AUX1 is a plasma-membrane auxin influx carrier of the AUX1/LAX branch of the amino acid/auxin permease superfamily. It imports indole-3-acetic acid through a proton-coupled mechanism and binds auxin in a central pocket of an 11-transmembrane-helix, monomeric LeuT-fold architecture. Polar and tissue-specific AUX1 distribution supports auxin delivery through the root apex and epidermis, root gravitropism, lateral-root development and root-hair positioning. AUX1 traffics through intracellular membrane compartments and acts redundantly with LAX carriers in some developmental and nematode-infection contexts. His249 is implicated in substrate binding, release and proton coupling; a fixed proton-to-auxin stoichiometry has not been established by the structural studies.
Definition: Enables the transfer of auxin (indole-3-acetic acid) from one side of a membrane to the other, coupled to the transport of a proton in the same direction, driven by the transmembrane proton-motive force.
Justification: AUX1 mediates proton-driven, pH-dependent auxin uptake and AUX/LAX proteins act as IAA-H+ symporters; a substrate-specific symporter term would capture both the mechanism (proton coupling) and the substrate (auxin), which neither GO:0010328 (substrate-specific, mechanism-agnostic) nor GO:0015293 (mechanism only) fully expresses.
Parent term: symporter activity
Supporting Evidence:
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0003333 amino acid transmembrane transport | IEA GO_REF:0000108 | UNDECIDED | Summary: Amino-acid substrate assignment remains unresolved for AUX1. Reason: AUX1 is an AAAP-family carrier with directly demonstrated IAA uptake. The recovered 2025 target structures and uptake assays establish auxin recognition but do not test and exclude amino-acid turnover. Neither broad family membership nor preference for IAA settles this separate substrate claim. Retain uncertainty rather than inferring loss of amino-acid transport from its auxin role. Supporting Evidence: PMID:40720658 These results confirm AUX1 as a direct mediator of active auxin influx. |
| GO:0005886 plasma membrane | IEA GO_REF:0000044 | ACCEPT | Summary: AUX1 is a multi-pass integral plasma membrane protein, established by experimental localization in root cells. This UniProt subcellular-location mapping is consistent with the curated Cell membrane location. Reason: Plasma membrane localization is well supported experimentally (PMID 11641271, PMID 16690816, PMID 17114355) and is the functional compartment where AUX1 imports auxin. The IEA mapping is correct. Supporting Evidence: PMID:11641271 AUX1, asymmetrically localized to the plasma membrane of root protophloem cells, is proposed to promote the acropetal, post-phloem movement of auxin to the root apex. file:ARATH/AUX1/AUX1-deep-research-falcon.md AUX1 localizes to the **plasma membrane** in heterologous expression (EYFP-AUX1 in oocytes), where it mediates pH-dependent, saturable IAA uptake. |
| GO:0060919 auxin import into cell | IEA GO_REF:0000108 | ACCEPT | Summary: This biological-process term is inferred from the molecular function GO:0010328 (auxin influx transmembrane transporter activity) and exactly captures the core role of AUX1 - importing auxin (IAA) into cells. It is strongly supported by direct experimental transport data. Reason: Auxin import into cells is the defining function of AUX1, demonstrated by saturable pH-dependent 3H-IAA uptake in AUX1-expressing oocytes and by impaired IAA accumulation in aux1 mutant root apices. The inter-ontology inference is biologically accurate and represents a core function. Supporting Evidence: PMID:16677815 Upon expression of AUX1 in Xenopus oocytes, saturable, pH-dependent uptake of 3H-IAA was measured. PMID:11641271 MS analysis shows that IAA accumulation in aux1 mutant root apices is impaired, consistent with an AUX1 phloem unloading function. file:ARATH/AUX1/AUX1-deep-research-falcon.md the dominant **regulated cellular uptake** is via **influx carriers** such as AUX1/LAX proteins. Reviews emphasize that AUX1/LAX transporters are **major auxin influx carriers** required to establish auxin gradients that drive development. |
