JAR1 (JASMONATE RESISTANT 1; also FIN219 and GH3.11) is a cytoplasmic GH3-family acyl acid-amido synthetase of the ANL adenylate-forming enzyme superfamily. It activates jasmonic acid by ATP-dependent adenylation and then conjugates it to an amino acid, with a strong preference for L-isoleucine, producing jasmonoyl-L-isoleucine (JA-Ile), the bioactive jasmonate perceived by the COI1-JAZ co-receptor. Loss of JAR1 strongly reduces JA-Ile levels and causes jasmonate insensitivity in root growth, gene induction, guard-cell signaling and induced systemic resistance, while residual JA-Ile formation in jar1 mutants indicates partial redundancy with other conjugating activities. JAR1 is auxin- and wound-inducible, and as FIN219 it also acts in phytochrome A-mediated far-red light responses, where its activity is enhanced by interaction with the tau-class glutathione S-transferase FIP1 (GSTU20).
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005515 protein binding | IPI PMID:28223489 Structural basis of jasmonate-amido synthetase FIN219 in com... | MODIFY | Summary: JAR1/FIN219 forms a complex with the tau-class glutathione S-transferase FIP1 (GSTU20), which enhances its adenylation activity. Reason: Protein binding is uninformative; the partner is an enzyme, and the more informative enzyme binding term is already annotated for the same interaction (PMID:17220357). Proposed replacements: enzyme binding Supporting Evidence: PMID:28223489 the adenylation activity per mole of FIN219–FIP1 was approximately double the adenylation activity per mole of FIN219 alone |
| GO:0005524 ATP binding | IDA PMID:28223489 Structural basis of jasmonate-amido synthetase FIN219 in com... | KEEP AS NON CORE | Summary: Crystal structures of FIN219/JAR1 show ATP bound in the active site after JA binding. Reason: ATP is a substrate of the ligase; binding is part of the core catalytic activity rather than a separate function. Supporting Evidence: PMID:28223489 Interestingly, neither ATP nor isoleucine could bind directly to FIN219 or to the FIN219–FIP1 complex unless JA had been bound first |
| GO:0005524 ATP binding | ISS PMID:12084835 Jasmonate response locus JAR1 and several related Arabidopsi... | KEEP AS NON CORE | Summary: JAR1 belongs to the adenylate-forming firefly luciferase superfamily and uses ATP to adenylate JA. Reason: ATP binding is a necessary feature of the ligase mechanism, not an independent function. Supporting Evidence: PMID:12084835 An ATP-PPi isotope exchange assay was used to demonstrate adenylation activity in a glutathione S-transferase-JAR1 fusion protein. |
| GO:0005634 nucleus | ISM GO_REF:0000122 | MARK AS OVER ANNOTATED | Summary: Subcellular-location prediction (AtSubP) of nuclear localization. Reason: Experimental localization places FIN219/JAR1 in the cytoplasm in both darkness and light, with no nuclear signal reported; the prediction is not supported for this soluble enzyme. Supporting Evidence: PMID:10921909 GUS–FIN219 was located in the cytoplasm both in darkness and in the light |
| GO:0005737 cytoplasm | IBA GO_REF:0000033 | ACCEPT | Summary: Cytoplasmic localization, inferred electronically/phylogenetically, agrees with direct localization evidence. Reason: Consistent with IDA evidence (PMID:10921909) for cytoplasmic FIN219/JAR1. Supporting Evidence: PMID:10921909 GUS–FIN219 was located in the cytoplasm both in darkness and in the light |
| GO:0005737 cytoplasm | IDA PMID:10921909 FIN219, an auxin-regulated gene, defines a link between phyt... | ACCEPT | Summary: GUS-FIN219 localizes to the cytoplasm in darkness and light. Reason: Direct localization evidence consistent with a soluble cytosolic conjugating enzyme. Supporting Evidence: PMID:10921909 GUS–FIN219 was located in the cytoplasm both in darkness and in the light |
