GI encodes Arabidopsis GIGANTEA, a conserved plant-specific regulatory protein in the GIGANTEA/PTHR36319 family. GI has no known catalytic activity; its best supported molecular role is as a timing-dependent nuclear and cytoplasmic interaction hub/coregulator. In the photoperiodic flowering pathway, GI forms blue-light-dependent complexes with FKF1/ZTL-family F-box proteins and binds CDF and other DNA-binding transcriptional regulators to control CO and FT expression. In the circadian clock, GI stabilizes ZTL-family F-box proteins and contributes to robust circadian rhythms and temperature compensation. GI also participates in cold, oxidative, shade, salt, and hormone/stress responses, but many of those phenotypes are downstream or context-specific consequences of its core clock/photoperiod regulatory functions.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0006355 regulation of DNA-templated transcription | IDA PMID:17872410 FKF1 and GIGANTEA complex formation is required for day-leng... | MODIFY | Summary: The Sawa et al. study directly supports transcriptional regulation: GI and FKF1 regulate CO transcription, GI binds the CO repressor CDF1, and the GI-FKF1-CDF1 complex associates with CO chromatin. The existing term is correct but too broad for the reported positive control of CO transcription. Reason: Replace the broad parent with the more specific positive regulation of RNA polymerase II transcription, reflecting de-repression/activation of CO expression by the GI-FKF1-CDF1 module. Proposed replacements: positive regulation of transcription by RNA polymerase II Supporting Evidence: PMID:17872410 The timing of this interaction regulates the timing of daytime CO expression. FKF1 function is dependent on GI, which interacts with a CO repressor, CYCLING DOF FACTOR 1 (CDF1), and controls CDF1 stability. GI, FKF1, and CDF1 proteins associate with CO chromatin. |
| GO:0007623 circadian rhythm | IDA PMID:17872410 FKF1 and GIGANTEA complex formation is required for day-leng... | MODIFY | Summary: GI is a well-supported regulator of circadian outputs and clock protein stability, but the term "circadian rhythm" is a broad process rather than the regulatory role of the GI gene product. Mizoguchi et al. and Kim et al. support a more specific regulation-of-circadian-rhythm annotation. Reason: GI regulates circadian rhythm robustness, phase, and ZTL/TOC1 proteostasis; GO:0042752 is more informative than the broad process term. Proposed replacements: regulation of circadian rhythm Supporting Evidence: PMID:16006578 Therefore, GI plays a general role in controlling circadian rhythms, and this is different from its effect on the amplitude of expression of CO and FT. file:ARATH/GI/GI-deep-research-falcon.md GI participates in circadian timing by controlling post-translational stability of key clock proteins through interactions with F-box photoreceptors PMID:17704763 This mechanism of establishing and sustaining robust oscillations of ZTL results in the high-amplitude TOC1 rhythms necessary for proper clock function. |
| GO:0009409 response to cold | IMP PMID:16231185 Involvement of GIGANTEA gene in the regulation of the cold s... | KEEP AS NON CORE | Summary: The cold-response annotation is supported by mutant and expression evidence: GI is cold-induced and gi-3 plants are more freezing sensitive. This is a real stress-response role, but it is not the primary conserved function of GI. Reason: Keep as a non-core process annotation because the evidence supports GI involvement in cold stress tolerance, while the core function remains clock/photoperiod regulatory control. Supporting Evidence: PMID:16231185 GI gene was induced by cold stress, but not by salt, mannitol, and abscisic acid. Moreover, gi-3 plants showed an increased sensitivity to freezing stress. |
| GO:0009637 response to blue light | IDA PMID:17872410 FKF1 and GIGANTEA complex formation is required for day-leng... | MODIFY | Summary: Blue light is mechanistically relevant because GI forms light-dependent complexes with FKF1/ZTL-family F-box proteins. However, the experiment supports blue-light signaling through the FKF1-GI timing module more specifically than a generic response-to-blue-light annotation. Reason: Replace with blue light signaling pathway to capture the blue-light-dependent FKF1-GI complex formation that controls photoperiodic timing. Proposed replacements: blue light signaling pathway Supporting Evidence: PMID:17872410 We demonstrate that FKF1 and GI proteins form a complex in a blue-light-dependent manner. |