| GO:0005515 protein binding | IPI PMID:32612234 Extensive signal integration by the phytohormone protein net... | REMOVE | Summary: This generic protein binding annotation derives from a large-scale phytohormone interactome screen; the WITH/FROM partner is UniProtKB:Q9FZ33 (AXR4), the ER accessory protein required for AUX1 trafficking to the plasma membrane. The term protein binding is uninformative about molecular function. Reason: GO:0005515 protein binding is too generic to convey a meaningful molecular function and is discouraged as a core annotation. The biologically relevant interaction (AUX1 with AXR4) reflects a chaperone/trafficking relationship rather than the activity of AUX1 itself, and is better represented by the trafficking biology described in PMID:16690816 than by a bare binding term. Supporting Evidence: PMID:32612234 we experimentally generated a systems-level map of the Arabidopsis phytohormone signalling network, consisting of more than 2,000 binary protein-protein interactions. PMID:16690816 AXR4 is a previously unidentified accessory protein of the endoplasmic reticulum (ER) that regulates localization of AUX1 but not of PIN proteins. file:ARATH/AUX1/AUX1-deep-research-falcon.md The 2024 study provides biochemical evidence that AXR4 **physically interacts** with AUX1 and **reduces AUX1 aggregation in a dose-dependent fashion**, supporting a model in which AXR4 functions as an **ER accessory/chaperone-like factor** enabling proper folding/ER exit and plasma-membrane targeting of AUX1. |
| GO:0010262 somatic embryogenesis | IEP PMID:36345646 Endogenous auxin maintains embryonic cell identity and promo... | KEEP AS NON CORE | Summary: AUX1 (as part of the AUX1/LAX influx carrier system together with PIN efflux carriers) contributes to polar auxin transport required for somatic embryo development. This is an auxin-transport-dependent developmental process, peripheral to the core transport function of AUX1 and involving redundancy with LAX/PIN family members. Reason: The paper shows that polar auxin transport, with AUX1/LAX influx and PIN1 efflux carriers as drivers, is required for the transition of embryonic cells to proembryos and later differentiation. This is a legitimate downstream developmental role but is a pleiotropic consequence of AUX1 transport activity rather than a core molecular function, and is shared redundantly across the family. Supporting Evidence: PMID:36345646 polar auxin transport, with AUXIN/LIKE-AUX influx and PIN-FORMED1 efflux carriers as important drivers, is required for the transition of embryonic cells to proembryos and, later, for correct cell fate specification and differentiation. |
| GO:0010262 somatic embryogenesis | IMP PMID:36345646 Endogenous auxin maintains embryonic cell identity and promo... | KEEP AS NON CORE | Summary: Duplicate of the somatic embryogenesis annotation from the same study, here with mutant-phenotype evidence. AUX1/LAX-mediated auxin import contributes to somatic embryo development as part of polar auxin transport. Reason: Same rationale as the IEP annotation from the same study (PMID:36345646), a genuine but peripheral, redundantly shared developmental role downstream of AUX1 auxin transport activity. Retained as non-core. Duplicate terms with different evidence codes are acceptable. Supporting Evidence: PMID:36345646 the stronger embryo defects observed after combining mutations in influx and efflux carriers indicate a cooperative function between auxin influx and efflux carriers in controlling embryo development |
| GO:0009624 response to nematode | HEP PMID:16478044 Nematode-induced changes of transporter gene expression in A... | KEEP AS NON CORE | Summary: AUX1 contributes redundantly to the host auxin-transport response during cyst-nematode infection. Reason: The original expression survey alone does not establish a transport contribution to infection. Independent native genetics in PMID:21156858 shows reduced cyst-nematode infectivity in aux1 lax3 and quadruple influx-carrier mutants, although the aux1 single mutant is unaffected. This supports a redundant, contextual role in auxin delivery during feeding-site formation, not direct nematode recognition or an AUX1-specific effector interaction. Supporting Evidence: PMID:21156858 We observed no decrease in H. schachtii infectivity in aux1 and lax3 single mutants. However, a decrease was observed in both the aux1lax3 double mutant and the aux1lax1lax2lax3 quadruple mutant. |