| GO:0005737 cytoplasm | IEA GO_REF:0000044 | ACCEPT | Summary: Cytoplasmic localization, inferred electronically/phylogenetically, agrees with direct localization evidence. Reason: Consistent with IDA evidence (PMID:10921909) for cytoplasmic FIN219/JAR1. Supporting Evidence: PMID:10921909 GUS–FIN219 was located in the cytoplasm both in darkness and in the light |
| GO:0005773 vacuole | HDA PMID:14760709 Large-scale characterization of integral proteins from Arabi... | MARK AS OVER ANNOTATED | Summary: JAR1 was detected in a large-scale proteomic survey of vacuolar membrane preparations. Reason: High-throughput organelle proteomics detects abundant soluble cytosolic contaminants; JAR1 is a soluble cytoplasmic enzyme with no transmembrane segment and direct localization shows cytoplasm. Not a credible functional location. Supporting Evidence: PMID:10921909 GUS–FIN219 was located in the cytoplasm both in darkness and in the light |
| GO:0009585 red, far-red light phototransduction | IMP PMID:10921909 FIN219, an auxin-regulated gene, defines a link between phyt... | KEEP AS NON CORE | Summary: fin219 mutants have a far-red-specific long-hypocotyl phenotype and suppress a cop1 allele, placing FIN219/JAR1 in phytochrome A signaling. Reason: A genuine but pleiotropic light-signaling role, likely linked to jasmonate/light crosstalk; not the core enzymatic function. Supporting Evidence: PMID:10921909 One suppressor mutation isolated also exhibited a far-red-specific long hypocotyl phenotype in a wild-type background. |
| GO:0009611 response to wounding | IEP PMID:18247047 The role of JAR1 in Jasmonoyl-L: -isoleucine production duri... | KEEP AS NON CORE | Summary: Wounding rapidly increases JAR1 transcript and JA-Ile levels. Reason: JAR1 is wound-inducible and responsible for most wound-induced JA-Ile, but jar1 had little effect on several wound-induced genes; wound response is a downstream physiological context. Supporting Evidence: PMID:18247047 JAR1 transcript also increased dramatically in wounded tissue, reaching a maximum after about 1 h. |
| GO:0009627 systemic acquired resistance | IEP PMID:17419843 Pathogen-associated molecular pattern recognition rather tha... | MARK AS OVER ANNOTATED | Summary: Expression-based (IEP) association of JAR1 with systemic acquired resistance triggered by non-host bacteria or PAMPs. Reason: SAR is salicylic-acid dependent; the abstract describes SA/PR-gene-based SAR and does not report a JAR1 requirement. An expression change alone does not establish participation of the JA-conjugating enzyme in SAR. |
| GO:0009640 photomorphogenesis | IMP PMID:10921909 FIN219, an auxin-regulated gene, defines a link between phyt... | KEEP AS NON CORE | Summary: fin219 mutants have a far-red-specific long-hypocotyl phenotype and suppress a cop1 allele, placing FIN219/JAR1 in phytochrome A signaling. Reason: A genuine but pleiotropic light-signaling role, likely linked to jasmonate/light crosstalk; not the core enzymatic function. Supporting Evidence: PMID:10921909 One suppressor mutation isolated also exhibited a far-red-specific long hypocotyl phenotype in a wild-type background. |
| GO:0009694 jasmonic acid metabolic process | IDA PMID:22628555 Structural basis for prereceptor modulation of plant hormone... | ACCEPT | Summary: JAR1 conjugates JA to amino acids, converting it to the active JA-Ile; this is jasmonic acid metabolism. Reason: JA-Ile formation is the metabolic step catalyzed by JAR1. GO has no JA-Ile biosynthesis term, so jasmonic acid metabolic process is the appropriate process. Supporting Evidence: PMID:22628555 Here, we report the crystal structures of benzoate-specific Arabidopsis thaliana AtGH3.12/PBS3 and jasmonic acid-specific AtGH3.11/JAR1. |
