AtHKT1;1 (HKT1, At4g10310) is a plasma-membrane cation transporter of the HKT/Trk/Ktr superfamily and the sole HKT-family member in Arabidopsis thaliana. It is a Class I HKT transporter that functions in planta as a sodium-selective uniporter. Its central physiological role is sodium retrieval and recirculation; it unloads Na+ from the xylem sap into xylem-parenchyma cells (and is implicated in Na+ loading into the phloem in shoots and unloading in roots), thereby limiting Na+ accumulation in photosynthetic shoot tissues and conferring tolerance to salt stress. The protein has a K-channel-like four transmembrane-pore-transmembrane architecture but, unlike potassium channels, lacks a conserved glycine in its first pore loop (position 68), which accounts for its selectivity for Na+ over K+; in planta it does not transport K+ and instead influences K+/Na+ balance indirectly through its effect on Na+ homeostasis. AtHKT1;1 is expressed in vascular tissues of all organs, predominantly in the phloem and in xylem-parenchyma cells, and its locus underlies natural variation in leaf Na+ content among Arabidopsis accessions.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
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GO:0005886
plasma membrane
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IEA
GO_REF:0000044 |
ACCEPT |
Summary: Electronic subcellular-location mapping placing HKT1 at the plasma membrane.
Reason: Plasma membrane is the correct and core localization, independently confirmed by direct immunoelectron microscopy of AtHKT1 in xylem-parenchyma cells (PMID:16359386). This IEA annotation is consistent with the curated UniProt subcellular location.
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
Plasma membrane (cell membrane), multi-pass membrane protein
|
|
GO:0006812
monoatomic cation transport
|
IEA
GO_REF:0000002 |
MODIFY |
Summary: Family-level electronic annotation to a generic cation-transport term.
Reason: Correct in essence (HKT1 transports a monovalent cation) but too general. The physiologically relevant species transported in planta is Na+, so a sodium ion transport term is more informative.
Proposed replacements:
sodium ion transport
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
It is a Class I HKT transporter that functions in planta as a Na+-selective uniporter
|
|
GO:0006813
potassium ion transport
|
IEA
GO_REF:0000117 |
MARK AS OVER ANNOTATED |
Summary: ARBA machine-learning electronic annotation to potassium ion transport.
Reason: This is a family/name-derived electronic inference. The Arabidopsis protein is Na+-selective and does not transport K+ in planta; UniProt states it "Does not transport K(+)". The K+-related function is at most an indirect consequence of Na+ homeostasis, so direct K+ transport is an over-annotation rather than the gene's activity.
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
it lacks a conserved Gly at position 68, explaining why it does not act as a K(+) transporter
|
|
GO:0008324
monoatomic cation transmembrane transporter activity
|
IEA
GO_REF:0000002 |
MODIFY |
Summary: Family-level electronic molecular-function annotation to generic cation transporter activity.
Reason: Correct but too general. The experimentally demonstrated and core molecular function is sodium ion transmembrane transporter activity; replace the generic parent with the specific Na+ term.
Proposed replacements:
sodium ion transmembrane transporter activity
Supporting Evidence:
PMID:10759522
AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
|
|
GO:0015079
potassium ion transmembrane transporter activity
|
IEA
GO_REF:0000002 |
MARK AS OVER ANNOTATED |
Summary: InterPro family-level electronic annotation of potassium ion transmembrane transporter activity.
Reason: This K+-specific molecular-function term is inherited from the HKT/Trk/Ktr family signature and the wheat ortholog's high-affinity K+ behavior, but AtHKT1;1 is Na+-selective and does NOT transport K+ in planta (it lacks the conserved Gly-68 of K+-permeable HKTs; only a <2-fold K+ effect in heterologous systems). The potassium transport function is therefore an over-annotation. The correct Na+ molecular function is captured separately by the ACCEPTed GO:0015081 (sodium ion transmembrane transporter activity, IDA), so this K+ term is flagged as over-annotated rather than re-pointed at the Na+ term — consistent with the three parallel K+ biological-process annotations in this file, which are likewise marked as over-annotated.
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
it lacks a conserved Gly at position 68, explaining why it does not act as a K(+) transporter
file:ARATH/HKT1/HKT1-deep-research-falcon.md
K+ currents were indistinguishable between WT and athkt1;1 stelar cells, arguing against a primary K+ transport role in planta
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|
GO:0016020
membrane
|
IEA
GO_REF:0000120 |
MODIFY |
Summary: Generic membrane localization from combined automated methods.
Reason: Correct but uninformatively general; the specific and supported location is the plasma membrane.
Proposed replacements:
plasma membrane
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
Plasma membrane (cell membrane), multi-pass membrane protein
|
|
GO:0035725
sodium ion transmembrane transport
|
IEA
GO_REF:0000108 |
ACCEPT |
Summary: Electronic annotation (inter-ontology link from MF GO:0015081) to the sodium ion transmembrane transport process.
Reason: This accurately captures the core in-planta process; HKT1 mediates Na+ movement across the plasma membrane. Supported by direct functional and genetic evidence.
Supporting Evidence:
PMID:10759522
AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
|
|
GO:0046873
metal ion transmembrane transporter activity
|
IEA
GO_REF:0000117 |
MODIFY |
Summary: ARBA electronic annotation to generic metal ion transmembrane transporter activity.
Reason: Correct (Na+ is a metal ion) but too general. The specific, experimentally supported molecular function is sodium ion transmembrane transporter activity.
Proposed replacements:
sodium ion transmembrane transporter activity
Supporting Evidence:
PMID:10759522
AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
|
|
GO:0055085
transmembrane transport
|
IEA
GO_REF:0000002 |
MODIFY |
Summary: Family-level electronic annotation to the most generic transport process term.
Reason: Correct but far too general to be informative; replace with the specific sodium ion transmembrane transport process.
Proposed replacements:
sodium ion transmembrane transport
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
It is a Class I HKT transporter that functions in planta as a Na+-selective uniporter
|
|
GO:0071805
potassium ion transmembrane transport
|
IEA
GO_REF:0000002 |
MARK AS OVER ANNOTATED |
Summary: InterPro family-level electronic annotation to potassium ion transmembrane transport.
Reason: Family/name-derived electronic inference. AtHKT1;1 does not transport K+ in planta; any K+ effect is indirect via Na+ homeostasis. Direct K+ transmembrane transport is an over-annotation. The biologically relevant process is sodium ion transmembrane transport (already annotated via GO:0035725).
Supporting Evidence:
file:ARATH/HKT1/HKT1-notes.md
it lacks a conserved Gly at position 68, explaining why it does not act as a K(+) transporter
file:ARATH/HKT1/HKT1-deep-research-falcon.md
K+ currents were indistinguishable between WT and athkt1;1 stelar cells, arguing against a primary K+ transport role in planta
|
|
GO:0005739
mitochondrion
|
ISM
GO_REF:0000122 |
REMOVE |
Summary: Sequence-based (AtSubP) prediction placing HKT1 in the mitochondrion.
Reason: This is a purely computational (ISM) subcellular-localization prediction, not experimental evidence. It is contradicted by direct immunoelectron microscopy and promoter-GUS data localizing AtHKT1 to the plasma membrane of xylem-parenchyma cells, and by the curated UniProt cell-membrane location. The mitochondrial prediction is a clearly-wrong electronic annotation.
Supporting Evidence:
PMID:16359386
AtHKT1 is targeted to the plasma membrane in xylem parenchyma cells in leaves
|
|
GO:0006814
sodium ion transport
|
IMP
PMID:15486089 Microarray-based rapid cloning of an ion accumulation deleti... |
ACCEPT |
Summary: Mutant phenotype (FN1148 AtHKT1 deletion) showing altered shoot/root Na+ distribution, supporting a role in sodium ion transport.
Reason: Experimental IMP evidence; the 523-bp AtHKT1 deletion causes shoot Na+ overaccumulation and root Na+ underaccumulation, and AtHKT1 cDNA complements the salt sensitivity, directly tying HKT1 to in-planta Na+ transport. Core process.
Supporting Evidence:
PMID:15486089
the deletion within the AtHKT1 gene is responsible for the sodium overaccumulation in shoots and leaf sodium sensitivity of the FN1148 mutant
|
|
GO:0009651
response to salt stress
|
IGI
PMID:11698666 AtHKT1 is a salt tolerance determinant that controls Na(+) e... |
ACCEPT |
Summary: Genetic interaction (hkt1 suppresses sos3-1 salt hypersensitivity) establishing HKT1 as a salt-tolerance determinant.
Reason: Experimental IGI evidence; hkt1 loss-of-function mutations suppress NaCl hypersensitivity of sos3-1 and alter intracellular Na+/K+, defining HKT1 as a salt-tolerance determinant. This is a core biological process for the gene.
Supporting Evidence:
PMID:11698666
AtHKT1 is a salt tolerance determinant that controls Na + entry
|
|
GO:0005886
plasma membrane
|
IDA
PMID:16359386 Enhanced salt tolerance mediated by AtHKT1 transporter-induc... |
ACCEPT |
Summary: Direct immunoelectron microscopy localizing AtHKT1 to the plasma membrane of xylem-parenchyma cells.
Reason: Direct experimental evidence (IDA) for the core and correct subcellular localization. Strongest support among the plasma-membrane annotations.
