SOS1 (also called NHX7) is a plasma-membrane sodium/proton (Na+/H+) antiporter of the monovalent cation:proton antiporter-1 (CPA1) family. The protein has roughly twelve N-terminal transmembrane helices that form the ion-translocation domain and a large (~700 residue) cytoplasmic C-terminal tail that mediates regulation. SOS1 catalyzes electroneutral exchange of intracellular Na+ (or Li+) for extracellular H+, driven by the inwardly directed proton-motive force established by plasma-membrane H+-ATPases, thereby extruding toxic Na+ from the cytosol to the apoplast. SOS1 is expressed most strongly in root tip epidermal cells and in parenchyma cells at the xylem/symplast boundary of roots, stems and leaves, where it controls the Na+ load of the xylem sap and mediates long-distance Na+ transport between root and shoot. It is the effector of the Salt Overly Sensitive (SOS) signaling pathway, in which the calcium sensor CBL4/SOS3 activates the protein kinase CIPK24/SOS2, which phosphorylates the C-terminal autoinhibitory domain of SOS1 to relieve autoinhibition and activate transport. By exporting Na+ and helping maintain cytosolic ion and pH homeostasis, SOS1 is a principal determinant of plant salt tolerance; its activity also modulates apoplastic pH and reactive-oxygen-species signaling under stress.
Definition: The directed movement of sodium ions from the cytosol to the extracellular space across the plasma membrane, as carried out by a plasma-membrane sodium/proton antiporter.
Justification: The dominant physiological mode of SOS1 is Na+ efflux (export) from the cytosol to the apoplast for detoxification. The existing GOA term GO:0098719 captures Na+ import across the plasma membrane, but no equally specific export term is annotated; an export-directed sodium transport term would more precisely represent the core detoxification function. Not added as a NEW annotation because a verified GO ID for plasma-membrane sodium export could not be confirmed in this session.
Parent term: sodium ion transport
Supporting Evidence:
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0051453 regulation of intracellular pH | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: As an electroneutral Na+/H+ antiporter, SOS1 couples cytosolic Na+ efflux to H+ influx and so influences cytosolic and apoplastic pH. This is a real consequence of antiport activity but is secondary to the core Na+ detoxification role. Reason: The phylogenetically inferred (IBA) regulation of intracellular pH is consistent with the mechanism of a CPA1-family Na+/H+ exchanger, and SOS1 has been reported to affect H+ transport and apoplastic alkalinization even without salt stress. However, pH regulation is a downstream effect of the antiport reaction rather than the central biological role, which is Na+ detoxification and salt tolerance. Supporting Evidence: PMID:17996020 The plasma membrane Na + /H + antiporter SOS1 has also been shown to affect H + transport even in the absence of salt stress |
| GO:0098719 sodium ion import across plasma membrane | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: SOS1 transports Na+ across the plasma membrane. Its core physiological mode is Na+ efflux (export) from the cytosol for detoxification; the import direction captured by this term is a secondary, condition-dependent mode (xylem retrieval of Na+ under severe salt stress), reflecting the intrinsic reversibility of the antiporter. Reason: The IBA term captures plasma-membrane Na+ transport, but specifically in the import direction. The directionality (import vs export) of an electroneutral antiporter depends on the prevailing Na+ and H+ gradients; experimental and modeling work shows SOS1 can both load Na+ into and retrieve Na+ from the xylem. However, the defining, core physiological function of SOS1 is Na+ EXPORT/efflux from the cytosol (and proposed_new_terms request an explicit export term as the missing core function). Na+ import is a secondary, condition-dependent xylem-retrieval mode under severe stress, so this import annotation is retained as non-core rather than as the core sodium-transport function. Supporting Evidence: PMID:11884687 SOS1 functions in retrieving Na + from the xylem stream under severe salt stress, whereas under mild salt stress it may function in loading Na + into the xylem. file:ARATH/SOS1/SOS1-deep-research-falcon.md consistent with roles in both direct Na+ efflux at the root surface and regulation of long-distance Na+ transport via xylem loading/unloading |