| GO:0009908 flower development | TAS PMID:10202817 Auxin polar transport and flower formation in Arabidopsis th... | MARK AS OVER ANNOTATED | Summary: TAS annotation of GI to flower development attributed to a paper on auxin polar transport and floral meristem formation (pin mutants, HFCA phenocopy) that also used a late-flowering mutant; the cached abstract does not mention GI and the full text is unavailable. Independently of this source, GI's well-established role is in the timing of the floral transition (photoperiodic induction of CO and FT), not in floral organ or floral meristem development per se. Reason: Not removed, because the curator may have read a GI-relevant statement in the full text. But flower development (GO:0009908) overstates GI's role: gi mutants flower late but form normal flowers, and GI's flowering function is captured more precisely by the photoperiodic flowering terms already on GI (positive regulation of long-day photoperiodism, flowering). Supporting Evidence: PMID:17872410 The FLAVIN-BINDING, KELCH REPEAT, F-BOX 1 (FKF1), and GIGANTEA (GI) proteins regulate CO transcription in Arabidopsis. |
| GO:0010218 response to far red light | IMP PMID:18790998 Acceleration of flowering during shade avoidance in Arabidop... | MODIFY | Summary: Low red:far-red conditions require GI and CO to fully accelerate flowering in long days. The source supports a shade/far-red effect on the photoperiodic flowering pathway rather than direct far-red photoreceptor activity or a broad far-red response by GI. Reason: The more accurate annotation is regulation of photoperiodism, flowering, because the phenotype measured was shade/far-red acceleration of flowering through the GI-CO pathway. Proposed replacements: regulation of photoperiodism, flowering Supporting Evidence: PMID:18790998 A low red to far-red ratio required the photoperiod-pathway genes GIGANTEA (GI) and CONSTANS (CO) to fully accelerate flowering in long days and did not promote flowering in short days. |
| GO:0010378 temperature compensation of the circadian clock | IMP PMID:16617099 The molecular basis of temperature compensation in the Arabi... | ACCEPT | Summary: The annotation is well supported. Gould et al. show that GI contributes to temperature compensation and rhythmic robustness at high and low temperatures through temperature-dependent effects on the Arabidopsis clock network. Reason: Temperature compensation is a specific, experimentally supported component of GI's circadian regulatory role. Supporting Evidence: PMID:16617099 At 27 degrees C, a dynamic balance between GI and LHY allows temperature compensation in wild-type plants, but circadian function is impaired in lhy and gi mutant plants. |
| GO:0042542 response to hydrogen peroxide | IMP PMID:9681039 Oxidative stress tolerance and longevity in Arabidopsis: the... | KEEP AS NON CORE | Summary: Kurepa et al. report increased paraquat and hydrogen peroxide tolerance in gi mutants. This supports GI involvement in oxidative-stress response, but the phenotype is pleiotropic and not a core molecular function. Reason: Keep as non-core because the evidence is a stress-tolerance phenotype rather than the central clock/photoperiod mechanism of GI. Supporting Evidence: PMID:9681039 In addition, the gi-3 mutant was more tolerant to hydrogen peroxide. |
| GO:0042752 regulation of circadian rhythm | IMP PMID:16006578 Distinct roles of GIGANTEA in promoting flowering and regula... | ACCEPT | Summary: This annotation is directly supported. GI overexpression and gi mutants alter circadian rhythms under multiple light/dark regimes, and the authors conclude that GI has a general role in circadian rhythm control. Reason: Regulation of circadian rhythm is one of the two main experimentally supported functions of GI. Supporting Evidence: PMID:16006578 Therefore, GI plays a general role in controlling circadian rhythms, and this is different from its effect on the amplitude of expression of CO and FT. |
| GO:0048578 positive regulation of long-day photoperiodism, flowering | IMP PMID:16006578 Distinct roles of GIGANTEA in promoting flowering and regula... | ACCEPT | Summary: The annotation is well supported by genetic and expression evidence. GI promotes flowering under long days by increasing CO and FT mRNA abundance downstream of the circadian oscillator. Reason: Positive regulation of long-day photoperiodic flowering is a core GI biological process. Supporting Evidence: PMID:16006578 These experiments demonstrated that GI acts between the circadian oscillator and CO to promote flowering by increasing CO and FT mRNA abundance. |