| GO:0009694 jasmonic acid metabolic process | IMP PMID:15258265 The oxylipin signal jasmonic acid is activated by an enzyme ... | ACCEPT | Summary: jar1 mutants have strongly reduced JA-Ile, and JAR1 expression restores it, demonstrating JAR1 acts in JA metabolism in planta. Reason: Genetic evidence that JAR1 performs the JA to JA-Ile conversion in vivo; core process. Supporting Evidence: PMID:15258265 JA-Ile was found at 29.6 pmole g(-1) fresh weight (FW) in the wild type but was more than sevenfold lower in two jar1 alleles. |
| GO:0009753 response to jasmonic acid | IMP PMID:11607311 Methyl jasmonate inhibition of root growth and induction of ... | KEEP AS NON CORE | Summary: jar1 was isolated as a mutant with reduced sensitivity to MeJA inhibition of root growth. Reason: JA insensitivity of jar1 results from the failure to convert JA into bioactive JA-Ile (JA-Ile rescues jar1); the response is downstream of the core enzymatic role. Supporting Evidence: PMID:11607311 An ethyl methanesulfonate mutant (jar1) with decreased sensitivity to MeJA inhibition of root elongation was isolated and characterized. PMID:15258265 Unlike free JA, JA-Ile inhibited root growth in jar1-1 to the same extent as in the wild type |
| GO:0009753 response to jasmonic acid | IMP PMID:15064385 Cytoplasmic alkalization precedes reactive oxygen species pr... | KEEP AS NON CORE | Summary: jar1-1 guard cells are insensitive to methyl jasmonate. Reason: Reflects lack of JA-Ile production; downstream of the core enzymatic role. Supporting Evidence: PMID:15064385 Stomata of jar1-1 mutant plants are insensitive to MJ but are able to close in response to ABA. |
| GO:0009864 induced systemic resistance, jasmonic acid mediated signaling pathway | IMP PMID:9724702 A novel signaling pathway controlling induced systemic resis... | KEEP AS NON CORE | Summary: Rhizobacteria-mediated ISR is blocked in jar1, establishing a requirement for jasmonate responsiveness. Reason: Classic genetic evidence (Pieterse et al. 1998) that JAR1-dependent jasmonate responsiveness is required for ISR; a physiological output of JA-Ile formation, not the core enzymatic function. Supporting Evidence: PMID:9724702 we demonstrate that signal transduction leading to P. fluorescens WCS417r-mediated ISR requires responsiveness to jasmonate and ethylene and is dependent on NPR1. |
| GO:0009864 induced systemic resistance, jasmonic acid mediated signaling pathway | IMP PMID:9724702 A novel signaling pathway controlling induced systemic resis... | KEEP AS NON CORE | Summary: Rhizobacteria-mediated ISR is blocked in jar1, establishing a requirement for jasmonate responsiveness. Reason: Classic genetic evidence (Pieterse et al. 1998) that JAR1-dependent jasmonate responsiveness is required for ISR; a physiological output of JA-Ile formation, not the core enzymatic function. Supporting Evidence: PMID:9724702 we demonstrate that signal transduction leading to P. fluorescens WCS417r-mediated ISR requires responsiveness to jasmonate and ethylene and is dependent on NPR1. |
| GO:0010046 response to mycotoxin | IMP PMID:11041879 Fumonisin B1-induced cell death in arabidopsis protoplasts r... | KEEP AS NON CORE | Summary: Fumonisin B1-induced protoplast cell death requires JA responsiveness and is reduced in jar1-1 protoplasts. Reason: Indirect phenotype downstream of JA signaling. Supporting Evidence: PMID:11041879 or from jar1-1 or etr1-1 mutant plants, which are insensitive to jasmonate (JA) or ethylene (ET), respectively. |
| GO:0010119 regulation of stomatal movement | IMP PMID:15064385 Cytoplasmic alkalization precedes reactive oxygen species pr... | KEEP AS NON CORE | Summary: MeJA-induced stomatal closure requires JAR1. Reason: Guard-cell JA signaling is a downstream output of JA-Ile formation. Supporting Evidence: PMID:15064385 Stomata of jar1-1 mutant plants are insensitive to MJ but are able to close in response to ABA. |