| GO:0005886 plasma membrane | IEA GO_REF:0000044 | ACCEPT | Summary: SOS1 is a multi-pass plasma-membrane protein, confirmed experimentally by SOS1-GFP confocal imaging in transgenic Arabidopsis. Reason: The UniProt subcellular-location mapping agrees with direct experimental evidence and with the protein's transmembrane topology. This is the core cellular location of SOS1. Supporting Evidence: PMID:11884687 Confocal imaging of a SOS1-green fluorescent protein fusion protein in transgenic Arabidopsis plants indicated that SOS1 is localized in the plasma membrane. |
| GO:0006812 monoatomic cation transport | IEA GO_REF:0000002 | ACCEPT | Summary: SOS1 transports the monovalent cations Na+ (and Li+) across the plasma membrane. This is a correct but generic parent of the specific sodium-transport annotations. Reason: InterPro-based generic cation-transport term is accurate; it is broader than the specific sodium transport terms but not misleading, so it is retained. Supporting Evidence: PMID:10823923 The transmembrane region of SOS1 has significant sequence similarities to plasma membrane Na + /H + antiporters from bacteria and fungi. |
| GO:0015297 antiporter activity | IEA GO_REF:0000002 | ACCEPT | Summary: SOS1 is a secondary active antiporter that exchanges Na+ for H+. This generic antiporter term is correct but less informative than the specific sodium:proton antiporter activity. Reason: The InterPro-derived term is a correct parent of GO:0015385 (sodium:proton antiporter activity); the more specific term is also annotated, so this broader term is acceptable as-is. Supporting Evidence: file:ARATH/SOS1/SOS1-uniprot.txt Acts in electroneutral exchange of protons for cations such as Na(+) or Li(+) across plasma membrane. |
| GO:0015385 sodium:proton antiporter activity | IEA GO_REF:0000002 | ACCEPT | Summary: This is the core molecular function of SOS1: electroneutral exchange of intracellular Na+ for extracellular H+ across the plasma membrane, verified by a curated catalytic activity (RHEA:29419) and by complementation of a yeast Na+-transport mutant. Reason: Strong convergent evidence (InterPro/IBA, UniProt catalytic activity, and functional yeast complementation showing Na+-specific transport) supports GO:0015385 as the central molecular function. It is the most informative MF term available and represents the core activity. Supporting Evidence: PMID:11884687 SOS1 activity was specific for Na + because the plant protein was inefficient for K + efflux or uptake in vivo file:ARATH/SOS1/SOS1-uniprot.txt Acts in electroneutral exchange of protons for cations such as Na(+) or Li(+) across plasma membrane. file:ARATH/SOS1/SOS1-deep-research-falcon.md SOS1/NHX7 mediates active Na+ efflux from the cytosol in exchange for H+, lowering cytosolic Na+ during salt stress. |
| GO:0016020 membrane | IEA GO_REF:0000002 | ACCEPT | Summary: SOS1 is an integral membrane protein with ~12 transmembrane helices. The term is a correct but generic parent of the specific plasma-membrane location. Reason: InterPro-derived generic membrane localization is accurate; the specific plasma-membrane term is also annotated, so this broader term is retained as-is. Supporting Evidence: PMID:10823923 predicted to encode a 127-kDa protein with 12 transmembrane domains in the N-terminal part and a long hydrophilic cytoplasmic tail in the C-terminal part |