Supporting Evidence:
PMID:16359386
AtHKT1 is targeted to the plasma membrane in xylem parenchyma cells in leaves
file:ARATH/HKT1/HKT1-deep-research-falcon.md
AtHKT1;1 is supported as a **plasma membrane** protein active in **root stelar/vascular cells** (often described as xylem-parenchyma associated)
|
|
GO:0006813
potassium ion transport
|
IMP
PMID:16359386 Enhanced salt tolerance mediated by AtHKT1 transporter-induc... |
MARK AS OVER ANNOTATED |
Summary: Mutant-phenotype annotation to potassium ion transport based on altered xylem K+ content in athkt1 alleles.
Reason: This TAIR IMP annotation reflects an indirect, secondary effect on K+, not direct K+ transport by HKT1. The paper itself states the influence on K+ is smaller, inverse, and that "K+ transport may be indirectly affected". Annotating HKT1 to potassium ion transport over-states an indirect downstream consequence as a transport function; the gene does not transport K+ in planta. (The annotation is not removed because it rests on an experimental phenotype, but the K+-transport term is an over-annotation.)
Supporting Evidence:
PMID:16359386
suggesting that K+ transport may be indirectly affected
|
|
GO:0006814
sodium ion transport
|
IMP
PMID:16359386 Enhanced salt tolerance mediated by AtHKT1 transporter-induc... |
ACCEPT |
Summary: Mutant-phenotype evidence that athkt1 alleles increase xylem-sap Na+ and reduce phloem-sap Na+, supporting HKT1's role in Na+ transport.
Reason: Experimental IMP evidence for the core in-planta process; disruption alters Na+ distribution between xylem and phloem and across shoot/root.
Supporting Evidence:
PMID:16359386
AtHKT1 disruption alleles caused large increases in the Na+ content of the xylem sap and conversely reduced the Na+ content of the phloem sap
|
|
GO:0006970
response to osmotic stress
|
IEP
PMID:16359386 Enhanced salt tolerance mediated by AtHKT1 transporter-induc... |
KEEP AS NON CORE |
Summary: Expression-pattern (IEP) annotation; AtHKT1 expression is modulated by osmolality of non-ionic compounds.
Reason: Supported by the cited paper (AtHKT1 expression responds to non-ionic osmolality and AtHKT1 mediates osmolality balance between xylem vessels and parenchyma). This is a real but peripheral aspect relative to the gene's core Na+-transport / salt-tolerance role; retain as non-core. IEP is expression-based, not a demonstration of involvement in osmotic-stress response per se.
Supporting Evidence:
PMID:16359386
The expression of AtHKT1 was modulated not only by the concentrations of Na+ and K+ but also by the osmolality of non-ionic compounds
|
|
GO:0009651
response to salt stress
|
IMP
PMID:12727868 Functional analysis of AtHKT1 in Arabidopsis shows that Na(+... |
ACCEPT |
Summary: Mutant-phenotype evidence (sas2-1/sas2-2 = AtHKT1) that disruption increases NaCl sensitivity, establishing a role in salt-stress response.
Reason: Experimental IMP evidence; sas2 (athkt1) plants show increased NaCl sensitivity with reduced growth and death under moderate salinity, demonstrating HKT1's core role in salt-stress tolerance via Na+ recirculation.
Supporting Evidence:
PMID:12727868
The sas2 plants displayed increased sensitivity to NaCl, with reduced growth and even death under moderate salinity
|
|
GO:0006814
sodium ion transport
|
IDA
PMID:10759522 The Arabidopsis HKT1 gene homolog mediates inward Na(+) curr... |
ACCEPT |
Summary: Direct functional evidence that AtHKT1 mediates inward Na+ currents in Xenopus oocytes and Na+ uptake in yeast.
Reason: Direct assay (IDA) demonstrating Na+ transport activity; core function.
Supporting Evidence:
PMID:10759522
AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
|
|
GO:0015081
sodium ion transmembrane transporter activity
|
IDA
PMID:10759522 The Arabidopsis HKT1 gene homolog mediates inward Na(+) curr... |
ACCEPT |
Summary: Direct electrophysiological evidence that AtHKT1 enables selective Na+ transmembrane transport.
Reason: Direct assay (IDA) establishing the core molecular function; selective Na+ uniport, independent of external K+. This is the primary, correct molecular function and the target term for the over-general and K+ MF annotations above.
Supporting Evidence:
PMID:10759522
AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes, and the presence of external K + did not affect the AtHKT1-mediated ion conductance
file:ARATH/HKT1/HKT1-deep-research-falcon.md
encodes a **plasma-membrane Na\(\+\)-selective transporter** that functions predominantly in **root vascular (stelar/xylem-parenchyma) cells**
|
=== UNIPROT METADATA ===
UniProt ID: Q84TI7
Entry Name: HKT1_ARATH
Gene Name: HKT1
Protein Name: Sodium transporter HKT1
Organism: Arabidopsis thaliana (Mouse-ear cress)
NCBI Taxonomy ID: 3702
Function: Sodium transporter protein, which plays a central role in plant tolerance to salt. Upon prolongated exposure to high concentrations, Na(+) translocates from the roots to the transpiring leaves where it can increase to toxic level. Involved in Na(+) recirculation from shoots to roots, probably by mediating Na(+) loading into the phloem sap in shoots and unloading in roots, thereby removing large amounts of Na(+) from the shoot. Does not transport K(+) but regulates K(+) nutrient status via its ability to facilitate Na(+) homeostasis. Probably not involved in root uptake of Na(+).
Subcellular Location: Cell membrane; Multi-pass membrane protein.
======================
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HKT1 (AtHKT1;1) encodes a plasma-membrane Na(+)-selective transporter that functions predominantly in root vascular (stelar/xylem-parenchyma) cells to control long-distance Na(+) distribution and protect shoots from Na(+) over-accumulation during salinity stress. In vivo electrophysiology in native cells supports passive, channel-like Na(+) conductance with strong Na(+) preference over K(+), aligning with salt-tolerance phenotypes of hkt1 loss-of-function mutants (xue2011athkt1;1mediatesnernstian pages 1-2, hauser2010aconservedprimary pages 5-6).
Two major 2024 advances refine regulation and developmental context for GO review. First, SOS3/CBL4 was identified as a Ca(\2+)-sensor “switch” that promotes proteasome-dependent HKT1;1 degradation under salt/Ca(\2+) signals, inversely coordinating HKT1;1 with SOS1 localization and thereby shifting net Na(+) partitioning (PNAS, published 2024-02; https://doi.org/10.1073/pnas.2320657121) (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 6-7, gamezarjona2024inverseregulationof media c615254c). Second, during seed germination, CaCl2-mediated salt tolerance depends on HKT1;1 and involves radicle-focused expression and a negative regulator PP2C49, linking HKT1;1 to ion homeostasis and germination success under salt (Plant Physiology, published 2024-12; https://doi.org/10.1093/plphys/kiad651) (chandran2024calciumregulationof pages 2-3, chandran2024calciumregulationof pages 5-7).
No evidence in the retrieved Arabidopsis literature supports HKT1;1 roles in apoptosis, developmental cell death programs, neuronal functions, inflammatory signaling, pyroptosis, synaptic remodeling, or nuclear/cytosolic signaling complexes; these appear to be non-applicable cross-domain concepts for this plant ion transporter (xue2011athkt1;1mediatesnernstian pages 1-2, chandran2024calciumregulationof pages 3-5).
In vivo electrophysiology (native Arabidopsis cells): AtHKT1;1-dependent currents were detected in GFP-labeled root stelar protoplasts in wild type but were absent in athkt1;1 mutants, providing direct evidence that AtHKT1;1 mediates these currents. The currents were carried by Na(+), showed little voltage dependence, and exhibited Nernstian shifts in reversal potential with altered NaCl gradients, consistent with passive Na(+) conductance. Importantly, K(+) currents were indistinguishable between WT and athkt1;1, supporting Na(+)-over-K(+) selectivity (PLoS ONE; published 2011-09; https://doi.org/10.1371/journal.pone.0024725) (xue2011athkt1;1mediatesnernstian pages 1-2).
Heterologous expression context: HKT1;1 was initially characterized via expression in Xenopus oocytes/yeast, generally supporting Na(+) transport. However, reports of Na(+)/K(+) symport can vary by heterologous system and ionic conditions; therefore, for GO MF in Arabidopsis, the in vivo stelar-cell electrophysiology provides the most directly transferable substrate-specific evidence (waters2013planthighaffinitypotassium pages 3-5, xue2011athkt1;1mediatesnernstian pages 1-2).
No evidence in the retrieved sources indicates that HKT1;1 requires proteolytic processing or a cleavage-based maturation mechanism for activity. Instead, the best-supported “maturation-like” control is post-translational regulation of abundance/stability (Section 4) rather than proteolytic activation (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 1-2).
Shoot protection via xylem Na(+) retrieval/unloading: Loss-of-function studies synthesized in Plant, Cell & Environment review evidence indicate that AtHKT1;1 plays a direct role in excluding Na(+) from xylem vessels (often described as retrieval/unloading of Na(+) from xylem sap into adjacent parenchyma), thereby preventing toxic Na(+) accumulation in aerial tissues under salinity. Under salinity, athkt1;1 null alleles show elevated Na(+) in shoots and xylem sap, and a markedly reduced shoot K(+)/Na(+) ratio; the review reports quantitative ion-ratio data (Table 1) contrasting WT versus athkt1;1 (Plant, Cell & Environment; published 2010-04; https://doi.org/10.1111/j.1365-3040.2009.02056.x) (hauser2010aconservedprimary pages 5-6, hauser2010aconservedprimary pages 2-3).
