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Plant Physiology 146:1459-1468 (2008) © 2008 American Society of Plant Biologists Jasmonate Signaling: Toward an Integrated ViewCommonwealth Scientific and Industrial Research Organization Plant Industry, Queensland Bioscience Precinct, St. Lucia, Queensland 4067, Australia
Oxylipins are biologically active signaling molecules derived from oxygenated polyunsaturated fatty acids and are found ubiquitously in most living organisms. In mammals, the eicosanoids, which include prostaglandins, are one of the best-studied groups of biologically important oxylipins. In addition to their essential roles in numerous other physiological functions, eicosanoids function as signaling molecules in vertebrate and invertebrate animals and in eukaryotic microbes (Stanley, 2006  ).
The discovery of prostaglandins and related biologically active substances was recognized by the award of a Nobel Prize in Physiology or Medicine in 1982. Shortly after this, the pioneering work published in Plant Physiology by Vick and Zimmerman (1984)
The biosynthesis of JAs has recently been reviewed (Wasternack, 2007
Our aim in this Update article is to briefly review these recent findings that have added fresh insights into our understanding of how JA signals are transmitted within the cell. Our particular focus will be on the roles of a recently discovered class of repressors whose destruction through a COI1-mediated ubiquitination pathway is required for the transcriptional activation of the JA-dependent gene expression. In addition, the emerging roles of the transcriptional regulator JIN1/MYC2 that acts immediately downstream from these repressors in coordinating a transcriptional cascade will be briefly reviewed. Finally, positive and negative feedback loops regulating JA biosynthesis and signaling and some recent examples of interactions between JA and other hormonal signaling pathways will be considered. Readers particularly interested in JA biosynthesis should refer to other recent reviews on this topic (Browse, 2005 ; Wasternack, 2007).
Many plant processes are controlled by repressors of downstream transcriptional networks, and the degradation of these repressors under external stimuli and by plant hormones provides a rapid regulatory trigger system. The involvement of protein degradation pathways in JA signaling became apparent after the identification of the COI1 gene encoding an F-box protein with Leu repeats (Xie et al., 1998 ). Indeed, COI1 or SCFCOI1 is an integral part of a highly conserved multi-protein complex called the SCF E3 ubiquitin ligase complex. The SCF complex is found in all eukaryotes and consists of a Skp1 (S-phase kinase-associated protein)-related protein, a cullin, a RING-box protein, and an F-box protein. The SCF complex is involved in marking proteins with ubiquitin tags to facilitate their degradation by the 26S proteasome (for review, see Stone and Callis, 2007). The F-box protein component (e.g. SCFCOI1) is known to be responsible for the specificity of the SCF complexes to particular targets. However, as stated above, repressor proteins potentially targeted by SCFCOI1 have been unknown. Recently, three laboratories have simultaneously converged on a family of genes that fulfils this role.
The cloning of mutated genes in JA-insensitive mutants has so far provided vital information about the signaling events involved in this pathway. In contrast to the recessive coi1, jar1, and jin1 mutations, the relatively less-studied jai3 mutation confers a dominant JA insensitivity phenotype (Chini et al., 2007
Thines et al. (2007)
How does JA- and SCFCOI1-dependent degradation of JAZ repressors transcriptionally regulate the JA signaling pathway? JAZ proteins do not contain any DNA-binding domain. This is an indication that they may interact with other proteins to regulate gene expression (see also Vanholme et al., 2007
Another member of the JAZ family, JASMONATE ASSOCIATED1 (JAS1), also appears to be involved in JA signaling (Yan et al., 2007
The finding that JA-Ile, a jasmonic acid-Ile conjugate, but not jasmonic acid itself, MeJA, COR, or the JA precursor 12-OPDA promotes the interaction between SCFCOI1-JAZ complexes in yeast two-hybrid assays (Thines et al., 2007 ) raises new questions regarding the exact nature of the JA signal(s) perceived by putative JA receptors. This finding might imply that jasmonic acid may not be the signal directly responsible for the activation of the JA signaling pathway, but possibly it undergoes further modifications to be converted to a biologically active signal. In contrast to this, in other hormone signaling pathways (e.g. auxin), conjugation of amino acids to plant hormones is often used as a versatile mechanism for rapid reduction of the hormone levels and, consequently, down-regulation of the signaling pathway (Woodward and Bartel, 2005). When required, hormone-amino acid conjugates are rapidly hydrolyzed to release the active hormone and this activates the signaling pathway. As mentioned above, the product of the JAR1 locus conjugates Ile to jasmonic acid. However, the jar1 mutant does not display all the defects observed in the coi1 mutant, suggesting that JA-Ile may not be the only signal responsible for the activation of the JA signaling pathway.
