COI1 is the F-box/LRR substrate-recognition subunit of the Arabidopsis SCF(COI1) ubiquitin ligase and a hormone-binding component of the COI1-JAZ jasmonate co-receptor. Bioactive jasmonate conjugates such as JA-Ile, and the bacterial mimic coronatine, promote association with JAZ repressors. COI1 recruits these repressors for SCF-dependent ubiquitylation and proteasomal degradation, releasing transcription factors to activate jasmonate responses. Inositol phosphate supports high-affinity co-receptor assembly. This mechanism controls defense, wound responses, root growth and reproductive development and integrates jasmonate signaling with light responses. In roots, COI1 also represses immunity-related gene expression independently of JA-Ile and promotes susceptibility to Verticillium longisporum. Complementation with a COI1 variant impaired in JAZ interaction supports separation of this repression from canonical JAZ perception. The molecular partners and requirement for SCF assembly in this root function remain unresolved.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0019005 SCF ubiquitin ligase complex | IDA PMID:12172031 The SCF(COI1) ubiquitin-ligase complexes are required for ja... | ACCEPT | Summary: COI1 is a component of SCF(COI1) E3 ubiquitin ligase complexes. Reason: The SCF complex context is central to COI1 function as an F-box substrate receptor. Supporting Evidence: PMID:12172031 In this study, we demonstrate that COI1 associates physically with AtCUL1, AtRbx1, and either of the Arabidopsis Skp1-like proteins ASK1 or ASK2 to assemble ubiquitin-ligase complexes, which we have designated SCF(COI1). |
| GO:1990756 ubiquitin-like ligase-substrate adaptor activity | IDA PMID:20927106 Jasmonate perception by inositol-phosphate-potentiated COI1-... | NEW | Summary: COI1 is the F-box substrate-recognition/adaptor subunit of SCF(COI1), recruiting JAZ repressors in the jasmonate co-receptor complex. Reason: The seeded GO annotations capture SCF complex membership and degradation, but not the specific substrate-adaptor molecular function of COI1. Supporting Evidence: PMID:20927106 The F-box protein CORONATINE INSENSITIVE 1 (COI1) mediates jasmonate signalling by promoting hormone-dependent ubiquitylation and degradation of transcriptional repressor JAZ proteins. PMID:12172031 In this study, we demonstrate that COI1 associates physically with AtCUL1, AtRbx1, and either of the Arabidopsis Skp1-like proteins ASK1 or ASK2 to assemble ubiquitin-ligase complexes, which we have designated SCF(COI1). PMID:20927106 High-affinity hormone binding requires a bipartite JAZ degron sequence consisting of a conserved Ξ±-helix for COI1 docking and a loop region to trap the hormone in its binding pocket. |
| GO:0009901 anther dehiscence | IMP PMID:23573263 New clothes for the jasmonic acid receptor COI1: delayed abs... | KEEP AS NON CORE | Summary: COI1 affects anther dehiscence through jasmonate-dependent reproductive development. Reason: This is a downstream reproductive output of COI1 jasmonate signaling. Supporting Evidence: PMID:23573263 plants were functionally male sterile due to a lack of dehiscence |
| GO:0006952 defense response | TAS PMID:9582125 COI1: an Arabidopsis gene required for jasmonate-regulated d... | KEEP AS NON CORE | Summary: COI1 is required for jasmonate-regulated defense responses. Reason: Defense response is a major output, but the core role is SCF(COI1)-JAZ regulation of JA signaling. Supporting Evidence: PMID:9582125 The coi1 mutation defines an Arabidopsis gene required for response to jasmonates, which regulate defense against insects and pathogens, wound healing, and pollen fertility. |