| GO:0055085 transmembrane transport | IEA GO_REF:0000002 | ACCEPT | Summary: SOS1 mediates transmembrane transport of Na+ and H+ across the plasma membrane. Correct but generic parent of the specific sodium/proton transport terms. Reason: InterPro-based generic transmembrane-transport term is accurate and consistent with the antiporter mechanism; retained as a non-misleading parent. Supporting Evidence: file:ARATH/SOS1/SOS1-uniprot.txt Acts in electroneutral exchange of protons for cations such as Na(+) or Li(+) across plasma membrane. |
| GO:1902600 proton transmembrane transport | IEA GO_REF:0000002 | ACCEPT | Summary: As a Na+/H+ antiporter, SOS1 translocates H+ across the plasma membrane coupled to Na+ movement. Proton transport is an integral part of the antiport cycle. Reason: The curated catalytic activity explicitly involves H+ counter-transport (RHEA:29419), so proton transmembrane transport is a correct InterPro-derived annotation, consistent with the electroneutral antiport reaction. Supporting Evidence: file:ARATH/SOS1/SOS1-uniprot.txt Acts in electroneutral exchange of protons for cations such as Na(+) or Li(+) across plasma membrane. file:ARATH/SOS1/SOS1-deep-research-falcon.md Transport is driven by the proton electrochemical gradient generated by the plasma-membrane H+-ATPase. |
| GO:0005515 protein binding | IPI PMID:17023541 The plasma membrane Na+/H+ antiporter SOS1 interacts with RC... | REMOVE | Summary: This IPI annotation records the interaction between the SOS1 cytoplasmic tail and RCD1 (a regulator of oxidative-stress responses). The interaction is biologically meaningful but the generic 'protein binding' term conveys no specific molecular function. Reason: Per curation guidelines, the uninformative GO:0005515 term should not be retained as it does not describe SOS1 molecular function. The underlying RCD1 interaction is captured biologically by the oxidative-stress process annotations. Supporting Evidence: PMID:17023541 SOS1 interacts through its predicted cytoplasmic tail with RCD1, a regulator of oxidative-stress responses. |
| GO:0005515 protein binding | IPI PMID:21262798 Activation of the plasma membrane Na/H antiporter Salt-Overl... | REMOVE | Summary: This IPI annotation records interaction with CIPK24/SOS2, the kinase that phosphorylates and activates SOS1. Biologically important for regulation, but the generic 'protein binding' term is uninformative about molecular function. Reason: The generic protein-binding term should not be kept. The functionally relevant SOS2-SOS3 regulatory interaction is described by the protein's regulation and phosphorylation, and a kinase-binding/regulatory relationship is better captured elsewhere than by bare GO:0005515. Supporting Evidence: PMID:21262798 SOS1 is relieved from auto-inhibition upon phosphorylation of the auto-inhibitory domain by SOS2-SOS3. |
| GO:0015386 potassium:proton antiporter activity | EXP PMID:12239394 SOS1, a Genetic Locus Essential for Salt Tolerance and Potas... | MARK AS OVER ANNOTATED | Summary: A K+/H+ catalytic activity is curated for SOS1, but direct functional testing in yeast showed SOS1 is specific for Na+ and inefficient at K+ transport in vivo. The sos1 potassium-acquisition phenotype is an indirect, genetic consequence of disrupted Na+/H+ exchange and linked Na+/K+ exchange at the xylem/symplast boundary, not direct K+ transport by SOS1. Reason: PMID:12239394 (Wu et al. 1996) is a genetic-mapping study reporting that sos1 mutants are defective in high-affinity K+ uptake; it does not directly demonstrate SOS1-catalyzed K+/H+ antiport. Direct transport assays (PMID:11884687) show SOS1 is Na+-specific and inefficient for K+, and the K+ phenotype is best explained by coupled antiport activities at the xylem/symplast boundary. The K+/H+ antiporter MF therefore over-annotates the protein's intrinsic activity. Supporting Evidence: PMID:11884687 SOS1 activity was specific for Na + because the plant protein was inefficient for K + efflux or uptake in vivo PMID:12239394 sos1 mutants are defective in high-affinity potassium uptake |