| GO:0010193 response to ozone | IMP PMID:11006337 Jasmonic acid signaling modulates ozone-induced hypersensiti... | KEEP AS NON CORE | Summary: jar1 alters ozone-induced HR-like cell death. Reason: Indirect phenotype downstream of JA signaling. Supporting Evidence: PMID:11006337 Analyses of the responses to O(3) of the JA-signaling mutants jar1 and fad3/7/8 also demonstrated an antagonistic relationship between JA- and SA-signaling pathways in controlling the magnitude of O(3)-induced HR-like cell death. |
| GO:0010224 response to UV-B | IMP PMID:16639567 Solar ultraviolet-B radiation alters the attractiveness of A... | KEEP AS NON CORE | Summary: UV-B-induced deterrence of insect oviposition is lost in jar1-1. Reason: Indirect, JA-signaling dependent ecological phenotype; non-core. Supporting Evidence: PMID:16639567 The deterring effect of UV-B exposure on insect oviposition was absent in jar1-1, a mutant with impaired jasmonic acid (JA) sensitivity |
| GO:0016597 amino acid binding | IDA PMID:28223489 Structural basis of jasmonate-amido synthetase FIN219 in com... | KEEP AS NON CORE | Summary: Structural and binding studies show amino acid substrates (Ile, Leu, Val, Met) bind the FIN219/JAR1 active site after JA. Reason: Amino acid binding reflects substrate binding by the conjugating enzyme; L-leucine is a minor acceptor in vivo (JA-Ile is the main product), so this is non-core. Supporting Evidence: PMID:28223489 between apolar substrates (Ile, Leu, Val, and Met) and polar amino acids at the hydrophobic binding site PMID:28223489 Interestingly, neither ATP nor isoleucine could bind directly to FIN219 or to the FIN219–FIP1 complex unless JA had been bound first |
| GO:0016881 acid-amino acid ligase activity | IBA GO_REF:0000033 | ACCEPT | Summary: Phylogenetic (PAINT) inference that GH3 family members are acid-amino acid ligases. Reason: Correct parent of the experimentally established jasmonoyl-L-amino acid ligase activity; the GH3 family conjugates acyl acid hormones to amino acids. Retained as an accurate but more general statement of the core activity. Supporting Evidence: PMID:15258265 analysis of products produced in vitro by recombinant JAR1 demonstrated that this enzyme forms JA-amido conjugates with several amino acids, including JA-Ile. |
| GO:0018117 protein adenylylation | IDA PMID:28223489 Structural basis of jasmonate-amido synthetase FIN219 in com... | MODIFY | Summary: The adenylation measured for FIN219/JAR1 is of the jasmonic acid carboxyl group (acyl-adenylate formation), not of a protein. Reason: Protein adenylylation (AMPylation of proteins) misdescribes the assay: FIN219 adenylation activity was measured as pyrophosphate release from ATP during activation of JA, the first half-reaction of JA-amino acid conjugation. The appropriate process is jasmonic acid metabolic process. That term is already carried by JAR1 with stronger IDA/IMP evidence, so the replacement adds no new coverage; MODIFY rather than REMOVE records that this curator row describes a real JA-activation assay whose process was mis-typed. Proposed replacements: jasmonic acid metabolic process Supporting Evidence: PMID:28223489 the adenylation activity per mole of FIN219–FIP1 was approximately double the adenylation activity per mole of FIN219 alone PMID:12084835 An ATP-PPi isotope exchange assay was used to demonstrate adenylation activity in a glutathione S-transferase-JAR1 fusion protein. |
| GO:0019899 enzyme binding | IPI PMID:17220357 Glutathione S-transferase interacting with far-red insensiti... | KEEP AS NON CORE | Summary: FIN219/JAR1 interacts in vitro and in vivo with FIP1, a glutathione S-transferase with GST activity. Reason: A documented regulatory interaction that increases JAR1 activity; not the core catalytic function. Supporting Evidence: PMID:17220357 Here, we demonstrate that FIN219-interacting protein 1 (FIP1) interacts with FIN219 in vitro and in vivo |