| GO:0042742 defense response to bacterium | IMP PMID:16959575 Plant stomata function in innate immunity against bacterial ... | MARK AS OVER ANNOTATED | Summary: As reported in the uncached full text of Melotto et al., coronatine-mediated reopening of bacterium-closed stomata fails in the coi1-20 mutant, so COI1 genotype alters the outcome of stomatal bacterial defense; COI1 here mediates pathogen counter-defense rather than defense itself. Reason: PMID:16959575 is abstract-only in the cache and the abstract does not describe the coi1 assay, so the curator's IMP is not overruled and the row is not removed. However, the phenotype as described in the summary is pathogen counter-defense - the bacterial JA-Ile mimic coronatine is perceived by COI1 (PMID:20927106) and exploited to reopen stomata, so loss of COI1 increases rather than decreases stomatal defense. An involved_in "defense response to bacterium" assertion therefore overstates COI1's role in antibacterial defense. MODIFY to GO:0031348 negative regulation of defense response is not proposed because COI1 already carries that term (IMP, PMID:16732289) in this review. Supporting Evidence: PMID:20927106 JA-Ile that is functionally and structurally mimicked by the Pseudomonas syringae phytotoxin coronatine |
| GO:0050832 defense response to fungus | IMP PMID:17513501 ABA is an essential signal for plant resistance to pathogens... | MODIFY | Summary: The cited paper concerns the oomycete Pythium irregulare, not a fungus. Reason: The supported pathogen class is oomycete; the fungus term is taxonomically wrong for PMID:17513501. Proposed replacements: defense response to oomycetes Supporting Evidence: PMID:17513501 Analyses of Arabidopsis thaliana defense response to the damping-off oomycete pathogen Pythium irregulare show that resistance to P. irregulare requires a multicomponent defense strategy. |
| GO:0106167 extracellular ATP signaling | IMP PMID:30630869 Extracellular ATP Shapes a Defense-Related Transcriptome Bot... | KEEP AS NON CORE | Summary: COI1 is implicated in extracellular ATP-associated defense transcriptome responses. Reason: This is a pathway interaction/output, not the core COI1 molecular role. Supporting Evidence: PMID:30630869 In conclusion, we present a model ( Fig. 10 ) in which ATP binding to P2K1 results in defense gene activation, where more than half of ATP-responsive genes required signaling by one or more of the pathways through EIN2, NPR1, and COI1, but with a more substantial reliance on COI1. |
| GO:0009861 jasmonic acid and ethylene-dependent systemic resistance | TAS PMID:11418339 Genes controlling expression of defense responses in Arabido... | KEEP AS NON CORE | Summary: Rhizobacteria-induced systemic resistance (ISR) requires jasmonate responsiveness, which COI1 confers; the TAS annotation is an author-statement transfer of this pathway requirement to COI1. Reason: ISR is defined genetically by its dependence on JA and ethylene responsiveness, and COI1 is the JA-Ile receptor required for most JA-induced gene expression (about 84% of JA-induced genes; PMID:16021335). The cited sources (a 2001 defense-genetics review listing genes needed for JA-dependent signaling and ISR, and the COI1 cloning paper) support COI1 as a required JA-signaling component. A COI1-specific distal-resistance assay is not exposed in the cached abstracts, so the term is retained only as a non-core, downstream physiological output of JA perception, not as a core COI1 function. Supporting Evidence: PMID:16021335 COI1 is required for expression of approximately 84% of 212 genes induced by JA PMID:11418339 Genes required for jasmonic-acid-dependent signaling and for induced systemic resistance have also been identified. |
| GO:0009861 jasmonic acid and ethylene-dependent systemic resistance | TAS PMID:9582125 COI1: an Arabidopsis gene required for jasmonate-regulated d... | KEEP AS NON CORE | Summary: Rhizobacteria-induced systemic resistance (ISR) requires jasmonate responsiveness, which COI1 confers; the TAS annotation is an author-statement transfer of this pathway requirement to COI1. Reason: ISR is defined genetically by its dependence on JA and ethylene responsiveness, and COI1 is the JA-Ile receptor required for most JA-induced gene expression (about 84% of JA-induced genes; PMID:16021335). The cited sources (a 2001 defense-genetics review listing genes needed for JA-dependent signaling and ISR, and the COI1 cloning paper) support COI1 as a required JA-signaling component. A COI1-specific distal-resistance assay is not exposed in the cached abstracts, so the term is retained only as a non-core, downstream physiological output of JA perception, not as a core COI1 function. Supporting Evidence: PMID:16021335 COI1 is required for expression of approximately 84% of 212 genes induced by JA |