| GO:0005886 plasma membrane | ISM GO_REF:0000122 | ACCEPT | Summary: Computational (AtSubP) prediction of plasma membrane localization, consistent with the experimentally established multi-pass plasma membrane location of AUX1. Reason: Although the evidence is a sequence-based prediction (ISM), it agrees with direct experimental localization data (PMID:11641271, PMID:16690816) and with the multi-pass transmembrane topology of the protein. Correct, if redundant with the experimental plasma membrane annotations. Supporting Evidence: PMID:16690816 Loss of AXR4 resulted in abnormal accumulation of AUX1 in the ER of epidermal cells, indicating that the axr4 agravitropic phenotype is caused by defective AUX1 trafficking in the root epidermis. |
| GO:0048829 root cap development | IMP PMID:19952011 The AUX1 LAX family of auxin influx carriers is required for... | KEEP AS NON CORE | Summary: aux1 lax mutants have enlarged radicle root caps with altered columella cell number, size and organization, indicating that AUX1/LAX auxin influx carriers act redundantly in establishing embryonic root cap cell pattern. AUX1 contributes within this auxin-transport-dependent developmental process. Reason: Mutant phenotype evidence supports a role in root cap / embryonic root organization, but the effect is largely redundant within the AUX1/LAX family (strong defects require quadruple mutants) and is a developmental consequence of AUX1 auxin import activity rather than a distinct core function. Supporting Evidence: PMID:19952011 aux1 lax mutants have a larger radicle root cap than the wild type and this is associated with a significant increase in the root-cap cell number, average cell size, or both. |
| GO:0010011 auxin binding | IDA PMID:18614710 The binding of auxin to the Arabidopsis auxin influx transpo... | ACCEPT | Summary: AUX1 expressed in baculovirus-infected insect cell membranes binds IAA directly with a Kd of about 2.6 microM, comparable to its transport Km. Auxin analogues and influx inhibitors specifically displace IAA, confirming direct, specific binding of the auxin substrate. Reason: Direct assay evidence demonstrates specific binding of the transport substrate IAA to AUX1. This is a genuine molecular function reflecting the initial substrate-recognition event of the transport cycle and supports the transporter activity annotation. Supporting Evidence: PMID:18614710 These membranes proved suitable for determination of the binding of IAA to AUX1 and enabled us to determine a K(d) of 2.6 mum, comparable with estimates for the K(m) for IAA transport. file:ARATH/AUX1/AUX1-deep-research-falcon.md Binding assays yielded a reported **Kd β 2.6 Β΅M** and **Bmax β 11,800 fmol IAA/mg membrane protein**, with **maximal specific binding around pH 5β6**. |
| GO:0010311 lateral root formation | IGI PMID:18622388 The auxin influx carrier LAX3 promotes lateral root emergenc... | KEEP AS NON CORE | Summary: AUX1 functions with its paralog LAX3 in auxin influx that promotes lateral root development; LAX3 acts in cortical/epidermal cells overlaying primordia to promote emergence, while AUX1 contributes to lateral root formation through auxin distribution. Genetic interaction within the AUX1/LAX family. Reason: Supported by genetic-interaction evidence within the auxin influx carrier family. Lateral root formation is a real developmental output of AUX1-mediated auxin transport but is a downstream, partly redundant role rather than the core molecular function of AUX1. Supporting Evidence: PMID:18622388 Auxin induces the expression of a previously uncharacterized auxin influx carrier LAX3 in cortical and epidermal cells directly overlaying new primordia. file:ARATH/AUX1/AUX1-deep-research-falcon.md **aux1 mutants show ~50% reduction in emerged lateral roots**, supporting AUX1-mediated auxin uptake as a quantitative determinant of LR development. |