| GO:0003677 DNA binding | IDA PMID:40157149 GIGANTEA functions as a co-repressor of cold stress response... | MARK AS OVER ANNOTATED | Summary: The abstract indicates that GI affects histone acetylation and CBF binding at the COR15A promoter and forms a co-repressor complex with HOS15 and HD2C. It does not establish whether GI directly binds DNA or is detected at DNA through associated transcription/chromatin proteins. Reason: Full text is not open access (no PMC record in Europe PMC), so the assay behind the IDA could not be seen. GI has no recognised DNA-binding domain, and the abstract describes GI acting as a co-repressor with HOS15 and HD2C that reduces CBF binding at COR15A; GI detection at promoters (as also seen at CO and FT) is best explained by recruitment through DNA-binding partners. Direct sequence-independent DNA binding is therefore implausible as a GI molecular function; not removed because the curator saw data we could not. Supporting Evidence: PMID:40157149 Moreover, GI reduces histone acetylation and CBF binding at the COR15A promoter under cold stress, repressing COR15A gene expression. |
| GO:0005515 protein binding | IPI PMID:15155885 SPINDLY and GIGANTEA interact and act in Arabidopsis thalian... | REMOVE | Summary: GI-SPY interaction is supported by yeast two-hybrid, bacterial, and in vitro pull-down evidence. However, the generic protein binding term adds little functional information and the SPY interaction is not the central GI molecular role. Reason: Removal concerns only the uninformative protein binding term, not the validity of the interaction. The interaction is real, but generic protein binding is an uninformative term for GI and no specific GO molecular function term is clearly supported by the abstract alone. Supporting Evidence: PMID:15155885 GI and SPY also interacted in Escherichia coli and in vitro pull-down assays. |
| GO:0005515 protein binding | IPI PMID:17704763 ZEITLUPE is a circadian photoreceptor stabilized by GIGANTEA... | MODIFY | Summary: This annotation represents GI interaction with ZTL/FKF1/LKP2-family F-box photoreceptors. The source shows that GI stabilizes ZTL through a direct, blue-light-enhanced interaction. A specific ubiquitin protein ligase binding term is more informative than generic protein binding. Reason: ZTL-family proteins are F-box components of SCF ubiquitin ligase systems; the functionally meaningful activity is binding these ubiquitin ligase components to regulate clock protein stability. Proposed replacements: ubiquitin protein ligase binding Supporting Evidence: PMID:17704763 Here we show that GIGANTEA (GI) is essential to establish and sustain oscillations of ZTL by a direct protein-protein interaction. GI, a large plant-specific protein with a previously undefined molecular role, stabilizes ZTL in vivo. |
| GO:0005515 protein binding | IPI PMID:17872410 FKF1 and GIGANTEA complex formation is required for day-leng... | MODIFY | Summary: This annotation covers GI binding to FKF1 and the CO repressor CDF1. The generic protein binding term should be replaced by terms that describe the two mechanistically important binding classes: ubiquitin ligase component binding and DNA-binding transcription factor binding. Reason: The FKF1-GI-CDF1 mechanism is central to GI function, but GO:0005515 is too generic to capture it. Proposed replacements: ubiquitin protein ligase binding DNA-binding transcription factor binding Supporting Evidence: PMID:17872410 FKF1 function is dependent on GI, which interacts with a CO repressor, CYCLING DOF FACTOR 1 (CDF1), and controls CDF1 stability. |
| GO:0005515 protein binding | IPI PMID:19452453 Proteomic profiling of tandem affinity purified 14-3-3 prote... | REMOVE | Summary: The paper is a TAP-MS survey of Arabidopsis 14-3-3 omega complexes. The cached full text supports the general approach and the presence of many putative 14-3-3 clients, but the GI-specific supporting row appears to be in supplemental material that is not present in the cached text. Reason: Removal concerns only the uninformative protein binding term, not the validity of the interaction; the GI-specific identification could not be verified from the cached text, but the term would be uninformative either way. This is a high-throughput 14-3-3 omega TAP-MS client survey; the GI-specific identification is only in supplementary data and no functional role for a 14-3-3-GI association is established, so no informative replacement term applies. Supporting Evidence: PMID:19452453 The identification here of 121 putative clients provides support for in vivo 14-3-3 interactions with a diverse array of proteins |
| GO:0005515 protein binding | IPI PMID:21709243 GIGANTEA directly activates Flowering Locus T in Arabidopsis... | MODIFY | Summary: Sawa and Kay show that GI binds FT repressors SVP, TEM1, and TEM2 and is associated with FT promoter regions near SVP binding sites. The functionally informative term is DNA-binding transcription factor binding, not generic protein binding. Reason: GI's binding to FT repressors is part of transcriptional control of flowering time, so DNA-binding transcription factor binding better captures the molecular function. Proposed replacements: DNA-binding transcription factor binding Supporting Evidence: PMID:21709243 We found that GI can bind to three FT repressors: SHORT VEGETATIVE PHASE (SVP), TEMPRANILLO (TEM)1, and TEM2. |