| GO:0009867 jasmonic acid mediated signaling pathway | IMP PMID:17637677 JAZ repressor proteins are targets of the SCF(COI1) complex ... | ACCEPT | Summary: JA-Ile promotes COI1-JAZ1 interaction and SCF(COI1)-dependent JAZ1 degradation, initiating jasmonate signaling. Reason: This captures the central biological process controlled by COI1. Supporting Evidence: PMID:17637677 Jasmonate treatment causes JAZ1 degradation and this degradation is dependent on activities of the SCF(COI1) ubiquitin ligase and the 26S proteasome. |
| 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: Independent root experiments support COI1-mediated negative regulation of defense; the original mlo-paper experiment remains unverified. Reason: Retain the biological assertion using independent primary evidence from PMID:39945499 and PMID:34145662: coi1 roots derepress immunity-related genes, and interfering with that expression partially suppresses coi1-mediated Verticillium tolerance. This supports negative regulation of defense response in a root/pathogen context. It does not verify the different mlo experiment in the unchanged original_reference_id PMID:16732289, whose full text remains unavailable. The latter citation limitation is recorded separately in its reference review. The newer evidence supports the more informative defense-regulatory term already present here; a separate NEW assertion for the same term is not novel under the repository GOA validation model, and a generic parent is unnecessary. JA-Ile independence and JAZ-interaction-impaired complementation do not establish SCF independence or direct transcriptional repression. Supporting Evidence: PMID:39945499 The biggest difference between the transcriptomes was due to 316 immunity-related genes that were constitutively higher expressed in coi1 as compared to the susceptible genotypes. PMID:39945499 Interfering with the expression of a sub-group of these genes partially suppressed the coi1-mediated tolerance phenotype. PMID:34145662 On the other hand, genes affected by COI1 but not by JA-Ile were still strongly repressed by COI1AA . |
| GO:0009909 regulation of flower development | IMP PMID:20435902 Jasmonate and phytochrome A signaling in Arabidopsis wound a... | KEEP AS NON CORE | Summary: COI1 affects flower development through jasmonate signaling. Reason: Flower development is a downstream developmental output. Supporting Evidence: PMID:20435902 We previously noticed that coi1- 16 mutants flower early, and in some growth conditions display elongated, hyponastic petioles, and elongated hypocotyls, phenotypes that are classic indicators of deficient responses to light quality |
| GO:0010218 response to far red light | IMP PMID:20435902 Jasmonate and phytochrome A signaling in Arabidopsis wound a... | KEEP AS NON CORE | Summary: COI1/JAZ stability connects jasmonate signaling with far-red/shade responses. Reason: This is signaling cross-talk downstream of the core COI1-JAZ module. Supporting Evidence: PMID:20435902 Additionally, we demonstrate that the FR light-induced expression of transcription factor genes is dependent on CORONATINE INSENSITIVE1 (COI1), a central component of JA signaling, and is suppressed by JA. |
| GO:0009625 response to insect | IMP PMID:15923339 Major signaling pathways modulate Arabidopsis glucosinolate ... | KEEP AS NON CORE | Summary: COI1 affects constitutive glucosinolate levels and insect performance, although insect-induced glucosinolate accumulation in this study does not require COI1. Reason: Read the original full PMC1150428 article through the NCBI report endpoint: its Results report the best insect growth on coi1 and distinguish consumption from growth. The negative result for one induced-metabolite endpoint does not negate the broader response-to-insect annotation. The prior REMOVE conflated these endpoints. Retain insect interaction as a non-core physiological output. Supporting Evidence: PMID:15923339 Blocked JA signaling in coronatine-insensitive (coi1) and enhanced expression of SA-signaled disease resistance in hypersensitive response-like (hrl1) mutants reduced constitutive GS concentrations, |