| GO:0005886 plasma membrane | HDA PMID:14506206 Large-scale analysis of in vivo phosphorylated membrane prot... | ACCEPT | Summary: A large-scale plasma-membrane phosphoproteomics study identified SOS1 among plasma-membrane phosphoproteins, consistent with its plasma-membrane localization and its regulation by phosphorylation. Reason: High-throughput direct-assay evidence places SOS1 in the plasma membrane, in full agreement with experimental GFP localization and the protein's topology. Core location. Supporting Evidence: PMID:14506206 identification of plasma membrane phosphoproteins of Arabidopsis |
| GO:0009941 chloroplast envelope | HDA PMID:12938931 Proteomic study of the Arabidopsis thaliana chloroplastic en... | REMOVE | Summary: A single large-scale proteomic survey of a 'mixed' chloroplast envelope preparation listed SOS1 among 392 nonredundant proteins. This is inconsistent with the well-established plasma-membrane localization and biology of SOS1 and most likely reflects plasma-membrane contamination of the envelope fraction. Reason: The chloroplast-envelope assignment comes from an untargeted proteomics dataset prone to contamination, with no functional rationale; SOS1 has no role in chloroplast biology and is robustly localized to the plasma membrane by GFP imaging and topology. This annotation is judged incorrect. Supporting Evidence: PMID:12938931 "mixed" envelopes were subsequently isolated using sucrose step gradients PMID:11884687 Confocal imaging of a SOS1-green fluorescent protein fusion protein in transgenic Arabidopsis plants indicated that SOS1 is localized in the plasma membrane. |
| GO:0005886 plasma membrane | ISM GO_REF:0000122 | ACCEPT | Summary: Sequence-based (AtSubP) prediction of plasma-membrane localization, consistent with experimental evidence and topology. Reason: The predicted plasma-membrane location agrees with multiple lines of experimental evidence (GFP imaging, phosphoproteomics) and the multi-pass topology. Core location. Supporting Evidence: PMID:11884687 Confocal imaging of a SOS1-green fluorescent protein fusion protein in transgenic Arabidopsis plants indicated that SOS1 is localized in the plasma membrane. |
| GO:0071805 potassium ion transmembrane transport | IMP PMID:12239394 SOS1, a Genetic Locus Essential for Salt Tolerance and Potas... | KEEP AS NON CORE | Summary: sos1 mutants are defective in high-affinity K+ uptake and become K+-deficient under NaCl, but SOS1 does not directly transport K+; this is an indirect consequence of disrupted Na+/H+ exchange and the tight coupling of Na+ and K+ fluxes at the xylem/symplast boundary. Reason: The acts_upstream_of_or_within qualifier appropriately reflects an indirect genetic effect on K+ transport rather than direct catalysis. Direct assays show SOS1 is Na+-specific (PMID:11884687), so this should not be treated as a core function but is retained as a genuine, non-core physiological phenotype. Supporting Evidence: PMID:12239394 sos1 mutants are defective in high-affinity potassium uptake PMID:11884687 the proposed coupling between Na + and K + exchange at the xylem/symplast boundary also could provide an explanation for why sos1 mutant plants are not capable of growing on low K + culture medium |
| GO:2000377 regulation of reactive oxygen species metabolic process | IMP PMID:17023541 The plasma membrane Na+/H+ antiporter SOS1 interacts with RC... | KEEP AS NON CORE | Summary: Through interaction of its cytoplasmic tail with RCD1 and effects on apoplastic pH/NADPH-oxidase activity, SOS1 influences ROS-related gene expression and ROS accumulation under stress. This is a secondary regulatory role distinct from ion transport. Reason: Experimental genetic evidence supports a role for SOS1 in modulating ROS metabolism (sos1 mutants over-accumulate ROS under salt; SOS1 and RCD1 jointly control ROS-scavenging genes), but this is downstream of and secondary to the core Na+/H+ antiport function. Supporting Evidence: PMID:17023541 Several genes related to oxidative-stress tolerance were found to be regulated by both RCD1 and SOS1. |