| GO:0031348 negative regulation of defense response | IMP PMID:16732289 Conserved requirement for a plant host cell protein in powde... | KEEP AS NON CORE | Summary: IMP annotation from a study of mlo-mediated powdery mildew resistance in which jar1 was used in epistasis analysis; the JAR1-specific result was not seen. Reason: The full text (Consonni et al. 2006, Nat Genet) is not open access (no PMC/Europe PMC full text) and the cached record is abstract-only. The abstract states mlo resistance does not require JA signaling, and secondary summaries report that the mlo2 early-senescence phenotype is SA- but not JA-dependent, so the specific experiment behind this IMP could not be identified. Per project policy the experimental annotation is not overruled: a negative effect of JA signaling on (SA-type) defense outputs is biologically plausible and independently consistent with the JA-SA antagonism shown for jar1 in ozone-induced cell death (PMID:11006337). Retained as a non-core, indirect consequence of JA-Ile formation, not a direct JAR1 function. Supporting Evidence: PMID:11006337 Analyses of the responses to O(3) of the JA-signaling mutants jar1 and fad3/7/8 also demonstrated an antagonistic relationship between JA- and SA-signaling pathways in controlling the magnitude of O(3)-induced HR-like cell death. |
| GO:0070566 adenylyltransferase activity | IDA PMID:17291501 Substrate specificity and products of side-reactions catalyz... | KEEP AS NON CORE | Summary: JAR1 adenylates JA (acyl-AMP formation) and, as a side reaction, transfers AMP to tripolyphosphate to form p4A. Reason: Adenylyl transfer is the first partial reaction of the jasmonoyl-L-amino acid ligase mechanism; it is correct but subsumed by the overall ligase activity, which is the core function. Supporting Evidence: PMID:17291501 in the presence of ATP, Mg(2+), (-)-JA and tripolyphosphate the ligase produces adenosine 5'-tetraphosphate (p(4)A) PMID:12084835 An ATP-PPi isotope exchange assay was used to demonstrate adenylation activity in a glutathione S-transferase-JAR1 fusion protein. |
| GO:0070728 L-leucine binding | IDA PMID:28223489 Structural basis of jasmonate-amido synthetase FIN219 in com... | KEEP AS NON CORE | Summary: Structural and binding studies show amino acid substrates (Ile, Leu, Val, Met) bind the FIN219/JAR1 active site after JA. Reason: Amino acid binding reflects substrate binding by the conjugating enzyme; L-leucine is a minor acceptor in vivo (JA-Ile is the main product), so this is non-core. Supporting Evidence: PMID:28223489 between apolar substrates (Ile, Leu, Val, and Met) and polar amino acids at the hydrophobic binding site PMID:28223489 Interestingly, neither ATP nor isoleucine could bind directly to FIN219 or to the FIN219–FIP1 complex unless JA had been bound first |
| GO:0071365 cellular response to auxin stimulus | IEP PMID:10921909 FIN219, an auxin-regulated gene, defines a link between phyt... | KEEP AS NON CORE | Summary: FIN219/JAR1 expression is rapidly induced by auxin, as for other GH3 genes. Reason: Expression response only; it does not establish a role in auxin signaling. Kept as a non-core expression attribute. Supporting Evidence: PMID:10921909 Molecular characterization of FIN219 indicated that it encodes a cytoplasmic localized protein highly similar to the GH3 family of proteins and its expression is rapidly induced by auxin. |
| GO:0080123 jasmonoyl-L-amino acid ligase activity | EXP PMID:18247047 The role of JAR1 in Jasmonoyl-L: -isoleucine production duri... | ACCEPT | Summary: Kinetic analysis of recombinant JAR1 shows strong preference for isoleucine as the amino acid acceptor. Reason: Direct enzymology establishing the core JA-Ile synthetase activity of JAR1. Supporting Evidence: PMID:18247047 Kinetic analysis showed that JAR1 had a K (m) of 0.03 mM for Ile, which was 60-80-fold lower than for Leu, Val and Phe. |