| GO:0009753 response to jasmonic acid | IMP PMID:16021335 Expression profiling reveals COI1 to be a key regulator of g... | ACCEPT | Summary: COI1 is required for jasmonate-responsive gene expression. Reason: Jasmonate responsiveness is central to COI1 hormone perception and signaling. A broad response term still represents core biology; its breadth does not make the role peripheral. The cited primary study directly establishes COI1-dependent jasmonate responses. Supporting Evidence: PMID:16021335 We show that COI1 is required for expression of approximately 84% of 212 genes induced by JA, and for expression of approximately 44% of 153 genes induced by wounding. |
| GO:0009753 response to jasmonic acid | IMP PMID:17637677 JAZ repressor proteins are targets of the SCF(COI1) complex ... | ACCEPT | Summary: COI1 is required for jasmonate-responsive JAZ degradation and signaling. Reason: Jasmonate responsiveness is central to COI1 hormone perception and signaling. A broad response term still represents core biology; its breadth does not make the role peripheral. The cited primary study directly establishes COI1-dependent jasmonate responses. Supporting Evidence: PMID:17637677 Furthermore, the jasmonoyl-isoleucine (JA-Ile) conjugate, but not other jasmonate-derivatives such as jasmonate, 12-oxo-phytodienoic acid, or methyl-jasmonate, promotes physical interaction between COI1 and JAZ1 proteins in the absence of other plant proteins. |
| GO:0009611 response to wounding | IMP PMID:16021335 Expression profiling reveals COI1 to be a key regulator of g... | KEEP AS NON CORE | Summary: COI1 participates in wound-induced jasmonate responses. Reason: Wound response is a downstream JA output. Supporting Evidence: PMID:16021335 We show that COI1 is required for expression of approximately 84% of 212 genes induced by JA, and for expression of approximately 44% of 153 genes induced by wounding. |
| GO:0048364 root development | IMP PMID:27756820 Endogenous Bioactive Jasmonate Is Composed of a Set of (+)-7... | KEEP AS NON CORE | Summary: COI1 is required for root growth inhibition by bioactive jasmonate analogues. Reason: Full PMC5129707 Results and Fig.5 compare coi1-1 and wild-type root length: loss of COI1 prevents the analogue-dependent root inhibition. This is a verified developmental response downstream of receptor action. The partial cached text lacks that Results section; the companion primary SCF study also places COI1 in jasmonate-regulated root growth. Supporting Evidence: PMID:12172031 required for response to jasmonates (JAs), which regulate root growth, pollen fertility, wound healing, and defense against insects and pathogens. |
| GO:0031146 SCF-dependent proteasomal ubiquitin-dependent protein catabolic process | IMP PMID:17637675 The JAZ family of repressors is the missing link in jasmonat... | ACCEPT | Summary: COI1 directs JAZ repressors into SCF-dependent proteasomal degradation. Reason: This is a core mechanistic process for COI1 function. Supporting Evidence: PMID:17637675 Our results demonstrate that JAI3 and other JAZs are direct targets of the SCF(COI1) E3 ubiquitin ligase and jasmonate treatment induces their proteasome degradation. |
| GO:0009641 shade avoidance | IMP PMID:20435902 Jasmonate and phytochrome A signaling in Arabidopsis wound a... | KEEP AS NON CORE | Summary: COI1/JAZ stability links jasmonate signaling to shade avoidance. Reason: This is a downstream pathway-output/cross-talk annotation. Supporting Evidence: PMID:20435902 These mutants display exaggerated shade responses to low, but not high, R/FR ratio light, suggesting a role for JA in phytochrome A (phyA) signaling. |
| GO:0048443 stamen development | IMP PMID:27756820 Endogenous Bioactive Jasmonate Is Composed of a Set of (+)-7... | KEEP AS NON CORE | Summary: COI1-dependent jasmonate signaling affects reproductive phenotypes including male fertility and anther dehiscence. Reason: Full PMC5129707 Results and Fig.1 show restoration of fertility in opr3 but not coi1-1 after ligand treatment; this supports the source-specific COI1 reproductive requirement. PMID:23573263 independently documents failure of anther dehiscence. Retain stamen development as a downstream physiological role, without conflating ligand rescue of biosynthesis mutants with rescue of coi1. Supporting Evidence: PMID:23573263 plants were functionally male sterile due to a lack of dehiscence |