Mechanistic framing for GO: The most strongly supported BP annotations are therefore those tied to Na(+) homeostasis and long-distance Na(+) transport (vascular Na(+) distribution, shoot Na(+) exclusion), rather than broad, non-mechanistic “salt tolerance” descriptors alone (hauser2010aconservedprimary pages 5-6, xue2011athkt1;1mediatesnernstian pages 1-2).
Multiple reviews summarize a phloem Na(+) recirculation model (shoot-to-root return of Na(+) via phloem loading/unloading) as part of HKT1-type function, but also note controversy and emphasize xylem retrieval as the most consistently supported core mechanism. For GO BP review, this suggests cautious phrasing and careful evidence weighting when considering phloem-specific BP annotations (waters2013planthighaffinitypotassium pages 3-5, hauser2010aconservedprimary pages 2-3).
Chandran et al. (Plant Physiology; published 2024-12; https://doi.org/10.1093/plphys/kiad651) provide strong evidence that HKT1;1 contributes to seed germination under salt stress in a Ca(\2+)-dependent manner. Key statistics from germination assays include:
* On 150 mM NaCl, WT germination 68.2 ± 2.8% vs hkt1 33.7 ± 7.3%; on 200 mM NaCl, WT 2.6 ± 0.5% vs hkt1 1.3 ± 0.5%.
* Adding 10 mM CaCl2 increased WT germination to 85 ± 3.8% (150 mM NaCl) and 27 ± 7% (200 mM NaCl) but did not rescue hkt1 lines comparably, supporting a functional requirement for HKT1;1 in the Ca(\2+)-mediated germination response (chandran2024calciumregulationof pages 2-3).
* Ion-content (ionomics) during germination: under NaCl+CaCl2, WT contained 1.99 ± 0.12 µg Na(+)/seedling vs hkt1 3.1 ± 0.11 µg, and WT contained 1.04 ± 0.17 µg K(+)/seedling vs hkt1 0.42 ± 0.12 µg, implying HKT1;1 helps maintain Na(+) and K(+) homeostasis during germination under combined stress (chandran2024calciumregulationof pages 3-5).
For GO, this supports a developmental-stage/context-specific BP annotation (“seed germination under salt stress” or “salt stress response during germination”), but it should not displace vascular Na(+) redistribution as the gene’s primary well-established role across life stages (chandran2024calciumregulationof pages 1-2, hauser2010aconservedprimary pages 5-6).
Across in vivo functional data and summarized localization work, AtHKT1;1 is supported as a plasma membrane protein active in root stelar/vascular cells (often described as xylem-parenchyma associated). The electrophysiology was explicitly performed in root stelar cells, directly tying function to this cellular context (xue2011athkt1;1mediatesnernstian pages 1-2).
Gámez-Arjona et al. (PNAS; published 2024-02; https://doi.org/10.1073/pnas.2320657121) provide evidence that SOS3/CBL4 physically interacts with HKT1;1 and coordinates HKT1;1 turnover with SOS1 localization:
* Physical interaction: SOS3–HKT1;1 interaction was supported by BiFC mapping (Figure 5) and co-immunoprecipitation (Figure 6A), and a mutant SOS3-1 failed to bind HKT1;1 (gamezarjona2024inverseregulationof pages 4-5, gamezarjona2024inverseregulationof media c615254c).
* Functional relationship: In Xenopus oocytes, HKT1;1 yielded robust Na(+)-dependent currents, and co-expression of SOS3 did not change these currents, supporting regulation mainly via abundance/localization rather than direct gating modulation in this assay context (gamezarjona2024inverseregulationof pages 5-6).
For GO CC, this supports inclusion of plasma membrane and potentially a qualified statement regarding operation within a SOS pathway regulatory module, but the evidence is strongest for a regulatory interaction rather than a stable multi-protein transporter “complex” with a defined stoichiometry (gamezarjona2024inverseregulationof pages 6-7, gamezarjona2024inverseregulationof pages 4-5).
Gámez-Arjona et al. show that salt and Ca(\2+) signals trigger HKT1;1 protein degradation and that this requires SOS3/CBL4:
* In planta, 100 mM NaCl and 3 mM CaCl2 treatments reduced HKT1;1 abundance in HKT1 fusion lines, and HKT1:GFP was reported to gradually disappear over ~24 h under salt stress (gamezarjona2024inverseregulationof pages 5-6).
* The decline was proteasome-dependent, as it was prevented by MG132 (50 µM), a 26S proteasome inhibitor (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof media c615254c).
* Genetic evidence: salt-induced HKT1;1 degradation occurred in sos1-1 and sos2-2 backgrounds but was blocked in sos3-1, indicating SOS3 is necessary for this post-translational regulation (gamezarjona2024inverseregulationof pages 5-6).
This set of findings strongly supports GO annotations describing negative regulation of HKT1;1 protein stability/abundance during salt stress and provides a concrete mechanistic basis to separate “activation” concepts from “turnover” concepts (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 1-2).
Chandran et al. support a pathway where PP2C49 negatively regulates HKT1;1, and Ca(\2+) improves germination partly by downregulating PP2C49:
* On 200 mM NaCl, pp2c49 mutants germinated substantially better than WT (WT 2.6 ± 0.5% vs pp2c49 alleles ~26.75–41.5%, depending on allele), consistent with PP2C49 acting as a negative regulator in this context (chandran2024calciumregulationof pages 5-7).
* pp2c49-1 seedlings accumulated less Na(+) under NaCl (1.77 ± 0.3 µg vs WT 2.34 ± 0.28 µg) and maintained higher K(+) (1.6 ± 0.27 µg vs WT 0.55 ± 0.07 µg) (chandran2024calciumregulationof pages 5-7).
For GO review, PP2C49-related regulation is best treated as context-specific (germination/early seedling) unless corroborated across additional tissues/stages (chandran2024calciumregulationof pages 1-2).
Two evidence-derived tables summarizing recommended annotation strength and risks are provided below.
| Category | Claim/Proposed GO statement | Evidence type (assay) | Key quantitative/statistical details | Notes on specificity/transferability | Primary citation (with year, journal, URL) |
|---|---|---|---|---|---|
| Molecular Function | Sodium ion transmembrane transporter activity; AtHKT1;1 mediates Na+-selective passive transport / channel-like conductance in root stelar cells | In vivo patch clamp of GFP-labeled Arabidopsis root stelar protoplasts; heterologous expression in Xenopus oocytes and yeast; mutant comparison | AtHKT1;1-dependent currents were present in wild type but absent in athkt1;1; reversal potentials shifted in a Nernstian manner with NaCl gradients; K+ currents were indistinguishable between WT and mutant; removal of external Na+ reduced outward current (xue2011athkt1;1mediatesnernstian pages 1-2, xue2011athkt1;1mediatesnernstian pages 8-9) | Strongest MF annotation should be Na+ transport, not generic K+ transport. Reports of Na+/K+ symport in some heterologous systems are context-dependent and should not override in planta Na+-selective evidence for Arabidopsis HKT1;1 (waters2013planthighaffinitypotassium pages 3-5, pardo2011na+andk+ pages 9-11) | Xue et al. 2011, PLoS ONE, https://doi.org/10.1371/journal.pone.0024725 (xue2011athkt1;1mediatesnernstian pages 1-2, xue2011athkt1;1mediatesnernstian pages 8-9) |
| Biological Process | Sodium ion homeostasis / response to salt stress via retrieval of Na+ from xylem sap, limiting Na+ delivery to shoot and maintaining shoot K+/Na+ balance | Loss-of-function phenotyping; ionomics of shoots and xylem sap; physiological interpretation from mutant and transport studies | Three independent athkt1;1 null alleles showed elevated shoot and xylem sap Na+ and reduced shoot and xylem K+ under salinity; review table values include WT around 2.71, 0.41, 1.58, 0.21 vs athkt1;1 0.25, 0.03, 0.55, 0.08; mutants show leaf chlorosis and salt hypersensitivity (hauser2010aconservedprimary pages 5-6, hauser2010aconservedprimary pages 2-3) | This is a core BP for Arabidopsis HKT1;1. “Phloem recirculation” has historical support, but the most robust and least controversial process annotation is xylem Na+ unloading / shoot Na+ exclusion (hauser2010aconservedprimary pages 2-3, pardo2011na+andk+ pages 9-11) | Hauser & Horie 2010, Plant, Cell & Environment, https://doi.org/10.1111/j.1365-3040.2009.02056.x (hauser2010aconservedprimary pages 5-6, hauser2010aconservedprimary pages 2-3) |
