Jasmonate Signaling System in Plant Innate Immunity

Abstract

The plant immune system uses several second messengers to encode information generated by the pathogen-associated molecular patterns (PAMPs) and deliver the information downstream of plant pattern recognition receptors (PRRs) to proteins which decode/interpret signals and initiate defense gene expression. Plant hormones play important role in intercellular and systemic signaling systems in plant immunity. Jasmonic acid (JA) system is a key component in the complex plant hormone signaling systems. The production of jasmonic acid (JA) in plants is a tightly regulated process. In healthy unstressed plants, JA content is very low and PAMP cues enhance the biosynthesis and accumulation of JA in the PAMP-treated plant tissues. PAMP elicitor signals activate G-proteins and the activated G-proteins further switch on calcium ion channels. Ca2+ influx and subsequent Ca2+ wave (calcium signature) may activate NADPH oxidase and H2O2 production. The Ca2+ influx-mediated NO plays important role in JA biosynthesis. Co-expression of MAPK genes with the genes involved in the JA biosynthesis pathway suggests that MAPK cascades may also be involved in JA biosynthesis. COI1 is as a key player in the jasmonate perception and signal transduction pathway. JA receptor is a three-molecule co-receptor complex, consisting of COI1, JAZ, and inositol pentakisphosphate, all of which are indispensable for high-affinity hormone binding. The bioactive jasmonate-isoleucine (JA-Ile) promotes physical interaction between JAZ1 and COI1. The JA receptor JAZ proteins have been identified as suppressors of jasmonate signaling. NINJA is an adaptor protein that interacts with the ZIM domain of most JAZs. NINJA contains an EAR (for ERF-associated amphiphilic repression) motif that recruits the corepressor TOPLESS (TPL). JAZs are a scaffold on which the NINJA–TPL corepressor complex is assembled. Repression of JA response genes involves binding of JAZ to ‑NINJA, which contains an EAR motif that recruits the corepressor TPL, which may silence gene expression. In the absence of JA signal, JAZ proteins actively repress the transcription factor MYC2, which binds to cis-acting elements of JA response genes. In response to cues that up-regulate JA-Ile synthesis, the hormone triggers the specific binding of JAZ proteins to COI1, leading to poly-ubiquitination. Subsequent degradation of JAZ by the 26S proteasome relieves repression of MYC2 and probably other transcription factors, permitting the expression of jasmonate-responsive genes. MEDIATOR25 subunit of the Mediator complex is a positive regulator of jasmonate-responsive gene expression in Arabidopsis. MED25 functions in association with transcriptional regulators of the JA pathway. Histone deacetylase may regulate JA-mediated signaling systems. JA and ET pathways appear to function cooperatively in modulating plant immune responses. Ethylene signaling may render JA signaling insensitive to subsequent suppression by SA. JA may inhibit SA signaling and SA may suppress the biosynthesis of JA. SA suppresses JA signaling system by targeting GCC-box motifs in JA-responsive promoters. JA signaling may be integrated into early ABA signaling and may affect ABA receptor complexes to regulate downstream common signal components. MicroRNA-directed RNA silencing system triggers JA signaling by specifically activating biosynthesis of JA. JA-Ile may be the mobile signaling cue involved in the induced systemic resistance (ISR). JA-Ile may be synthesized de novo and transported into systemic tissues to trigger ISR. JA-mediated priming plays an important role in the ISR.