| GO:0080123 jasmonoyl-L-amino acid ligase activity | IDA PMID:15258265 The oxylipin signal jasmonic acid is activated by an enzyme ... | ACCEPT | Summary: Recombinant JAR1 forms JA-amido conjugates including JA-Ile, and jar1 mutants have strongly reduced JA-Ile. Reason: Founding biochemical and genetic demonstration of JAR1 as the jasmonoyl-amino acid conjugate synthetase; core function. Supporting Evidence: PMID:15258265 analysis of products produced in vitro by recombinant JAR1 demonstrated that this enzyme forms JA-amido conjugates with several amino acids, including JA-Ile. PMID:15258265 JA-Ile was found at 29.6 pmole g(-1) fresh weight (FW) in the wild type but was more than sevenfold lower in two jar1 alleles. |
| GO:0080123 jasmonoyl-L-amino acid ligase activity | IDA PMID:22628555 Structural basis for prereceptor modulation of plant hormone... | ACCEPT | Summary: Crystal structure and biochemistry of JA-specific AtGH3.11/JAR1 define the acyl acid and amino acid binding sites for conjugation. Reason: Structural/biochemical support for the JA-amino acid conjugating activity; core function. Supporting Evidence: PMID:22628555 Here, we report the crystal structures of benzoate-specific Arabidopsis thaliana AtGH3.12/PBS3 and jasmonic acid-specific AtGH3.11/JAR1. |
| GO:0080123 jasmonoyl-L-amino acid ligase activity | IEA GO_REF:0000120 | ACCEPT | Summary: Electronic transfer of jasmonoyl-L-amino acid ligase activity, consistent with experimental characterization of JAR1. Reason: The IEA agrees with direct biochemical evidence (PMID:15258265, PMID:18247047) and represents the core catalytic activity. Supporting Evidence: PMID:15258265 analysis of products produced in vitro by recombinant JAR1 demonstrated that this enzyme forms JA-amido conjugates with several amino acids, including JA-Ile. |
| GO:2000030 regulation of response to red or far red light | IMP PMID:17220357 Glutathione S-transferase interacting with far-red insensiti... | KEEP AS NON CORE | Summary: FIN219 together with its interactor FIP1 affects hypocotyl elongation under far-red light. Reason: Supports a light-response role of the FIN219-FIP1 module; non-core relative to JA-Ile synthesis. Supporting Evidence: PMID:17220357 these data indicate that FIP1 may interact with FIN219 to regulate cell elongation and flowering in response to light. |
| GO:2000377 regulation of reactive oxygen species metabolic process | IMP PMID:15064385 Cytoplasmic alkalization precedes reactive oxygen species pr... | KEEP AS NON CORE | Summary: MeJA-induced guard-cell ROS production is absent in jar1-1. Reason: Downstream of JA-Ile production in guard-cell signaling. Supporting Evidence: PMID:15064385 MJ induces H(2)O(2) production in both wild-type and ost1-2 guard cells, but not in jar1-1. |
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Download this section (compressed HTML)Q: Which enzymes account for the residual JA-Ile (about 10-15% of wild type) that accumulates in jar1 null mutants, and do they contribute in specific tissues?
Q: Is the far-red/phytochrome A phenotype of fin219 explained entirely by reduced JA-Ile production, or does FIN219 have a JA-Ile-independent light-signaling function?
Experiment: Complement fin219/jar1 null mutants with a catalytically dead JAR1 (acyl-adenylate motif mutant) and test far-red hypocotyl and jasmonate phenotypes in parallel with JA-Ile quantification.
Hypothesis: All FIN219/JAR1 phenotypes, including far-red light responses, require its JA-conjugating activity.
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