| Cellular Component | Plasma membrane, especially in root vascular/xylem parenchyma stelar cells where active Na+ retrieval occurs | Cell-type-resolved electrophysiology in stelar cells; GFP-marked vascular cells; microscopy and localization evidence summarized from primary studies | AtHKT1;1 currents were measured directly in root stelar cells; protein is described as localized to the plasma membrane of xylem parenchyma; expression is vascular-preferential and associated with xylem and phloem adjacent tissues (xue2011athkt1;1mediatesnernstian pages 1-2, hauser2010aconservedprimary pages 2-3, pardo2011na+andk+ pages 9-11) | Strong CC annotation: plasma membrane. More specific placement in xylem parenchyma plasma membrane is well supported in Arabidopsis; avoid unsupported annotations to cytosol, nucleus, or organelles (xue2011athkt1;1mediatesnernstian pages 1-2, waters2013planthighaffinitypotassium pages 5-7) | Xue et al. 2011, PLoS ONE, https://doi.org/10.1371/journal.pone.0024725; corroborating localization evidence summarized in Hauser & Horie 2010, Plant, Cell & Environment, https://doi.org/10.1111/j.1365-3040.2009.02056.x (xue2011athkt1;1mediatesnernstian pages 1-2, hauser2010aconservedprimary pages 2-3, pardo2011na+andk+ pages 9-11) |
| Regulation/Maturation | Post-translational negative regulation of HKT1;1 protein stability by SOS3/CBL4 under salt and Ca2+ stress; salt triggers 26S proteasome-dependent degradation of HKT1;1 | Co-IP; BiFC mapping of SOS3-HKT1;1 interaction; HKT1:GFP and HKT1:CFP stability assays in planta; salt and Ca2+ treatments; MG132 proteasome inhibition; oocyte electrophysiology | 100 mM NaCl and 3 mM CaCl2 reduced HKT1;1 abundance; HKT1:GFP gradually disappeared within 24 h; degradation was blocked by 50 µM MG132; degradation occurred in sos1-1 and sos2-2 but was blocked in sos3-1; SOS3 interacted with an HKT1;1 cytosolic loop, while SOS3 co-expression did not alter HKT1 transport currents directly in oocytes (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 6-7, gamezarjona2024inverseregulationof pages 4-5, gamezarjona2024inverseregulationof media c615254c) | Strong evidence for regulation of localization and stability, but not for proteolytic maturation or activation cleavage of HKT1;1. GO review should prefer regulation terms over processing terms (gamezarjona2024inverseregulationof pages 1-2, gamezarjona2024inverseregulationof pages 2-3) | Gámez-Arjona et al. 2024, PNAS, https://doi.org/10.1073/pnas.2320657121 (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 6-7, gamezarjona2024inverseregulationof pages 4-5, gamezarjona2024inverseregulationof media c615254c) |
| Biological Process | Seed germination under salt stress; HKT1;1 contributes to Ca2+-dependent salt tolerance during germination, linked to Na+ and K+ homeostasis and radicle-focused expression | Germination assays; promoter and reporter analysis; RT-qPCR by tissue; transgenic radicle-specific expression; ionomics; mutant analysis of hkt1 and pp2c49 | WT germination on 150 mM / 200 mM NaCl was 68.2 ± 2.8% / 2.6 ± 0.5%; hkt1 was 33.7 ± 7.3% / 1.3 ± 0.5%; 10 mM CaCl2 improved WT to 85 ± 3.8% / 27 ± 7% but not hkt1; with NaCl plus CaCl2, WT seedling Na+ was 1.99 ± 0.12 µg vs hkt1 3.1 ± 0.11 µg, and WT K+ was 1.04 ± 0.17 µg vs hkt1 0.42 ± 0.12 µg; radicle-specific HKT1;1 restored germination to 31 ± 5.6% under 200 mM NaCl (chandran2024calciumregulationof pages 3-5, chandran2024calciumregulationof pages 2-3) | Useful as a context-specific BP annotation in Arabidopsis, but not as central as vascular Na+ homeostasis. Best treated as a specialized developmental and stress context rather than the primary biological role of HKT1;1 (chandran2024calciumregulationof pages 1-2, chandran2024calciumregulationof pages 12-13) | Chandran et al. 2024, Plant Physiology, https://doi.org/10.1093/plphys/kiad651 (chandran2024calciumregulationof pages 3-5, chandran2024calciumregulationof pages 2-3, chandran2024calciumregulationof pages 1-2, chandran2024calciumregulationof pages 12-13) |
| Regulation/Maturation | PP2C49 negatively regulates HKT1;1 function during germination, and Ca2+ relieves this inhibition by reducing PP2C49 expression | Mutant germination assays; ionomics; RT-qPCR and GUS; transcriptomics | pp2c49 mutants germinated better than WT on 200 mM NaCl: 28 ± 8.16%, 26.75 ± 5.7%, and 41.5 ± 8.1% vs WT 2.6 ± 0.5%; under NaCl, pp2c49-1 had lower Na+ (1.77 ± 0.3 µg vs WT 2.34 ± 0.28 µg) and higher K+ (1.6 ± 0.27 µg vs WT 0.55 ± 0.07 µg); PP2C49 transcript decreased −3.29-fold with CaCl2 in transcriptome analysis using FC cutoff ** | 1.25 | ** and P ≤ 0.05 (chandran2024calciumregulationof pages 5-7) |
Table: This table summarizes the strongest GO-relevant evidence for Arabidopsis HKT1;1 across molecular function, biological process, cellular component, and regulation. It separates core annotations from context-specific regulatory findings useful for annotation review.
| Potential GO annotation (MF/BP/CC) | Support level | Evidence summary | Common over-extensions/pitfalls | Recommended curation note |
|---|---|---|---|---|
| Na+ transmembrane transport (MF) | Strong | In vivo patch clamp in Arabidopsis root stelar cells showed AtHKT1;1-dependent Na+ currents absent in athkt1;1 mutants, with Nernstian shifts in reversal potential; heterologous systems also support predominant Na+ transport (xue2011athkt1;1mediatesnernstian pages 1-2, hauser2010aconservedprimary pages 5-6) | Mislabeling as generic cation or K+ transporter because of HKT family name/history | Curate as sodium ion transmembrane transporter activity; this is the best-supported core molecular function |
| K+ transport (MF) | Weak | K+ currents were indistinguishable between WT and athkt1;1 stelar cells, arguing against a primary K+ transport role in planta; K+ phenotypes appear secondary to Na+ homeostasis changes (xue2011athkt1;1mediatesnernstian pages 1-2, hauser2010aconservedprimary pages 5-6) | Inferring direct K+ transport from altered shoot/root K+ content under salt stress | Avoid direct K+ transporter annotation unless tied to clearly qualified indirect/homeostatic effects |
| Na+/K+ symport (MF) | Weak | Some heterologous assays/reviews note Na+/K+ symport under certain expression conditions, but Arabidopsis in planta evidence supports predominant Na+ selectivity and channel-like Na+ conductance (waters2013planthighaffinitypotassium pages 3-5, waters2013planthighaffinitypotassium pages 5-7, xue2011athkt1;1mediatesnernstian pages 1-2) | Treating heterologous-system behavior as definitive for native Arabidopsis function | If retained at all, annotate only with caution and note strong context dependence; not preferred as core MF |
| Xylem Na+ unloading / retrieval from xylem sap (BP) | Strong | Mutant and physiological evidence consistently support removal of Na+ from xylem sap, limiting shoot Na+ accumulation and protecting leaves under salinity (hauser2010aconservedprimary pages 5-6, hauser2010aconservedprimary pages 2-3, pardo2011na+andk+ pages 9-11) | Replacing direct transport activity terms with overly broad “salt tolerance” only | Curate as a core biological process role linked to long-distance Na+ distribution and shoot Na+ exclusion |
| Phloem Na+ loading / shoot-to-root Na+ recirculation (BP) | Moderate | Historical Arabidopsis models and reviews support phloem recirculation, but later literature emphasizes xylem retrieval as the least controversial principal role; evidence remains more interpretive than for xylem unloading (hauser2010aconservedprimary pages 2-3, waters2013planthighaffinitypotassium pages 3-5, waters2013planthighaffinitypotassium pages 15-18) | Elevating a debated transport-route model to sole or primary function | If annotated, qualify as supported but more controversial/contextual than xylem Na+ unloading |
| Seed germination under salt stress (BP) | Moderate | 2024 work showed hkt1 mutants are hypersensitive during germination, Ca2+ rescue depends on HKT1;1, and radicle-focused HKT1;1 expression improves germination and ion balance under salt (chandran2024calciumregulationof pages 3-5, chandran2024calciumregulationof pages 2-3, chandran2024calciumregulationof pages 1-2) | Promoting a developmental-stage-specific phenotype to the universal main role of HKT1;1 | Curate as context-specific salt-stress/germination role, not the primary species-wide function |
| Plasma membrane (CC) | Strong | HKT1;1 is localized to the plasma membrane of vascular/stelar/xylem parenchyma-associated cells, consistent with direct Na+ retrieval from xylem sap (xue2011athkt1;1mediatesnernstian pages 1-2, hauser2010aconservedprimary pages 2-3, pardo2011na+andk+ pages 9-11) | Using only “membrane” without specificity, or shifting to unsupported endomembrane/organelle locations | Curate as plasma membrane; where evidence model allows, note vascular/xylem parenchyma context |
| Cytosol / nucleus / chloroplast (CC) | Not supported | No gathered Arabidopsis evidence supports active AtHKT1;1 localization to cytosol, nucleus, or chloroplast; chloroplast HKT evidence is from a distant moss homolog and is not transferable to AtHKT1;1 (xue2011athkt1;1mediatesnernstian pages 1-2, waters2013planthighaffinitypotassium pages 5-7) | Transferring subcellular localizations across distant HKT homologs or from non-Arabidopsis systems | Do not annotate AtHKT1;1 to cytosol, nucleus, or chloroplast |