| GO:0000302 response to reactive oxygen species | IEP PMID:17996020 Reactive oxygen species mediate Na+-induced SOS1 mRNA stabil... | KEEP AS NON CORE | Summary: SOS1 mRNA is stabilized by ROS (H2O2) and SOS1 activity feeds back into apoplastic ROS production via pH changes and NADPH oxidase, linking SOS1 to the ROS response. A secondary, signaling-level role. Reason: Expression/phenotype evidence supports involvement of SOS1 in ROS responses, but this is an indirect signaling role downstream of its transport activity rather than a core function. Supporting Evidence: PMID:17996020 Stress-induced SOS1 mRNA stability is mediated by reactive oxygen species (ROS). |
| GO:0006979 response to oxidative stress | IMP PMID:17996020 Reactive oxygen species mediate Na+-induced SOS1 mRNA stabil... | KEEP AS NON CORE | Summary: sos1 mutants show altered oxidative-stress sensitivity (more tolerant to paraquat/methyl viologen), indicating SOS1 participates in oxidative-stress responses, with a proposed negative role mediated by apoplastic pH and NADPH oxidase. Reason: Mutant-phenotype evidence supports involvement in oxidative-stress responses, but as an indirect, secondary effect of SOS1 antiport activity on apoplastic pH and ROS production, not a core function. Supporting Evidence: PMID:17996020 mutations in the SOS1 gene render sos1 mutants more tolerant to paraquat, a non-selective herbicide causing oxidative stress, indicating that SOS1 plays negative roles in tolerance of oxidative stress |
| GO:0009651 response to salt stress | IEP PMID:17996020 Reactive oxygen species mediate Na+-induced SOS1 mRNA stabil... | ACCEPT | Summary: SOS1 is a salt-tolerance determinant; its mRNA is stabilized under salt stress and the protein extrudes toxic Na+, making salt-stress response a core biological process for SOS1. Reason: Multiple independent lines of evidence (expression induction by Na+, severe salt hypersensitivity of sos1 mutants, Na+ efflux activity) establish response to salt stress as a core process of SOS1. Supporting Evidence: PMID:17996020 Salt Overly Sensitive 1 (SOS1), a plasma membrane Na+/H+ antiporter in Arabidopsis, is a salt tolerance determinant crucial for the maintenance of ion homeostasis in saline stress conditions. |
| GO:0042542 response to hydrogen peroxide | IEP PMID:17996020 Reactive oxygen species mediate Na+-induced SOS1 mRNA stabil... | KEEP AS NON CORE | Summary: H2O2 treatment increases SOS1 mRNA stability, and SOS1 activity affects apoplastic H2O2 production, linking SOS1 to the hydrogen-peroxide response as a secondary signaling role. Reason: Expression evidence supports a connection between SOS1 and H2O2 responses, but this is downstream signaling/ROS biology, secondary to the core ion-transport function. Supporting Evidence: PMID:17996020 H2O2 treatment increases the stability of SOS1 mRNA. |
| GO:0005886 plasma membrane | IDA PMID:10823923 The Arabidopsis thaliana salt tolerance gene SOS1 encodes a ... | ACCEPT | Summary: Direct experimental evidence (TAIR IDA) supports plasma-membrane localization, consistent with the predicted multi-pass topology and similarity to bacterial/fungal plasma-membrane Na+/H+ antiporters. Reason: Direct-assay plasma-membrane localization agrees with all other location evidence; core cellular location of SOS1. Supporting Evidence: PMID:10823923 Phylogenetic analysis showed that SOS1 is more closely related to plasma membrane Na + /H + antiporters from microorganisms than to the vacuolar antiporters |