Interestingly, although JA-Ile produced by JAR1 promotes the interaction between JAZ and SCFCOI1, a recent report found that wound-induced expression JAZ and SCFCOI1-dependent genes in the jar1 mutant was similar to that in wild-type plants (Chung et al., 2008
As mentioned above, JAI3/JAZ3 most likely suppresses the transcription factor JIN1/MYC2, which, acting early on in the signaling pathway, can either positively or negatively modulate diverse JA-dependent functions. In particular, the JA-dependent expression of pathogen and insect defense genes is differentially regulated by JIN1/MYC2. In the jin1/myc2 mutant, JA-dependent induction of wound and insect response genes was significantly attenuated, and, as a result, jin1/myc2 mutant plants showed increased susceptibility to an insect pest (Dombrecht et al., 2007 ). In contrast, the JA-dependent induction of pathogen defense genes was heightened in the jin1/myc2 mutant, which showed increased resistance to bacterial and fungal pathogens (Anderson et al., 2004; Lorenzo et al., 2004). Accumulating evidence indicates that plants are able to coordinate their responses depending on the type of attack so that the metabolic cost of plant defense can be minimized. Indeed, although both herbivory and pathogen attack activate JA signaling, the defense genes that are activated are functionally specialized against insect pests or pathogens, respectively (De Vos et al., 2005). JIN1/MYC2 and similar other molecular switches might perhaps be required to fine-tune plant defense against different biological threats.
Recent research has also showed that, in addition to pathogen and insect defense, JIN1/MYC2 differentially regulates other JA-dependent functions in Arabidopsis. For instance, in addition to insect resistance, JIN1/MYC2 positively regulates JA-mediated oxidative stress tolerance and flavonoid metabolism. In contrast, JA-dependent pathogen defense and the biosynthesis of secondary metabolites (e.g. biosynthesis of indole glucosinolates) are negatively regulated by JIN1/MYC2 (Dombrecht et al., 2007
JIN1/MYC2 does not have any obvious roles in fertility, although this trait is regulated by SCFCOI1. Fertility might be controlled by other SCFCOI1-regulated transcription factors. Recent analysis of the T-DNA insertion mutants of the two JA-responsive MYB transcription factor genes, MYB21 and MYB24, indicated their involvement in fertility (Mandaokar et al., 2006 ), although whether these MYB transcription factors interact with SCFCOI1 and/or JAZ repressors is currently unknown.
The relatively broad effects of hormone signaling pathways on multiple plant physiological processes demand that signaling pathways are tightly and coordinately regulated, preferably at multiple points. So far, both negative and positive feedback regulatory loops that regulate JA biosynthesis and signaling have been identified. First, JA biosynthesis genes are activated by JAs, suggesting that JAs positively regulate their own biosynthesis through a positive feedback loop. The recent identification of the Arabidopsis FATTY ACID OXYGENATION UPREGULATED2 gene that encodes a Ca2+-permeant nonselective cation channel suggested that cation fluxes are an important part of this positive feedback loop (Bonaventure et al., 2007 ).