| Protein processing / proteolytic maturation (BP/MF) | Not supported | Recent evidence supports regulated degradation of HKT1;1, not proteolytic maturation or activating processing; no cleavage-dependent maturation mechanism was identified (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 1-2) | Confusing regulated turnover with maturation/processing annotations | Avoid protein maturation or proteolytic processing terms for HKT1;1 |
| Regulation via SOS3/CBL4-dependent proteasomal degradation (regulatory BP) | Strong | SOS3 physically interacts with HKT1;1, salt and Ca2+ reduce HKT1;1 abundance, MG132 blocks degradation, and degradation is lost in sos3 backgrounds, supporting SOS3-dependent 26S proteasome-mediated turnover (gamezarjona2024inverseregulationof pages 5-6, gamezarjona2024inverseregulationof pages 6-7, gamezarjona2024inverseregulationof pages 4-5, gamezarjona2024inverseregulationof media c615254c) | Misstating SOS3 as directly activating HKT1;1 transport rather than regulating abundance/stability | Curate as post-translational negative regulation of HKT1;1 stability/localization under salt/Ca2+ stress |
| PP2C49 regulation of HKT1;1 (regulatory BP) | Moderate | Germination-stage evidence indicates PP2C49 negatively regulates HKT1;1-associated salt tolerance and ion homeostasis; pp2c49 mutants germinate better and show improved ion profiles under salt (chandran2024calciumregulationof pages 5-7, chandran2024calciumregulationof pages 1-2) | Generalizing a germination-focused regulatory module to all tissues and life stages | Curate as context-specific negative regulation in germination/salt-response settings |
| Apoptosis / developmental cell death / neuronal / inflammatory / pyroptosis / synaptic remodeling (BP) | Not supported | No evidence in the gathered Arabidopsis HKT1;1 literature links this plant Na+ transporter to animal-like death, neuronal, immune-inflammatory, pyroptotic, or synaptic processes (hauser2010aconservedprimary pages 5-6, xue2011athkt1;1mediatesnernstian pages 1-2, chandran2024calciumregulationof pages 3-5) | Annotation drift from unrelated eukaryotic vocabularies or text-mining noise | Exclude these annotations entirely for AtHKT1;1 |
| Broad “salt tolerance” without mechanistic qualifier (BP) | Moderate | HKT1;1 clearly affects salt tolerance phenotypes, but the mechanistic basis is specifically Na+ distribution/homeostasis via vascular transport and regulation of shoot Na+ accumulation (hauser2010aconservedprimary pages 5-6, hauser2010aconservedprimary pages 2-3, gamezarjona2024inverseregulationof pages 5-6) | Using only broad stress-response labels and losing the direct process/mechanism | Prefer mechanistically specific BP terms over generic salt-tolerance annotations |
Table: This table summarizes the evidence strength and curation risks for likely GO annotations of Arabidopsis HKT1;1. It distinguishes strongly supported core functions from context-specific, controversial, or unsupported annotations to help prevent over-extension during review.
Across the retrieved Arabidopsis-focused sources, there is no support for HKT1;1 annotations related to apoptosis, pyroptosis, neuronal/synaptic remodeling, or inflammatory signaling, nor for localization to nucleus or cytosolic signaling complexes. These concepts are inconsistent with the experimentally supported identity of HKT1;1 as a plasma-membrane Na(+) transporter in vascular tissues (xue2011athkt1;1mediatesnernstian pages 1-2, chandran2024calciumregulationof pages 3-5).
This report is constrained to the papers successfully retrieved in-tool. Several classic primary papers on Arabidopsis HKT1;1 (e.g., xylem unloading genetics/localization studies often cited from mid-2000s) were not directly obtainable here, so GO reviewers may wish to consult those originals for additional localization granularity (e.g., immunolocalization and tissue-specific promoter data) beyond what is summarized in the available reviews (hauser2010aconservedprimary pages 2-3, waters2013planthighaffinitypotassium pages 3-5).
References
(xue2011athkt1;1mediatesnernstian pages 1-2): Shaowu Xue, Xuan Yao, Wei Luo, Deepa Jha, Mark Tester, Tomoaki Horie, and Julian I. Schroeder. Athkt1;1 mediates nernstian sodium channel transport properties in arabidopsis root stelar cells. PLoS ONE, 6:e24725, Sep 2011. URL: https://doi.org/10.1371/journal.pone.0024725, doi:10.1371/journal.pone.0024725. This article has 84 citations and is from a peer-reviewed journal.
(hauser2010aconservedprimary pages 5-6): Felix Hauser and Tomoaki Horie. A conserved primary salt tolerance mechanism mediated by hkt transporters: a mechanism for sodium exclusion and maintenance of high k(+)/na(+) ratio in leaves during salinity stress. Plant, cell & environment, 33 4:552-65, Apr 2010. URL: https://doi.org/10.1111/j.1365-3040.2009.02056.x, doi:10.1111/j.1365-3040.2009.02056.x. This article has 677 citations.
(gamezarjona2024inverseregulationof pages 5-6): Francisco Gámez-Arjona, Hee Jin Park, Elena García, Rashid Aman, Irene Villalta, Natalia Raddatz, Raul Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng-Yi Xu, Armando Albert, Woe-Yeon Kim, Jose M. Pardo, Clara Sánchez-Rodriguez, Dae-Jin Yun, and Francisco J. Quintero. Inverse regulation of sos1 and hkt1 protein localization and stability by sos3/cbl4 in arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America, Feb 2024. URL: https://doi.org/10.1073/pnas.2320657121, doi:10.1073/pnas.2320657121. This article has 45 citations and is from a highest quality peer-reviewed journal.
(gamezarjona2024inverseregulationof pages 6-7): Francisco Gámez-Arjona, Hee Jin Park, Elena García, Rashid Aman, Irene Villalta, Natalia Raddatz, Raul Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng-Yi Xu, Armando Albert, Woe-Yeon Kim, Jose M. Pardo, Clara Sánchez-Rodriguez, Dae-Jin Yun, and Francisco J. Quintero. Inverse regulation of sos1 and hkt1 protein localization and stability by sos3/cbl4 in arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America, Feb 2024. URL: https://doi.org/10.1073/pnas.2320657121, doi:10.1073/pnas.2320657121. This article has 45 citations and is from a highest quality peer-reviewed journal.
(gamezarjona2024inverseregulationof media c615254c): Francisco Gámez-Arjona, Hee Jin Park, Elena García, Rashid Aman, Irene Villalta, Natalia Raddatz, Raul Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng-Yi Xu, Armando Albert, Woe-Yeon Kim, Jose M. Pardo, Clara Sánchez-Rodriguez, Dae-Jin Yun, and Francisco J. Quintero. Inverse regulation of sos1 and hkt1 protein localization and stability by sos3/cbl4 in arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America, Feb 2024. URL: https://doi.org/10.1073/pnas.2320657121, doi:10.1073/pnas.2320657121. This article has 45 citations and is from a highest quality peer-reviewed journal.
(chandran2024calciumregulationof pages 2-3): Ancy E J Chandran, Aliza Finkler, Tom Aharon Hait, Yvonne Kiere, Sivan David, Metsada Pasmanik-Chor, and Doron Shkolnik. Calcium regulation of the arabidopsis na+/k+ transporter hkt1;1 improves seed germination under salt stress. Plant Physiology, 194:1834-1852, Dec 2024. URL: https://doi.org/10.1093/plphys/kiad651, doi:10.1093/plphys/kiad651. This article has 21 citations and is from a highest quality peer-reviewed journal.
(chandran2024calciumregulationof pages 5-7): Ancy E J Chandran, Aliza Finkler, Tom Aharon Hait, Yvonne Kiere, Sivan David, Metsada Pasmanik-Chor, and Doron Shkolnik. Calcium regulation of the arabidopsis na+/k+ transporter hkt1;1 improves seed germination under salt stress. Plant Physiology, 194:1834-1852, Dec 2024. URL: https://doi.org/10.1093/plphys/kiad651, doi:10.1093/plphys/kiad651. This article has 21 citations and is from a highest quality peer-reviewed journal.
(chandran2024calciumregulationof pages 3-5): Ancy E J Chandran, Aliza Finkler, Tom Aharon Hait, Yvonne Kiere, Sivan David, Metsada Pasmanik-Chor, and Doron Shkolnik. Calcium regulation of the arabidopsis na+/k+ transporter hkt1;1 improves seed germination under salt stress. Plant Physiology, 194:1834-1852, Dec 2024. URL: https://doi.org/10.1093/plphys/kiad651, doi:10.1093/plphys/kiad651. This article has 21 citations and is from a highest quality peer-reviewed journal.
(pardo2011na+andk+ pages 9-11): José M. Pardo and Francisco Rubio. Na+ and k+ transporters in plant signaling. ArXiv, pages 65-98, Sep 2011. URL: https://doi.org/10.1007/978-3-642-14369-4_3, doi:10.1007/978-3-642-14369-4_3. This article has 75 citations.