| GO:0001736 establishment of planar polarity | IGI PMID:17084699 Vectorial information for Arabidopsis planar polarity is med... | KEEP AS NON CORE | Summary: Combinatorial action of AUX1, EIN2 and GNOM provides vectorial information for planar polarity of root hair positioning; the auxin gradient is abolished in aux1 ein2 gnom triple mutants. AUX1 contributes by shaping the auxin gradient through its import activity. Reason: Genetic-interaction evidence supports a role in coordinating root epidermal planar polarity via auxin gradient formation. This is a developmental consequence of AUX1 auxin transport acting together with other genes, not a distinct core function of AUX1. Supporting Evidence: PMID:17084699 combinatorial action of the auxin influx carrier AUX1, ETHYLENE-INSENSITIVE2 (EIN2), and GNOM genes mediates the vector for coordinate hair positioning. file:ARATH/AUX1/AUX1-deep-research-falcon.md aux1 mutants have **shorter root hairs** (rescuable by exogenous auxin) and show **~30-fold higher frequency of double-hair formation**, indicating disrupted epidermal patterning/polarity. |
| GO:0048765 root hair cell differentiation | IGI PMID:17084699 Vectorial information for Arabidopsis planar polarity is med... | KEEP AS NON CORE | Summary: In aux1 ein2 gnom mutants, root hair positioning switches from polar to axial and the auxin gradient is lost, indicating AUX1 acts with EIN2 and GNOM in patterning root hair cells. The annotation captures the role of AUX1 in root hair development via auxin gradient formation. Reason: Supported by genetic interaction data showing AUX1 contributes to root hair cell polarity/positioning. This is a developmental output of AUX1 auxin import, peripheral to its core transport function. (UniProt also notes AUX1 involvement in trichoblast polarization and root hair elongation.) Supporting Evidence: PMID:17084699 In aux1;ein2;gnom eb triple mutant roots, hairs display axial (apical or basal) instead of coordinate polar (basal) position file:ARATH/AUX1/AUX1-deep-research-falcon.md The AUX/LAX overview reports AUX1 expression in **epidermal non-hair cells** and links AUX1 to root hair development and planar polarity. |
| GO:0010328 auxin influx transmembrane transporter activity | IDA PMID:16677815 High-affinity auxin transport by the AUX1 influx carrier pro... | ACCEPT | Summary: Heterologous expression of AUX1 in Xenopus oocytes confers saturable, pH-dependent high-affinity 3H-IAA uptake that is reduced by 2,4-D and 1-NOA and by mutations that abrogate AUX1 function in planta. This directly demonstrates that AUX1 is an auxin influx transmembrane transporter and is the core molecular function. Reason: This is the central, experimentally validated molecular function of AUX1. Direct transport assays in a heterologous system, plus the genotype-phenotype concordance of transport-abrogating mutations, provide strong IDA support. Represents the core function of the gene. Supporting Evidence: PMID:16677815 Mutations in AUX1 that abrogate physiological responses to IAA in planta resulted in loss or reduction of 3H-IAA uptake in AUX1-expressing oocytes. PMID:16677815 The measured Km for AUX1-mediated uptake of 3H-IAA was at concentrations at which physiological responses are observed for exogenously added IAA and 2,4-D. file:ARATH/AUX1/AUX1-deep-research-falcon.md Direct functional evidence from heterologous expression in **Xenopus oocytes** demonstrates that AUX1 transports **IAA** with high affinity and saturable kinetics. |
| GO:0015171 amino acid transmembrane transporter activity | ISS PMID:9484486 The Arabidopsis AUX1 gene: a model system to study mRNA proc... | UNDECIDED | Summary: Amino-acid substrate assignment remains unresolved for AUX1. Reason: AUX1 is an AAAP-family carrier with directly demonstrated IAA uptake. The recovered 2025 target structures and uptake assays establish auxin recognition but do not test and exclude amino-acid turnover. Neither broad family membership nor preference for IAA settles this separate substrate claim. Retain uncertainty rather than inferring loss of amino-acid transport from its auxin role. Supporting Evidence: PMID:40720658 These results confirm AUX1 as a direct mediator of active auxin influx. |
