The wound hormone jasmonate

Abstract

Plant tissues are highly vulnerable to injury by herbivores, pathogens, mechanical stress, and other environmental insults. Optimal plant fitness in the face of these threats relies on complex signal transduction networks that link damage-associated signals to appropriate changes in metabolism, growth, and development. Many of these wound-induced adaptive responses are triggered by de novo synthesis of the plant hormone jasmonate (JA). Recent studies provide evidence that JA mediates systemic wound responses through distinct cell autonomous and non-autonomous pathways. In both pathways, bioactive JAs are recognized by an F-box protein-based receptor system that couples hormone binding to ubiquitin-dependent degradation of transcriptional repressor proteins. These results provide a framework for understanding how plants recognize and respond to tissue injury.

Fig. 1

The biologically synthesized form of jasmonic acid, (3R,7S)-JA (also known as (+)-7-iso-JA), is metabolized to various bioactive and non-bioactive derivatives. JA carboxyl methyltransferase (JMT) converts (3R,7S)-JA to the volatile compound, methyl-JA (MeJA). The reverse reaction is catalyzed by MeJA esterase (MJE). (3R,7S)-JA is also converted to the active form of the hormone, (3R,7S)-JA-L-Ile (also known as (+)-7-iso-JA-L-Ile), via JAR1-mediated conjugation to L-isoleucine. (3R,7S)-JA-L-Ile may epimerize to the more stable (3R,7R)-JA-L-Ile stereoisomer (also known as (-)-JA-L-Ile) in which the side chains at position 7 and 3 are in the trans orientation with respect to one another. (3R,7S)-JA can be conjugated other amino acids to produce various JA-amino acid conjugates (JACs). Both free and amino acid-conjugated forms of (3R,7S)-JA are subject to several other modifications (boxed).

Fig. 2

Role of JA in plant responses to tissue injury. Local response: tissue damage results in the production of plant- and attacker-derived signals (either chemical or physical in nature) that are recognized by pattern recognition receptors (PRRs) at the cell surface. By mechanisms that are largely unknown, this recognition event activates de novo synthesis of JA and JA-Ile. JA-Ile is the active signal for SCF^COI1/26 proteasome-mediated degradation of JAZ proteins that repress transcription factors (TFs) involved in the expression of defense-related traits. Systemic response: wound-induced systemic defense responses are mediated by two distinct pathways involving JA. In the cell-nonautonomous pathway, JA (or a derivative) produced in the damaged leaf is translocated to distal sites (e.g., an undamaged leaf) where it triggers JA responses in target cells. In the cell autonomous pathway, wound-induced production of a mobile signal (other than JA) activates JA/JA-Ile synthesis and subsequent responses in distal tissues. The two pathways may work synergistically to optimize the spatial and temporal expression of responses elicited by various forms of tissue injury. For simplicity, the figure does not include pathogen-and microbe-associated molecular patterns (PAMPs/MAMPs) that may also activate JA-based defenses.