(waters2013planthighaffinitypotassium pages 3-5): Shane Waters, Matthew Gilliham, and Maria Hrmova. Plant high-affinity potassium (hkt) transporters involved in salinity tolerance: structural insights to probe differences in ion selectivity. International Journal of Molecular Sciences, 14:7660-7680, Apr 2013. URL: https://doi.org/10.3390/ijms14047660, doi:10.3390/ijms14047660. This article has 161 citations.
(gamezarjona2024inverseregulationof pages 1-2): Francisco Gámez-Arjona, Hee Jin Park, Elena García, Rashid Aman, Irene Villalta, Natalia Raddatz, Raul Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng-Yi Xu, Armando Albert, Woe-Yeon Kim, Jose M. Pardo, Clara Sánchez-Rodriguez, Dae-Jin Yun, and Francisco J. Quintero. Inverse regulation of sos1 and hkt1 protein localization and stability by sos3/cbl4 in arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America, Feb 2024. URL: https://doi.org/10.1073/pnas.2320657121, doi:10.1073/pnas.2320657121. This article has 45 citations and is from a highest quality peer-reviewed journal.
(hauser2010aconservedprimary pages 2-3): Felix Hauser and Tomoaki Horie. A conserved primary salt tolerance mechanism mediated by hkt transporters: a mechanism for sodium exclusion and maintenance of high k(+)/na(+) ratio in leaves during salinity stress. Plant, cell & environment, 33 4:552-65, Apr 2010. URL: https://doi.org/10.1111/j.1365-3040.2009.02056.x, doi:10.1111/j.1365-3040.2009.02056.x. This article has 677 citations.
(chandran2024calciumregulationof pages 1-2): Ancy E J Chandran, Aliza Finkler, Tom Aharon Hait, Yvonne Kiere, Sivan David, Metsada Pasmanik-Chor, and Doron Shkolnik. Calcium regulation of the arabidopsis na+/k+ transporter hkt1;1 improves seed germination under salt stress. Plant Physiology, 194:1834-1852, Dec 2024. URL: https://doi.org/10.1093/plphys/kiad651, doi:10.1093/plphys/kiad651. This article has 21 citations and is from a highest quality peer-reviewed journal.
(gamezarjona2024inverseregulationof pages 4-5): Francisco Gámez-Arjona, Hee Jin Park, Elena García, Rashid Aman, Irene Villalta, Natalia Raddatz, Raul Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng-Yi Xu, Armando Albert, Woe-Yeon Kim, Jose M. Pardo, Clara Sánchez-Rodriguez, Dae-Jin Yun, and Francisco J. Quintero. Inverse regulation of sos1 and hkt1 protein localization and stability by sos3/cbl4 in arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America, Feb 2024. URL: https://doi.org/10.1073/pnas.2320657121, doi:10.1073/pnas.2320657121. This article has 45 citations and is from a highest quality peer-reviewed journal.
(xue2011athkt1;1mediatesnernstian pages 8-9): Shaowu Xue, Xuan Yao, Wei Luo, Deepa Jha, Mark Tester, Tomoaki Horie, and Julian I. Schroeder. Athkt1;1 mediates nernstian sodium channel transport properties in arabidopsis root stelar cells. PLoS ONE, 6:e24725, Sep 2011. URL: https://doi.org/10.1371/journal.pone.0024725, doi:10.1371/journal.pone.0024725. This article has 84 citations and is from a peer-reviewed journal.
(waters2013planthighaffinitypotassium pages 5-7): Shane Waters, Matthew Gilliham, and Maria Hrmova. Plant high-affinity potassium (hkt) transporters involved in salinity tolerance: structural insights to probe differences in ion selectivity. International Journal of Molecular Sciences, 14:7660-7680, Apr 2013. URL: https://doi.org/10.3390/ijms14047660, doi:10.3390/ijms14047660. This article has 161 citations.
(gamezarjona2024inverseregulationof pages 2-3): Francisco Gámez-Arjona, Hee Jin Park, Elena García, Rashid Aman, Irene Villalta, Natalia Raddatz, Raul Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng-Yi Xu, Armando Albert, Woe-Yeon Kim, Jose M. Pardo, Clara Sánchez-Rodriguez, Dae-Jin Yun, and Francisco J. Quintero. Inverse regulation of sos1 and hkt1 protein localization and stability by sos3/cbl4 in arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America, Feb 2024. URL: https://doi.org/10.1073/pnas.2320657121, doi:10.1073/pnas.2320657121. This article has 45 citations and is from a highest quality peer-reviewed journal.
(chandran2024calciumregulationof pages 12-13): Ancy E J Chandran, Aliza Finkler, Tom Aharon Hait, Yvonne Kiere, Sivan David, Metsada Pasmanik-Chor, and Doron Shkolnik. Calcium regulation of the arabidopsis na+/k+ transporter hkt1;1 improves seed germination under salt stress. Plant Physiology, 194:1834-1852, Dec 2024. URL: https://doi.org/10.1093/plphys/kiad651, doi:10.1093/plphys/kiad651. This article has 21 citations and is from a highest quality peer-reviewed journal.
(waters2013planthighaffinitypotassium pages 15-18): Shane Waters, Matthew Gilliham, and Maria Hrmova. Plant high-affinity potassium (hkt) transporters involved in salinity tolerance: structural insights to probe differences in ion selectivity. International Journal of Molecular Sciences, 14:7660-7680, Apr 2013. URL: https://doi.org/10.3390/ijms14047660, doi:10.3390/ijms14047660. This article has 161 citations.
AtHKT1;1 is the single HKT-family member in Arabidopsis thaliana. It is a Class I
HKT transporter that functions in planta as a Na+-selective uniporter in the
plasma membrane. Its physiological role is Na+ retrieval/recirculation: it unloads
Na+ from the xylem sap into xylem-parenchyma cells (and is also implicated in Na+
loading into phloem in shoots / unloading in roots), thereby limiting Na+ accumulation
in photosynthetic shoot tissue and conferring salt tolerance. It does NOT transport
K+ in planta; the "high-affinity K+ transporter" name is historical, inherited from
the wheat ortholog (TaHKT1), and does not reflect the Arabidopsis protein's selectivity.
The K+ molecular-function and K+-transport process annotations (GO:0015079, GO:0006813,
GO:0071805) are electronic (IEA InterPro/ARBA) inherited from the HKT/Trk/Ktr family
and from the wheat ortholog's high-affinity K+ behavior. The Arabidopsis protein is
Na+-selective; UniProt explicitly states it "does not transport K(+)" and the lone
Gly-68 absence is the structural explanation. These are therefore mapped toward the
Na+ counterparts (MODIFY) or marked as over-annotation rather than accepted, but not
blanket-removed as "wrong gene." The one TAIR IMP K+ annotation (GO:0006813,
PMID:16359386) reflects the indirect K+ effect ("K+ transport may be indirectly
affected") — kept as non-core / over-annotated since it is a downstream/indirect
consequence, not a direct K+ transport function.
id: Q84TI7
gene_symbol: HKT1
product_type: PROTEIN
status: INITIALIZED
taxon:
id: NCBITaxon:3702
label: Arabidopsis thaliana
description: >-
AtHKT1;1 (HKT1, At4g10310) is a plasma-membrane cation transporter of the
HKT/Trk/Ktr superfamily and the sole HKT-family member in Arabidopsis thaliana.
It is a Class I HKT transporter that functions in planta as a sodium-selective
uniporter. Its central physiological role is sodium retrieval and recirculation;
it unloads Na+ from the xylem sap into xylem-parenchyma cells (and is implicated
in Na+ loading into the phloem in shoots and unloading in roots), thereby
limiting Na+ accumulation in photosynthetic shoot tissues and conferring
tolerance to salt stress. The protein has a K-channel-like four
transmembrane-pore-transmembrane architecture but, unlike potassium channels,
lacks a conserved glycine in its first pore loop (position 68), which accounts
for its selectivity for Na+ over K+; in planta it does not transport K+ and
instead influences K+/Na+ balance indirectly through its effect on Na+
homeostasis. AtHKT1;1 is expressed in vascular tissues of all organs,
predominantly in the phloem and in xylem-parenchyma cells, and its locus
underlies natural variation in leaf Na+ content among Arabidopsis accessions.
existing_annotations:
- term:
id: GO:0005886
label: plasma membrane
evidence_type: IEA
original_reference_id: GO_REF:0000044
qualifier: located_in
review:
summary: Electronic subcellular-location mapping placing HKT1 at the plasma membrane.
action: ACCEPT
reason: Plasma membrane is the correct and core localization, independently confirmed by direct immunoelectron microscopy of AtHKT1 in xylem-parenchyma cells (PMID:16359386). This IEA annotation is consistent with the curated UniProt subcellular location.
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: Plasma membrane (cell membrane), multi-pass membrane protein
- term:
id: GO:0006812
label: monoatomic cation transport
evidence_type: IEA
original_reference_id: GO_REF:0000002
qualifier: involved_in
review:
summary: Family-level electronic annotation to a generic cation-transport term.
action: MODIFY
reason: Correct in essence (HKT1 transports a monovalent cation) but too general. The physiologically relevant species transported in planta is Na+, so a sodium ion transport term is more informative.
proposed_replacement_terms:
- id: GO:0006814
label: sodium ion transport
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: It is a Class I HKT transporter that functions in planta as a Na+-selective uniporter
- term:
id: GO:0006813
label: potassium ion transport
evidence_type: IEA
original_reference_id: GO_REF:0000117
qualifier: involved_in
review:
summary: ARBA machine-learning electronic annotation to potassium ion transport.
action: MARK_AS_OVER_ANNOTATED
reason: This is a family/name-derived electronic inference. The Arabidopsis protein is Na+-selective and does not transport K+ in planta; UniProt states it "Does not transport K(+)". The K+-related function is at most an indirect consequence of Na+ homeostasis, so direct K+ transport is an over-annotation rather than the gene's activity.