| GO:0005515 protein binding | IPI PMID:32612234 Extensive signal integration by the phytohormone protein net... | REMOVE | Summary: The source is a systems-level phytohormone protein interaction network. The cached abstract supports the overall network generation but does not expose GI-specific partner evidence or functional validation for these interactions. Reason: Removal concerns only the uninformative protein binding term, not the validity of the interaction; the GI-specific pairs could not be verified from the cached text, but the term would be uninformative either way. These are binary Y2H pairs from a systems-level phytohormone interactome without GI-specific functional validation; no informative replacement term can be assigned to the set of partners. Supporting Evidence: PMID:32612234 Here, we experimentally generated a systems-level map of the Arabidopsis phytohormone signalling network, consisting of more than 2,000 binary protein-protein interactions. |
| GO:0005515 protein binding | IPI PMID:40157149 GIGANTEA functions as a co-repressor of cold stress response... | MODIFY | Summary: The abstract supports GI association with the HOS15-HISTONE DEACETYLASE 2C complex and describes GI as a co-repressor in cold-response chromatin regulation. Generic protein binding is less informative than the corepressor/HDAC-associated activities reported. Reason: Replace generic protein binding with transcription corepressor activity and histone deacetylase binding, which better describe the HOS15-HD2C-GI mechanism visible in the abstract. Proposed replacements: transcription corepressor activity histone deacetylase binding Supporting Evidence: PMID:40157149 We further demonstrate that GI forms a co-repressor with HOS15 and HD2C, inhibiting CBF binding and preventing COR gene activation under normal conditions. |
| GO:2000028 regulation of photoperiodism, flowering | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: The InterPro2GO annotation from the GIGANTEA family is biologically correct, but it is broader and weaker than the experimental long-day photoperiodic flowering annotation already present for GI. Reason: Keep as a correct electronic family-level annotation, but prioritize the experimentally supported GO:0048578 term as core. Supporting Evidence: file:ARATH/GI/GI-uniprot.txt GO; GO:0048578; P:positive regulation of long-day photoperiodism, flowering; IMP:TAIR. |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: UniProt subcellular-location mapping to nucleus is correct and consistent with multiple experimental GI localization studies. It is redundant with direct IDA nucleus/nucleoplasm annotations. Reason: The duplicate electronic row is less informative than the experimental localization annotations, but the nucleus term itself is a core GI cellular location and should be handled consistently across duplicate GOA rows. Supporting Evidence: file:ARATH/GI/GI-uniprot.txt SUBCELLULAR LOCATION: Nucleus. Cytoplasm. |
| GO:0005634 nucleus | ISM GO_REF:0000122 | ACCEPT | Summary: The AtSubP prediction of nuclear localization agrees with direct experimental data showing nuclear/nucleoplasmic GI. It is correct but computational and redundant. Reason: The prediction is redundant with direct experimental evidence, but the nucleus term itself is a core GI cellular location and should be handled consistently across duplicate GOA rows. Supporting Evidence: PMID:10920210 Optical sectioning by using the green fluorescent protein-GI fusion protein showed green fluorescence throughout the nucleoplasm. |
| GO:0005634 nucleus | IDA PMID:16006578 Distinct roles of GIGANTEA in promoting flowering and regula... | ACCEPT | Summary: Functional GI:GFP localizes to the nucleus in transgenic Arabidopsis, and nuclear GI is mechanistically relevant to CO/FT regulation. Reason: Nucleus is a directly supported core cellular location for GI function in photoperiodic transcriptional control. Supporting Evidence: PMID:16006578 Functional GI:green fluorescent protein is localized to the nucleus in transgenic Arabidopsis plants, supporting the idea that GI regulates flowering in the nucleus. |