| GO:0010118 stomatal movement | IMP PMID:16959575 Plant stomata function in innate immunity against bacterial ... | KEEP AS NON CORE | Summary: As reported in the uncached full text of Melotto et al., coronatine-induced reopening of stomata closed in response to bacteria requires COI1 (coi1-20 guard cells fail to reopen), placing COI1 upstream of pathogen-modulated stomatal movement. Reason: PMID:16959575 is abstract-only in the cache; the coi1 stomatal assay is in the full text, which is not available here, so the curator IMP is retained rather than overruled. Stomatal movement is direction-neutral and is consistent with COI1 perceiving the JA-Ile mimic coronatine (PMID:20927106), which the pathogen uses to reopen stomata. It is a downstream physiological output of COI1-dependent perception, not a core COI1 function. No supporting quote is given because the cached abstract does not mention COI1, coronatine or jasmonate; the row rests on deference to the curator, who read the full text. |
| GO:0006511 ubiquitin-dependent protein catabolic process | TAS PMID:11019805 Protein degradation in signaling. | MODIFY | Summary: COI1 functions in ubiquitin-dependent degradation, but the SCF-dependent term is more precise. Reason: The original PMID:11019805 review abstract gives broad proteolysis context. The specific replacement is independently demonstrated by PMID:17637677, where JAZ1 degradation requires SCF(COI1) and the 26S proteasome; PMID:12172031 demonstrates SCF assembly. Thus this specialization uses explicit primary evidence rather than assuming the review abstract itself contains the mechanism. Proposed replacements: SCF-dependent proteasomal ubiquitin-dependent protein catabolic process Supporting Evidence: PMID:17637677 Jasmonate treatment causes JAZ1 degradation and this degradation is dependent on activities of the SCF(COI1) ubiquitin ligase and the 26S proteasome. |
| GO:0042562 hormone binding | IDA PMID:20927106 Jasmonate perception by inositol-phosphate-potentiated COI1-... | NEW | Summary: COI1 directly contacts JA-Ile within the COI1-JAZ co-receptor. Reason: Structural and pharmacological measurements establish a ligand pocket in COI1 and JA-Ile binding by the co-receptor. Hormone binding captures this experimentally supported MF separately from ubiquitin-ligase substrate adaptation. High-affinity perception requires JAZ, so this is not a claim that isolated COI1 is a complete high-affinity receptor. A specific JA-Ile-binding GO term was not found in the ontology search. Supporting Evidence: PMID:20927106 Here we present structural and pharmacological data to show that the true Arabidopsis jasmonate receptor is a complex of both COI1 and JAZ. COI1 contains an open pocket that recognizes the bioactive hormone (3R,7S)-jasmonoyl-l-isoleucine (JA-Ile) with high specificity. |
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Download this section (compressed HTML)Q: How do different JAZ degrons and inositol-phosphate cofactors alter the ligand selectivity of the COI1-JAZ co-receptor?
Q: Which COI1 developmental/defense outputs should be modeled as downstream targets rather than direct gene annotations?
Q: Which molecular partners mediate JA-Ile-independent root defense-gene repression by COI1, does it require SCF assembly, and can a residual contribution from JAZ proteins be excluded?
Experiment: Map COI1-dependent JAZ degradation and transcriptional release across developmental and defense contexts using matched proteomics and RNA-seq.
Hypothesis: JAZ degradation and transcriptional release differ in timing across developmental and defense contexts.
Experiment: Test whether eATP, far-red, and shade annotations require canonical JA-Ile/COI1/JAZ signaling or separate COI1 functions.
Hypothesis: COI1-dependent ATP and light responses require canonical ligand-dependent JAZ turnover.
Experiment: Compare root complementation of coi1 with wild-type COI1, the JAZ-interaction-impaired COI1 variant, and an SCF-assembly-defective COI1 variant while matching protein abundance and localization; assay root defense-gene expression and Verticillium tolerance, and verify SCF and JAZ interactions directly.
Hypothesis: JA-Ile-independent root repression is separable from canonical JAZ perception; testing SCF assembly distinguishes a noncanonical ubiquitin-ligase pathway from an SCF-independent function.
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