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: it lacks a conserved Gly at position 68, explaining why it does not act as a K(+) transporter
- term:
id: GO:0008324
label: monoatomic cation transmembrane transporter activity
evidence_type: IEA
original_reference_id: GO_REF:0000002
qualifier: enables
review:
summary: Family-level electronic molecular-function annotation to generic cation transporter activity.
action: MODIFY
reason: Correct but too general. The experimentally demonstrated and core molecular function is sodium ion transmembrane transporter activity; replace the generic parent with the specific Na+ term.
proposed_replacement_terms:
- id: GO:0015081
label: sodium ion transmembrane transporter activity
supported_by:
- reference_id: PMID:10759522
supporting_text: AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
- term:
id: GO:0015079
label: potassium ion transmembrane transporter activity
evidence_type: IEA
original_reference_id: GO_REF:0000002
qualifier: enables
review:
summary: InterPro family-level electronic annotation of potassium ion transmembrane transporter activity.
action: MARK_AS_OVER_ANNOTATED
reason: This K+-specific molecular-function term is inherited from the HKT/Trk/Ktr family signature and the wheat ortholog's high-affinity K+ behavior, but AtHKT1;1 is Na+-selective and does NOT transport K+ in planta (it lacks the conserved Gly-68 of K+-permeable HKTs; only a <2-fold K+ effect in heterologous systems). The potassium transport function is therefore an over-annotation. The correct Na+ molecular function is captured separately by the ACCEPTed GO:0015081 (sodium ion transmembrane transporter activity, IDA), so this K+ term is flagged as over-annotated rather than re-pointed at the Na+ term — consistent with the three parallel K+ biological-process annotations in this file, which are likewise marked as over-annotated.
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: it lacks a conserved Gly at position 68, explaining why it does not act as a K(+) transporter
- reference_id: file:ARATH/HKT1/HKT1-deep-research-falcon.md
supporting_text: K+ currents were indistinguishable between WT and athkt1;1 stelar cells, arguing against a primary K+ transport role in planta
- term:
id: GO:0016020
label: membrane
evidence_type: IEA
original_reference_id: GO_REF:0000120
qualifier: located_in
review:
summary: Generic membrane localization from combined automated methods.
action: MODIFY
reason: Correct but uninformatively general; the specific and supported location is the plasma membrane.
proposed_replacement_terms:
- id: GO:0005886
label: plasma membrane
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: Plasma membrane (cell membrane), multi-pass membrane protein
- term:
id: GO:0035725
label: sodium ion transmembrane transport
evidence_type: IEA
original_reference_id: GO_REF:0000108
qualifier: involved_in
review:
summary: Electronic annotation (inter-ontology link from MF GO:0015081) to the sodium ion transmembrane transport process.
action: ACCEPT
reason: This accurately captures the core in-planta process; HKT1 mediates Na+ movement across the plasma membrane. Supported by direct functional and genetic evidence.
supported_by:
- reference_id: PMID:10759522
supporting_text: AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
- term:
id: GO:0046873
label: metal ion transmembrane transporter activity
evidence_type: IEA
original_reference_id: GO_REF:0000117
qualifier: enables
review:
summary: ARBA electronic annotation to generic metal ion transmembrane transporter activity.
action: MODIFY
reason: Correct (Na+ is a metal ion) but too general. The specific, experimentally supported molecular function is sodium ion transmembrane transporter activity.
proposed_replacement_terms:
- id: GO:0015081
label: sodium ion transmembrane transporter activity
supported_by:
- reference_id: PMID:10759522
supporting_text: AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
- term:
id: GO:0055085
label: transmembrane transport
evidence_type: IEA
original_reference_id: GO_REF:0000002
qualifier: involved_in
review:
summary: Family-level electronic annotation to the most generic transport process term.
action: MODIFY
reason: Correct but far too general to be informative; replace with the specific sodium ion transmembrane transport process.
proposed_replacement_terms:
- id: GO:0035725
label: sodium ion transmembrane transport
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: It is a Class I HKT transporter that functions in planta as a Na+-selective uniporter
- term:
id: GO:0071805
label: potassium ion transmembrane transport
evidence_type: IEA
original_reference_id: GO_REF:0000002
qualifier: involved_in
review:
summary: InterPro family-level electronic annotation to potassium ion transmembrane transport.
action: MARK_AS_OVER_ANNOTATED
reason: Family/name-derived electronic inference. AtHKT1;1 does not transport K+ in planta; any K+ effect is indirect via Na+ homeostasis. Direct K+ transmembrane transport is an over-annotation. The biologically relevant process is sodium ion transmembrane transport (already annotated via GO:0035725).
supported_by:
- reference_id: file:ARATH/HKT1/HKT1-notes.md
supporting_text: it lacks a conserved Gly at position 68, explaining why it does not act as a K(+) transporter
- reference_id: file:ARATH/HKT1/HKT1-deep-research-falcon.md
supporting_text: K+ currents were indistinguishable between WT and athkt1;1 stelar cells, arguing against a primary K+ transport role in planta
- term:
id: GO:0005739
label: mitochondrion
evidence_type: ISM
original_reference_id: GO_REF:0000122
qualifier: located_in
review:
summary: Sequence-based (AtSubP) prediction placing HKT1 in the mitochondrion.
action: REMOVE
reason: This is a purely computational (ISM) subcellular-localization prediction, not experimental evidence. It is contradicted by direct immunoelectron microscopy and promoter-GUS data localizing AtHKT1 to the plasma membrane of xylem-parenchyma cells, and by the curated UniProt cell-membrane location. The mitochondrial prediction is a clearly-wrong electronic annotation.
supported_by:
- reference_id: PMID:16359386
supporting_text: AtHKT1 is targeted to the plasma membrane in xylem parenchyma cells in leaves
- term:
id: GO:0006814
label: sodium ion transport
evidence_type: IMP
original_reference_id: PMID:15486089
qualifier: acts_upstream_of_or_within
review:
summary: Mutant phenotype (FN1148 AtHKT1 deletion) showing altered shoot/root Na+ distribution, supporting a role in sodium ion transport.
action: ACCEPT
reason: Experimental IMP evidence; the 523-bp AtHKT1 deletion causes shoot Na+ overaccumulation and root Na+ underaccumulation, and AtHKT1 cDNA complements the salt sensitivity, directly tying HKT1 to in-planta Na+ transport. Core process.
supported_by:
- reference_id: PMID:15486089
supporting_text: the deletion within the AtHKT1 gene is responsible for the sodium overaccumulation in shoots and leaf sodium sensitivity of the FN1148 mutant
- term:
id: GO:0009651
label: response to salt stress
evidence_type: IGI
original_reference_id: PMID:11698666
qualifier: acts_upstream_of_or_within
review:
summary: Genetic interaction (hkt1 suppresses sos3-1 salt hypersensitivity) establishing HKT1 as a salt-tolerance determinant.
action: ACCEPT
reason: Experimental IGI evidence; hkt1 loss-of-function mutations suppress NaCl hypersensitivity of sos3-1 and alter intracellular Na+/K+, defining HKT1 as a salt-tolerance determinant. This is a core biological process for the gene.
supported_by:
- reference_id: PMID:11698666
supporting_text: AtHKT1 is a salt tolerance determinant that controls Na + entry
- term:
id: GO:0005886
label: plasma membrane
evidence_type: IDA
original_reference_id: PMID:16359386
qualifier: located_in
review:
summary: Direct immunoelectron microscopy localizing AtHKT1 to the plasma membrane of xylem-parenchyma cells.
action: ACCEPT
reason: Direct experimental evidence (IDA) for the core and correct subcellular localization. Strongest support among the plasma-membrane annotations.
supported_by:
- reference_id: PMID:16359386
supporting_text: AtHKT1 is targeted to the plasma membrane in xylem parenchyma cells in leaves
- reference_id: file:ARATH/HKT1/HKT1-deep-research-falcon.md
supporting_text: AtHKT1;1 is supported as a **plasma membrane** protein active in **root stelar/vascular cells** (often described as xylem-parenchyma associated)
- term:
id: GO:0006813
label: potassium ion transport
evidence_type: IMP
original_reference_id: PMID:16359386
qualifier: acts_upstream_of_or_within
review:
summary: Mutant-phenotype annotation to potassium ion transport based on altered xylem K+ content in athkt1 alleles.
action: MARK_AS_OVER_ANNOTATED
reason: This TAIR IMP annotation reflects an indirect, secondary effect on K+, not direct K+ transport by HKT1. The paper itself states the influence on K+ is smaller, inverse, and that "K+ transport may be indirectly affected". Annotating HKT1 to potassium ion transport over-states an indirect downstream consequence as a transport function; the gene does not transport K+ in planta. (The annotation is not removed because it rests on an experimental phenotype, but the K+-transport term is an over-annotation.)