| GO:0005634 nucleus | IDA PMID:19061637 COP1 and ELF3 control circadian function and photoperiodic f... | ACCEPT | Summary: This source studies COP1/ELF3 control of GI stability in the light-input, circadian, and photoperiodic flowering pathway. The cached text does not expose the exact localization result behind the GOA IDA, but nuclear GI is independently supported by Huq et al. and Mizoguchi et al. Reason: Accept the term as biologically correct using the broader experimental localization evidence for GI, while noting that the cached copy of the original source does not show the exact localization assay. Supporting Evidence: PMID:19061637 COP1 acts with ELF3 to mediate day length signaling from CRY2 to GI within the photoperiod flowering pathway. PMID:16006578 Functional GI:green fluorescent protein is localized to the nucleus in transgenic Arabidopsis plants |
| GO:0005654 nucleoplasm | IDA PMID:10920210 GIGANTEA is a nuclear protein involved in phytochrome signal... | ACCEPT | Summary: Huq et al. directly demonstrated nucleoplasmic localization of GI using GFP-GI fusion constructs and optical sectioning. This is the most specific directly supported nuclear localization term. Reason: Nucleoplasm is directly supported and consistent with GI's nuclear roles in transcriptional and chromatin-associated regulation. Supporting Evidence: PMID:10920210 Optical sectioning by using the green fluorescent protein-GI fusion protein showed green fluorescence throughout the nucleoplasm. |
| GO:0005737 cytoplasm | IEA GO_REF:0000044 | ACCEPT | Summary: UniProt maps GI to both nucleus and cytoplasm. Cytoplasmic GI is also consistent with the ZTL-family stabilization/proteostasis mechanism described in later studies and reviews. Reason: Cytoplasm is a core GI location because GI's ZTL/F-box protein stability functions include a cytoplasmic pool, even though this GOA row is electronically propagated from UniProt subcellular-location mapping. Supporting Evidence: file:ARATH/GI/GI-uniprot.txt SUBCELLULAR LOCATION: Nucleus. Cytoplasm. |
| GO:0003712 transcription coregulator activity | IDA | NEW | Summary: GI's photoperiodic flowering mechanism is best captured as transcription coregulator activity: GI does not have a demonstrated intrinsic sequence-specific DNA-binding activity, but it binds FKF1, CDF1, and FT repressors and is associated with CO/FT promoter regions to regulate transcriptional output. Reason: This term captures the core molecular function inferred from multiple direct GI chromatin-association and protein-complex studies better than the existing generic DNA binding and protein binding rows. Supporting Evidence: PMID:17872410 GI, FKF1, and CDF1 proteins associate with CO chromatin. PMID:21709243 Finally, our chromatin immunoprecipitation experiments showed that GI binds to FT promoter regions that are near the SVP binding sites. |
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Download this section (compressed HTML)Q: Does GI directly bind DNA at CO, FT, or COR promoters, or are published ChIP and promoter-association signals mediated entirely through DNA-binding transcription factors and chromatin-modifying complexes?
Suggested experts: Masaki Sawa, Steve A. Kay, Won Y. Kim
Q: Which of the high-throughput phytohormone-network interactions reported for GI are reproducible at endogenous protein levels and relevant to GI's physiological stress phenotypes?
Suggested experts: Pascal Falter-Braun
Q: What GO molecular function term best captures GI's scaffold/co-chaperone role with ZTL/FKF1/LKP2 and transcriptional repressors, given that generic protein binding is not informative?
Suggested experts: David E. Somers, Takato Imaizumi
Experiment: Test purified GI in EMSA or fluorescence anisotropy assays against CO, FT, and COR15A promoter fragments, then compare with ChIP-reChIP or CUT&RUN using tagged GI plus CDF1, SVP/TEM, HOS15, and HD2C in planta.
Hypothesis: GI promoter occupancy is mediated by partner transcription factors or chromatin complexes rather than sequence-specific DNA binding by GI itself.
Type: biochemical DNA-binding and chromatin-occupancy assay
Experiment: Reconstitute GI-ZTL/FKF1/LKP2 complexes with HSP90 in vitro and measure binding affinities, light dependence, and effects on F-box protein stability; validate key interfaces by endogenous genome-edited GI separation-of-function alleles.
Hypothesis: GI's core clock function depends on direct binding to ZTL/FKF1/LKP2 F-box proteins and HSP90-assisted stabilization of the ZTL-family complex.
Type: protein interaction and proteostasis assay
Experiment: Generate endogenous tagged GI lines and perform time-of-day-resolved interactome profiling under long-day control, blue light, cold, salt, and low red:far-red treatments, followed by reciprocal co-IP and phenotyping of partner-specific GI interface mutants.
Hypothesis: GI stress-response phenotypes are separable from its photoperiodic flowering and circadian functions through distinct partner complexes.
Type: endogenous interactomics and genetics
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