| GO:0009958 positive gravitropism | IMP PMID:8688077 Arabidopsis AUX1 gene: a permease-like regulator of root gra... | ACCEPT | Summary: aux1 mutations abolish root gravitropic curvature and confer auxin-resistant root growth; AUX1 is expressed in root apical tissues that regulate gravitropic curvature. AUX1-facilitated auxin uptake into distal elongation zone tissues is required for the differential growth underlying root gravitropism. Reason: Strong mutant-phenotype evidence establishes that AUX1 is required for root (positive) gravitropism, the phenotype for which the gene was named. This is a well-characterized, biologically central output of AUX1 auxin transport and is appropriately retained as a core process annotation. Supporting Evidence: PMID:8688077 Mutations within the AUX1 gene confer an auxin-resistant root growth phenotype and abolish root gravitropic curvature. PMID:11641271 AUX1 is necessary for root gravitropism by facilitating basipetal auxin transport to distal elongation zone tissues. file:ARATH/AUX1/AUX1-deep-research-falcon.md AUX1 is essential for gravitropism and mediates auxin movement from the **lateral root cap to the epidermis of the elongation zone**, enabling differential growth during bending |
| GO:0010311 lateral root formation | IMP PMID:17215297 Auxin-dependent regulation of lateral root positioning in th... | KEEP AS NON CORE | Summary: Lateral roots are spaced along the primary root in a regular pattern that correlates with gravity-induced waving and depends on AUX1; AUX1 contributes to auxin-dependent priming of pericycle cells for lateral root initiation. Mutant-phenotype evidence links AUX1 to lateral root positioning/formation. Reason: This is a duplicate lateral root formation term (here IMP from a positioning study) supporting a real developmental role of AUX1 downstream of its auxin transport activity. Retained as non-core, consistent with the IGI lateral-root annotation. Supporting Evidence: PMID:17215297 lateral roots are spaced along the main axis in a regular left-right alternating pattern that correlates with gravity-induced waving and depends on AUX1, an auxin influx carrier essential for gravitropic response. |
| GO:0009986 cell surface | IDA PMID:11641271 Localization of the auxin permease AUX1 suggests two functio... | MODIFY | Summary: AUX1 is an integral plasma membrane protein, asymmetrically localized to the plasma membrane of root protophloem cells. The cited study establishes plasma membrane localization; cell surface (GO:0009986) is a less precise rendering of the curated plasma membrane location. Reason: The experimental evidence supports plasma membrane localization rather than the more generic/loosely defined cell surface term. GO:0009986 (cell surface) refers to the external side/region of the cell surface and is not the most accurate description of a multi-pass integral membrane transporter. Replace with the plasma membrane term that the same data support. Proposed replacements: plasma membrane Supporting Evidence: PMID:11641271 AUX1, asymmetrically localized to the plasma membrane of root protophloem cells, is proposed to promote the acropetal, post-phloem movement of auxin to the root apex. |
| GO:0005768 endosome | IDA PMID:17114355 Subcellular trafficking of the Arabidopsis auxin influx carr... | KEEP AS NON CORE | Summary: Live-cell imaging shows AUX1 resides at the apical plasma membrane and at highly dynamic subpopulations of Golgi apparatus and endosomes in all cell types, with PM and intracellular pools interconnected by actin-dependent constitutive trafficking. The endosomal pool reflects AUX1 trafficking rather than its functional transport site. Reason: Direct imaging evidence supports endosomal localization as part of the constitutive trafficking itinerary of AUX1. It is a genuine location but represents the trafficking route to/from the plasma membrane, not the site where AUX1 performs auxin import. Retained as non-core. Supporting Evidence: PMID:17114355 AUX1 resides at the apical plasma membrane of protophloem cells and at highly dynamic subpopulations of Golgi apparatus and endosomes in all cell types. file:ARATH/AUX1/AUX1-deep-research-falcon.md in **axr4** mutants AUX1 is retained/accumulates in the **endoplasmic reticulum (ER)** rather than reaching the plasma membrane. |