JA also rapidly activates the transcription of genes encoding JAZ repressors (Chini et al., 2007
The roles of protein phosphorylation/dephosphorylation pathways in negative and positive regulation of JA biosynthesis and signaling are just emerging. Importantly, protein phosphorylation often precedes the ubiquitination process, which, as discussed above, is critical for the activation of the JA signaling pathway. Although whether Arabidopsis JAZ repressors are phosphorylated before being ubiquitinated is not known, a recent report indicated that PPS3, the potato homolog of JAI3/JAZ3, is phosphorylated by StMPK1, which shows close sequence similarity to Arabidopsis MPK6 (Katou et al., 2005
In addition to phosphorylation, protein dephosphorylation pathways modulate JA levels. For instance, in response to wounding, the PP2C-type phosphatase AP2C1 negatively regulates mitogen-activated protein kinase signaling pathways as deduced from the analysis of the Arabidopsis ap2c1 mutant, which contains increased levels of wound-induced JAs and displays enhanced resistance to a phytophagous mite (Schweighofer et al., 2007
It is becoming evident that plant hormone signaling pathways extensively interact during plant growth and development as well as during adaptation to biotic and abiotic stresses. This hormonal cross talk is indeed intriguingly complex and often dose-, species-, tissue-, and inducer-specific. The JA signaling pathway is no exception to this. Over the years, many components that are shared between JA and various other plant hormone signaling pathways have been identified. Cross talk is mostly inferred from the observation that genetic ablation of the individual shared components (or nodes) compromises both pathways or if one hormone brings about physiological changes mainly by promoting the synthesis or action of another hormone.
The mutually antagonistic interactions between salicylic acid (SA) and JA pathways first became evident from the analysis of SA- and JA-marker gene expression in SA and JA signaling mutants in Arabidopsis. Indeed, mutations that disrupt JA signaling (e.g. coi1) lead to the enhanced basal and inducible expression of the SA marker gene PR1, while mutations that disrupt SA signaling (e.g. npr1) lead to the concomitant increases in the basal or induced levels of the JA marker gene PDF1.2. Interestingly, exogenous SA promotes the JA-dependent induction of the defense gene PDF1.2 when applied at low concentrations. However, at higher SA concentrations, the induction of PDF1.2 by JA is reduced, leading to the proposal that the interaction between these two pathways might be dose dependent (Mur et al., 2006 ). Plants treated with SA or inoculated with virulent strains of P. syringae pv. tomato show compromised resistance to Alternaria brassicicola, a necrotrophic pathogen sensitive to JA-dependent defenses, possibly due to suppression of JA-dependent defenses known to be effective against necrotrophic pathogens (Spoel et al., 2007). Interestingly, however, inoculations with an avirulent strain of P. syringae that trigger hypersensitive response do not compromise A. brassicicola resistance, suggesting that cross talk between SA and JA signaling is also specific to pathogen strain (Spoel et al., 2007).
The antagonistic interaction between SA and JA signaling is at least partly mediated by NONINDUCIBLE PR1 (NPR1), a master regulator of SA signaling, but also responds to oxidative events (Spoel et al., 2003
Acting downstream from NPR1, WRKY70 is a versatile transcription factor with roles in multiple signaling pathways and physiological processes. WRKY70 regulates the antagonistic interactions between SA and JA pathways (Fig. 1). Overexpression of WRKY70 leads to the constitutive expression of the SA-responsive PR genes and increased resistance to SA-sensitive pathogens but reduces resistance to JA-sensitive pathogens. In contrast, suppression of WRKY70 leads to increased expression from JA-responsive genes and increased resistance to a pathogen sensitive to JA-dependent defenses (Li et al., 2004a
The Arabidopsis mpk4 mutant exhibits constitutively active SA-dependent defense responses (e.g. increased SA levels, constitutive expression of PR1, and increased resistance to P. syringae) in the absence of pathogen attack. In contrast, the JA-dependent induction of the PDF1.2 gene was abolished in the mpk4 mutant (Petersen et al., 2000
In addition to COI1, the transcriptional regulator JIN1/MYC2 also has a role in antagonizing SA signaling in plants during infection by P. syringae. Increased PR1 expression and resistance is found in P. syringae-infected jin1/myc2 plants that show increased resistance to this pathogen (Laurie-Berry et al., 2006
The interaction between JA and ethylene signaling is rather complex, and both synergistic and antagonistic interactions have been reported, depending on the stress conditions examined. Adding to this complexity, the role of ethylene in biotrophic pathogen-plant interactions could be different than that in necrotrophic pathogen-plant interactions (Broekaert et al., 2006 ). JA and ethylene synergistically induce a subset of defense genes following pathogen inoculation in Arabidopsis. For instance, induction of PDF1.2 by A. brassicicola requires both JA and ethylene signaling pathways (Penninckx et al., 1998). The cellulose synthase gene CeSA3/CEV1 controls a point of convergence between these two pathways as a negative regulator of both pathways, as deduced from the analysis of the cev1 mutant that displays constitutively active JA and ethylene responses (Ellis et al., 2002). The ETHYLENE RESPONSE FACTOR1 transcription factor also functions at the crossroad of JA and ethylene signaling as a positive regulator of both pathways (Lorenzo et al., 2003).