| GO:0042542 response to hydrogen peroxide | IMP PMID:17023541 The plasma membrane Na+/H+ antiporter SOS1 interacts with RC... | KEEP AS NON CORE | Summary: sos1 mutants show altered sensitivity to H2O2/apoplastic ROS, supporting involvement of SOS1 in the hydrogen-peroxide response via its role in oxidative-stress tolerance with RCD1. Reason: Mutant-phenotype evidence supports involvement in H2O2 responses, but as a secondary, indirect role downstream of SOS1 antiport activity and the SOS1-RCD1 module, not a core function. Supporting Evidence: PMID:17023541 Like rcd1 mutants, sos1 mutant plants show an altered sensitivity to oxidative stresses. |
| GO:0005886 plasma membrane | IDA PMID:11884687 The putative plasma membrane Na(+)/H(+) antiporter SOS1 cont... | ACCEPT | Summary: Direct experimental localization by SOS1-GFP confocal imaging in transgenic Arabidopsis demonstrates plasma-membrane localization. Reason: This is the strongest direct evidence for the core plasma-membrane location of SOS1. Supporting Evidence: PMID:11884687 Confocal imaging of a SOS1-green fluorescent protein fusion protein in transgenic Arabidopsis plants indicated that SOS1 is localized in the plasma membrane. file:ARATH/SOS1/SOS1-deep-research-falcon.md SOS1:GFP becomes increasingly recruited to the plasma membrane over |
| GO:0006814 sodium ion transport | IMP PMID:11874577 Salt causes ion disequilibrium-induced programmed cell death... | ACCEPT | Summary: SOS1 mediates Na+ transport across the plasma membrane and is required to limit cytosolic Na+ accumulation; sodium ion transport is a core process for this antiporter. Reason: Although PMID:11874577 uses the sos1 mutant only as a salt-sensitive genetic background (salt-induced programmed cell death), sodium ion transport is firmly established as a core SOS1 function by direct transport assays (PMID:11884687) and UniProt. The annotation is correct; supporting evidence is drawn from the directly relevant transport literature. Supporting Evidence: PMID:11884687 SOS1 is a plasma membrane Na + transporter essential for controlling long-distance Na + movement in plants. file:ARATH/SOS1/SOS1-deep-research-falcon.md SOS1/NHX7 mediates active Na+ efflux from the cytosol in exchange for H+, lowering cytosolic Na+ during salt stress. PMID:11874577 salt-sensitive mutants of yeast (cnb1Delta) and Arabidopsis (sos1) exhibit substantially more profound PCD symptoms, indicating that salt-induced PCD is mediated by ion disequilibrium |
| GO:0009651 response to salt stress | IMP PMID:12239394 SOS1, a Genetic Locus Essential for Salt Tolerance and Potas... | ACCEPT | Summary: sos1 mutants are >20-fold more sensitive to NaCl, establishing SOS1 as essential for the response to salt stress. Reason: Loss-of-function mutant phenotype (extreme NaCl hypersensitivity) directly supports the core role of SOS1 in salt-stress response. Supporting Evidence: PMID:12239394 their growth was >20 times more sensitive to inhibition by NaCl file:ARATH/SOS1/SOS1-deep-research-falcon.md Loss-of-function sos mutants (sos1, sos2, sos3) exhibit strong salt sensitivity, supporting the conclusion that the SOS pathway is essential for salt tolerance through ion homeostasis maintenance |
| GO:0009651 response to salt stress | IMP PMID:10823923 The Arabidopsis thaliana salt tolerance gene SOS1 encodes a ... | ACCEPT | Summary: The SOS1 locus is essential for salt tolerance; sos1 mutations render plants extremely sensitive to high Na+ and SOS1 expression is induced by NaCl. Core biological process. Reason: Cloning and mutant analysis establish SOS1 as required for the salt-stress response, a core function. Duplicate IMP support across independent studies is appropriate. Supporting Evidence: PMID:10823923 sos1 mutations render plants more sensitive to growth inhibition by high Na + and low K + environments |
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Q: Does SOS1 directly bind 14-3-3 proteins at the SOS2-phosphorylated RIDSPSK motif, as for the related plasma-membrane H+-ATPase, and does this modulate activation?
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