supported_by:
- reference_id: PMID:16359386
supporting_text: suggesting that K+ transport may be indirectly affected
- term:
id: GO:0006814
label: sodium ion transport
evidence_type: IMP
original_reference_id: PMID:16359386
qualifier: acts_upstream_of_or_within
review:
summary: Mutant-phenotype evidence that athkt1 alleles increase xylem-sap Na+ and reduce phloem-sap Na+, supporting HKT1's role in Na+ transport.
action: ACCEPT
reason: Experimental IMP evidence for the core in-planta process; disruption alters Na+ distribution between xylem and phloem and across shoot/root.
supported_by:
- reference_id: PMID:16359386
supporting_text: AtHKT1 disruption alleles caused large increases in the Na+ content of the xylem sap and conversely reduced the Na+ content of the phloem sap
- term:
id: GO:0006970
label: response to osmotic stress
evidence_type: IEP
original_reference_id: PMID:16359386
qualifier: acts_upstream_of_or_within
review:
summary: Expression-pattern (IEP) annotation; AtHKT1 expression is modulated by osmolality of non-ionic compounds.
action: KEEP_AS_NON_CORE
reason: Supported by the cited paper (AtHKT1 expression responds to non-ionic osmolality and AtHKT1 mediates osmolality balance between xylem vessels and parenchyma). This is a real but peripheral aspect relative to the gene's core Na+-transport / salt-tolerance role; retain as non-core. IEP is expression-based, not a demonstration of involvement in osmotic-stress response per se.
supported_by:
- reference_id: PMID:16359386
supporting_text: The expression of AtHKT1 was modulated not only by the concentrations of Na+ and K+ but also by the osmolality of non-ionic compounds
- term:
id: GO:0009651
label: response to salt stress
evidence_type: IMP
original_reference_id: PMID:12727868
qualifier: acts_upstream_of_or_within
review:
summary: Mutant-phenotype evidence (sas2-1/sas2-2 = AtHKT1) that disruption increases NaCl sensitivity, establishing a role in salt-stress response.
action: ACCEPT
reason: Experimental IMP evidence; sas2 (athkt1) plants show increased NaCl sensitivity with reduced growth and death under moderate salinity, demonstrating HKT1's core role in salt-stress tolerance via Na+ recirculation.
supported_by:
- reference_id: PMID:12727868
supporting_text: The sas2 plants displayed increased sensitivity to NaCl, with reduced growth and even death under moderate salinity
- term:
id: GO:0006814
label: sodium ion transport
evidence_type: IDA
original_reference_id: PMID:10759522
qualifier: acts_upstream_of_or_within
review:
summary: Direct functional evidence that AtHKT1 mediates inward Na+ currents in Xenopus oocytes and Na+ uptake in yeast.
action: ACCEPT
reason: Direct assay (IDA) demonstrating Na+ transport activity; core function.
supported_by:
- reference_id: PMID:10759522
supporting_text: AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes
- term:
id: GO:0015081
label: sodium ion transmembrane transporter activity
evidence_type: IDA
original_reference_id: PMID:10759522
qualifier: enables
review:
summary: Direct electrophysiological evidence that AtHKT1 enables selective Na+ transmembrane transport.
action: ACCEPT
reason: Direct assay (IDA) establishing the core molecular function; selective Na+ uniport, independent of external K+. This is the primary, correct molecular function and the target term for the over-general and K+ MF annotations above.
supported_by:
- reference_id: PMID:10759522
supporting_text: AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes, and the presence of external K + did not affect the AtHKT1-mediated ion conductance
- reference_id: file:ARATH/HKT1/HKT1-deep-research-falcon.md
supporting_text: encodes a **plasma-membrane Na\(\+\)-selective transporter** that functions predominantly in **root vascular (stelar/xylem-parenchyma) cells**
core_functions:
- description: Functions as a sodium-selective plasma-membrane transporter (Na+ uniporter) that mediates Na+ movement across the plasma membrane; does not transport K+ in planta
supported_by:
- reference_id: PMID:10759522
supporting_text: AtHKT1 functioned as a selective Na + uptake transporter in Xenopus laevis oocytes, and the presence of external K + did not affect the AtHKT1-mediated ion conductance
molecular_function:
id: GO:0015081
label: sodium ion transmembrane transporter activity
directly_involved_in:
- id: GO:0035725
label: sodium ion transmembrane transport
locations:
- id: GO:0005886
label: plasma membrane
- description: Mediates Na+ retrieval and recirculation by unloading Na+ from the xylem sap into xylem-parenchyma cells and recirculating Na+ from shoots to roots, protecting photosynthetic shoot tissues from Na+ over-accumulation
supported_by:
- reference_id: PMID:16359386
supporting_text: AtHKT1 disruption alleles caused large increases in the Na+ content of the xylem sap and conversely reduced the Na+ content of the phloem sap
- reference_id: PMID:12727868
supporting_text: AtHKT1 is involved in Na + recirculation from shoots to roots
- reference_id: file:ARATH/HKT1/HKT1-deep-research-falcon.md
supporting_text: Involved in Na(+) recirculation from shoots to roots, probably by mediating Na(+) loading into the phloem sap in shoots and unloading in roots, thereby removing large amounts of Na(+) from the shoot
molecular_function:
id: GO:0015081
label: sodium ion transmembrane transporter activity
directly_involved_in:
- id: GO:0006814
label: sodium ion transport
locations:
- id: GO:0005886
label: plasma membrane
- description: Acts as a determinant of salt-stress tolerance and Na+ homeostasis; loss of function causes shoot Na+ over-accumulation and salt hypersensitivity
supported_by:
- reference_id: PMID:11698666
supporting_text: AtHKT1 is a salt tolerance determinant that controls Na + entry
- reference_id: PMID:12727868
supporting_text: The sas2 plants displayed increased sensitivity to NaCl, with reduced growth and even death under moderate salinity
directly_involved_in:
- id: GO:0009651
label: response to salt stress
- id: GO:0006814
label: sodium ion transport
references:
- id: file:ARATH/HKT1/HKT1-deep-research-falcon.md
title: "Falcon/Edison deep research report: HKT1"
findings: []
reference_review:
relevance: HIGH
correctness: VERIFIED
review_notes: "AI-generated (Falcon/Edison) deep-research synthesis used as supporting context; trace individual claims to primary literature before treating as definitive."
- id: GO_REF:0000002
title: Gene Ontology annotation through association of InterPro records with GO terms
findings: []
- id: GO_REF:0000044
title: Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
findings: []
- id: GO_REF:0000108
title: Automatic assignment of GO terms using logical inference, based on on inter-ontology links
findings: []
- id: GO_REF:0000117
title: Electronic Gene Ontology annotations created by ARBA machine learning models
findings: []
- id: GO_REF:0000120
title: Combined Automated Annotation using Multiple IEA Methods
findings: []
- id: GO_REF:0000122
title: AtSubP analysis
findings: []
- id: PMID:10759522
title: The Arabidopsis HKT1 gene homolog mediates inward Na(+) currents in xenopus laevis oocytes and Na(+) uptake in Saccharomyces cerevisiae.
findings: []
reference_review:
relevance: HIGH
correctness: VERIFIED
review_notes: PubMed-verified abstract. Directly establishes the core molecular function (selective Na+ transport, K+-independent) in heterologous systems and shows AtHKT1 differs from the wheat HKT1; only a <2-fold K+ effect in E. coli, no K+ uptake complementation in yeast.
- id: PMID:11698666
title: AtHKT1 is a salt tolerance determinant that controls Na(+) entry into plant roots.
findings: []
reference_review:
relevance: HIGH
correctness: VERIFIED
review_notes: PubMed-verified abstract. Genetic suppression of sos3-1 hypersensitivity by hkt1 establishes HKT1 as a salt-tolerance determinant. Title and abstract phrase a role in "high affinity K+ uptake", but this is an indirect K+/Na+-ratio effect, not direct K+ transport.
- id: PMID:12727868
title: Functional analysis of AtHKT1 in Arabidopsis shows that Na(+) recirculation by the phloem is crucial for salt tolerance.
findings: []
reference_review:
relevance: HIGH
correctness: VERIFIED
review_notes: Full text available and PubMed-verified. sas2-1/sas2-2 = AtHKT1; establishes phloem-restricted expression, Na+ recirculation shoot-to-root, and that AtHKT1 is NOT involved in root Na+ uptake (influx higher in mutant).
- id: PMID:15486089
title: Microarray-based rapid cloning of an ion accumulation deletion mutant in Arabidopsis thaliana.
findings: []
reference_review:
relevance: HIGH
correctness: VERIFIED
review_notes: Full text available and PubMed-verified. Independent AtHKT1 deletion allele (FN1148) confirms HKT1 controls shoot/root Na+ distribution; complementation by AtHKT1 cDNA.
- id: PMID:16359386
title: Enhanced salt tolerance mediated by AtHKT1 transporter-induced Na unloading from xylem vessels to xylem parenchyma cells.
findings: []
reference_review:
relevance: HIGH
correctness: VERIFIED
review_notes: PubMed-verified abstract. Direct IDA evidence for plasma-membrane localization in xylem-parenchyma cells and for selective Na+ unloading from xylem; explicitly notes K+ effects are indirect.