In contrast to these synergistic interactions, JA and ethylene signaling pathways act in a mutually antagonistic fashion in modulating ozone-induced cell death. Most, if not all, JA signaling and biosynthetic mutants show increased ozone sensitivity. In contrast to the effect of JA signaling, the ethylene signaling pathway promotes ozone-induced spread of lesion development (for review, see Overmyer et al., 2003
As discussed above, protein degradation pathways play essential roles not only in JA but also in light and auxin signaling. Not surprisingly, therefore, most cross talk among these pathways revolves around the SCF E3 ubiquitin ligase and the COP9 signalosome (CSN) complexes. For instance, mutations in CULLIN1/AUXIN RESISTANT6 (AXR6) component of the SCF ubiquitin ligase and CSN complexes compromise auxin, JA, and light responses. The axr6 mutant shows reduced sensitivity to JA and auxin (Feng et al., 2003 ; Ren et al., 2005) and hypersensitivity to far-red light (Quint et al., 2005). A direct interaction between CSN and SCFCOI1 has been shown. CSN reduction-of-function plants show a JA-insensitive root elongation phenotype and reduced expression from JA-responsive genes (Feng et al., 2003). AXR1, which encodes a subunit of the RUB1-activating enzyme that regulates the protein degradation activity of SCF complexes, regulates both SCFTIR1 and SCFCOI1 involved in auxin and JA signaling, respectively (Schwechheimer et al., 2002). The axr1 mutant shows reduced sensitivity to both JA and auxin (Tiryaki and Staswick, 2002). SUPPRESSOR OF THE G2 ALLELE OF skp1-4b is required for both SCFTIR-mediated auxin and SCFCOI1-mediated JA responses (Gray et al., 2003). Auxin and JA pathways are also interlinked at the level of ARFs. At least two ARFs, ARF6 and ARF8, are required for JA biosynthesis and flower fertility (Fig. 1). In addition to defective auxin responses, the arf6/arf8 double mutant shows JA deficiency, aberrant flower development, and reduced expression of several JA biosynthesis genes in flowers (Nagpal et al., 2005). JA activates expression from auxin biosynthesis genes (Dombrecht et al., 2007), while auxin activates expression of JA biosynthesis genes (Tiryaki and Staswick, 2002). These examples clearly illustrate that auxin and JA signaling are intimately interlinked. The Arabidopsis phytochrome mutants hy1 and hy2 show a JA overproduction phenotype and constitutive activation of the JA-inducible and SCFCOI1-dependent defense genes (Zhai et al., 2007). Importantly, JIN1/MYC2 acts as a negative regulator of blue light-mediated photomorphogenic growth and blue and far-red light-regulated gene expression in Arabidopsis (Yadav et al., 2005).
