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 |
|---|---|---|---|
| GO:0005886 plasma membrane | 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 |
| 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** |
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