of
JA-Ile required the JA biosynthetic
enzyme 12-oxo-phytodienoic acid (
OPDA)
reductase 3 (OPR3) in undamaged responding leaves, but not in wounded leaves, and was largely dependent on the JA-conjugating
enzyme JAR1. Interestingly, the
wound-induced synthesis of JA/
JA-Ile in systemic leaves was correlated with a rapid decline in
OPDA levels. These results are consistent with a model in which a rapidly transmitted
wound signal triggers the systemic synthesis of JA, which, upon conversion to
JA-Ile, activates the expression of early response genes by the SCF(COI1)/JAZ pathway.