Both antagonistic and synergistic interactions occur between abscisic acid (ABA) and JA signaling in Arabidopsis. Both ABA and MeJA induce stomatal closure, most likely by triggering the production of reactive oxygen species (ROS) in stomatal guard cells (Munemasa et al., 2007 ). The coi1 mutation disrupts only MeJA-mediated ROS production without influencing ABA-mediated ROS production, suggesting that COI1 acts upstream from the convergence of ABA and MeJA signaling pathways.
JIN1/MYC2, a negative regulator of JA-dependent pathogen defense gene expression, positively regulates ABA-dependent drought responses (Anderson et al., 2004
Nevertheless, JA and ABA activate a large subset of genes also activated by the pathogenic oomycete Pythium irregulare. This effect of ABA is proposed to be due to the effect of this root-infecting pathogen to impose water stress in plants by clogging the vasculature (Adie et al., 2007
As exemplified throughout this article, the genetic and genomic resources available in Arabidopsis have been a driving force behind the recent discoveries made regarding how JA signals are transmitted. Some of the JA signaling components that have been identified in Arabidopsis have also been functionally analyzed in a few other dicot species, such as tobacco (Paschold et al., 2007 ; Rayapuram and Baldwin, 2007; Wang et al., 2008) and tomato (Boter et al., 2004; Li et al., 2004b; Thines et al., 2007), where they have been shown to be largely conserved. However, currently there is very little evidence regarding the actual roles of the Arabidopsis JA signaling genes in monocots. In crop plants that are not particularly amenable to functional studies (e.g. due to genetic redundancy and/or technical difficulties associated with genetic transformation), functional homology to Arabidopsis JA signaling genes was established based on the successful restoration of the wild-type phenotype when the cloned crop gene of interest was introduced into the well-characterized Arabidopsis mutant (e.g. coi1) defective for the same JA signaling component (Wang et al., 2005).
The recent discovery of JAZ repressors in Arabidopsis and tomato has not only revealed new mechanical insights into JA signaling but also reinforced the notion that signal-mediated degradation of repressors is a common theme used in plant hormone signaling. The JAZ family contains at least 12 members in Arabidopsis (Vanholme et al., 2007
The discovery of JAZ repressors has also led to the proposal that the complexes between SCFCOI1 and different JAZ proteins might be the sites of reception of different JA signals (Parry and Estelle, 2006
Given the redundancy of receptors for other plant hormones, it would not be surprising that multiple JA receptors exist in plants. Indeed, not all JA responses are SCFCOI1 dependent (Devoto et al., 2005 It is becoming evident that signaling cascades regulated by protein phosphorylation/dephosphorylation have roles in regulating JA signaling, although JA signaling components phosphorylated/dephosphorylated by these pathways are mostly unknown. Despite observations of extensive interactions between JA and other hormonal signaling pathways, our knowledge on the molecular mechanisms involved in these interactions is also still rudimentary. Nevertheless, this complex interaction among signaling networks is a testament to the plant's ability to integrate diverse signals from multiple sources so expediently that a finely tuned output can be produced and thereby provide adaptation to its environment. We expect that the elucidation of the intricate interactions between JA and other signaling pathways will continue to be a fertile area for future research.
Owing to space limitations, not all relevant work on this topic could be cited. We thank Bruno Dombrecht, Louise Thatcher, and Brendan Kidd for useful discussions, Louise Thatcher and Brendan Kidd for critical manuscript reading, and two anonymous reviewers for useful comments. Received December 30, 2007; accepted February 4, 2008; published April 8, 2008.
The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Kemal Kazan (kemal.kazan{at}csiro.au). www.plantphysiol.org/cgi/doi/10.1104/pp.107.115717 * Corresponding author; e-mail kemal.kazan{at}csiro.au.
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OXYLIPINS AS SIGNALING MOLECULES...
ACTIVATION OF JA SIGNALING...
-linolenic acid liberated from membrane phospholipids by the action of phospholipase A. 
3 was transgenically expressed in Arabidopsis, a coi1-like phenotype characterized by male sterility, JA insensitivity, and increased resistance to infection by the bacterial pathogen P. syringae pv. tomato was observed. JAZ1