| GO:0005794 Golgi apparatus | IDA PMID:17114355 Subcellular trafficking of the Arabidopsis auxin influx carr... | KEEP AS NON CORE | Summary: Same live-cell imaging study shows AUX1 in dynamic subpopulations of the Golgi apparatus, interconnected with the plasma membrane pool by actin-dependent trafficking. The Golgi pool reflects the biosynthetic/trafficking route rather than the functional site of auxin transport. Reason: Direct imaging supports a Golgi-associated pool of AUX1 as part of its trafficking pathway. Legitimate localization but peripheral to the functional plasma membrane site of auxin import; retained as non-core. Supporting Evidence: PMID:17114355 AUX1 resides at the apical plasma membrane of protophloem cells and at highly dynamic subpopulations of Golgi apparatus and endosomes in all cell types. file:ARATH/AUX1/AUX1-deep-research-falcon.md AUX1 (and LAX2) maturation and delivery to the plasma membrane. |
| GO:0005886 plasma membrane | IDA PMID:16690816 AXR4 is required for localization of the auxin influx facili... | ACCEPT | Summary: AUX1 normally localizes to the plasma membrane; loss of the ER accessory protein AXR4 causes abnormal AUX1 accumulation in the ER, demonstrating that correct AUX1 plasma membrane targeting is AXR4-dependent. Direct experimental support for plasma membrane localization. Reason: Direct assay evidence (IDA) for the functional plasma membrane location of AUX1, the compartment where it imports auxin. Core localization; duplicate of the IEA/ISM plasma membrane annotations with stronger experimental backing. Supporting Evidence: PMID:16690816 Loss of AXR4 resulted in abnormal accumulation of AUX1 in the ER of epidermal cells, indicating that the axr4 agravitropic phenotype is caused by defective AUX1 trafficking in the root epidermis. |
| GO:0009926 auxin polar transport | TAS PMID:16839804 Auxin transport: a field in flux. | ACCEPT | Summary: AUX1 is one of the carrier proteins that mediate carrier-based polar auxin transport, contributing the influx (uptake) component alongside PIN efflux carriers. The review (TAS) places AUX1 within the polar auxin transport system that establishes directional auxin fluxes in the root apex. Reason: The auxin import activity of AUX1 is an integral part of carrier-mediated polar auxin transport; this process annotation accurately reflects its contribution to directional auxin movement. Well supported by the transport literature and represents a core biological process for AUX1. Supporting Evidence: PMID:16839804 Auxin moves between plant cells through a combination of membrane diffusion and carrier-mediated transport. Several classes of membrane proteins that facilitate auxin uptake and efflux have recently been identified in Arabidopsis. PMID:11641271 AUX1, asymmetrically localized to the plasma membrane of root protophloem cells, is proposed to promote the acropetal, post-phloem movement of auxin to the root apex. file:ARATH/AUX1/AUX1-deep-research-falcon.md AUX1/LAX transporters are **major auxin influx carriers** required to establish auxin gradients that drive development. |
| GO:0015293 symporter activity | IEA PMID:18614710 The binding of auxin to the Arabidopsis auxin influx transpo... | NEW | Summary: AUX1 mediates proton-coupled auxin uptake; exact coupling stoichiometry is not assigned. Reason: Retain the inherited proposal for proton-coupled symport as a distinct coupling property of auxin uptake. The oocyte assay establishes pH-dependent IAA influx, and the 2025 structures, pH-dependent binding and His249 mutagenesis support the coupling model. PMID:40720658 treats His249 protonation as a mechanistic model; it does not measure an integer H+:IAA stoichiometry. Supporting Evidence: PMID:16677815 Upon expression of AUX1 in Xenopus oocytes, saturable, pH-dependent uptake of 3H-IAA was measured. PMID:40720658 These findings support a model where protonation and deprotonation of the NΞ΄1 atom of His249 are coupled to the binding and release of IAA, respectively. |
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Q: What structural features (from the recent cryo-EM structures) determine proton coupling and the asymmetric (polar) plasma membrane localization of AUX1 in protophloem cells?
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