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The gene odr-1 (synonym gcy-10; locus R01E6.1; UniProt B1Q257) encodes a receptor-type guanylyl cyclase (rGC) in Caenorhabditis elegans. The protein is also known as "Odorant response abnormal protein 1," reflecting its original identification in behavioral screens for mutants with specific olfactory defects (bargmann2006chemosensationinc. pages 10-12). ODR-1 belongs to the adenylyl cyclase class-4/guanylyl cyclase protein family and possesses characteristic domains including a periplasmic-binding-protein-like extracellular domain (ECD), a transmembrane segment, a kinase homology domain (KHD), a hinge region, and a carboxy-terminal cyclase catalytic domain (ferkey2021chemosensorysignaltransduction pages 34-35).
The following table summarizes the key molecular and functional properties of ODR-1:
| Property | Details |
|---|---|
| Gene name/synonyms | odr-1; synonym gcy-10; protein described as receptor-type guanylate cyclase / Odorant response abnormal protein 1 in Caenorhabditis elegans (bargmann2006chemosensationinc. pages 10-12) |
| UniProt accession | B1Q257 (user-supplied target identity) |
| Protein type | Single-pass receptor-type guanylyl cyclase (rGC) in the adenylyl cyclase class-4/guanylyl cyclase family; function is mediated primarily by its intracellular cyclase domain rather than the extracellular domain in olfactory signaling (ferkey2021chemosensorysignaltransduction pages 35-35, bargmann2006chemosensationinc. pages 10-12) |
| Enzymatic reaction | Catalyzes GTP → cGMP; like other rGCs, catalytic activity requires dimerization of cyclase domains to form the active site for cGMP synthesis (ferkey2021chemosensorysignaltransduction pages 34-35, usuyama2012amodelof pages 2-3) |
| Dimerization partner | Strong evidence supports functional partnership with DAF-11; ODR-1 and DAF-11 likely form an obligate heterodimer because each individually lacks key catalytic residues, but together can form an active catalytic site (bargmann2006chemosensationinc. pages 10-12, ferkey2021chemosensorysignaltransduction pages 35-35) |
| Neurons expressing ODR-1 | Reported in AWC, AWB, ASI, ASJ, and ASK sensory neurons; canonical olfactory roles are best established in AWC and AWB, with ASK/ASI/ASJ implicated in broader cGMP signaling and circuit modulation (bargmann2006chemosensationinc. pages 10-12, sojka2025anextensivegap pages 2-4, wu2022positiveinteractionbetween pages 2-4) |
| Subcellular localization | Functions at sensory cilia/ciliated sensory endings as a transmembrane rGC; recent work also links ODR-1 to regulation of AWC cilia and dendrite state, and odr-1 mutants show distorted AWC cilia morphology (sun2025multipleregulatorsconstrain pages 1-2, ferkey2021chemosensorysignaltransduction pages 18-19) |
| Key pathway components (upstream and downstream) | Upstream: odor-responsive GPCR signaling and the Gα subunit ODR-3; ODR-1 is thought to be regulated mainly via intracellular/G-protein-linked mechanisms rather than classical extracellular ligand binding in AWC. Core transduction: ODR-1/DAF-11 → cGMP → TAX-2/TAX-4 CNG channels → Ca2+ influx/voltage-gated Ca2+ channels. Adaptation/plasticity: EGL-4/PKG, HPL-2, phosphodiesterases, and calcium-dependent feedback regulators. In another circuit context, ODR-1-generated cGMP can travel via gap junctions to ASH to modulate nociception (ferkey2021chemosensorysignaltransduction pages 35-35, usuyama2012amodelof pages 2-3, bargmann2006chemosensationinc. pages 10-12, ferkey2021chemosensorysignaltransduction pages 18-19, sojka2025anextensivegap pages 1-2) |
| Primary biological functions | Required for AWC- and AWB-mediated olfactory behaviors, especially chemotaxis to attractive volatile odorants and aspects of repellent sensing; contributes to olfactory adaptation/plasticity through cGMP-EGL-4 signaling; also has non-cell-autonomous modulatory roles in sensory circuits by supplying cGMP that dampens ASH aversive signaling (bargmann2006chemosensationinc. pages 10-12, ferkey2021chemosensorysignaltransduction pages 18-19, sojka2025anextensivegap pages 1-2) |
| Known phenotypes of odr-1 mutants | Mutants are defective in AWC/AWB olfactory responses and chemotaxis to AWC-sensed odors; can show altered olfactory adaptation/plasticity, hypersensitivity in ASH-mediated aversive responses when ODR-1-derived cGMP modulation is lost, and distorted AWC cilia morphology in recent studies; dauer formation is reported as largely normal compared with daf-11 mutants (bargmann2006chemosensationinc. pages 10-12, sojka2025anextensivegap pages 2-4, sojka2025anextensivegap pages 1-2, sun2025multipleregulatorsconstrain pages 1-2) |
Table: This table summarizes the main molecular, cellular, and functional properties of the C. elegans ODR-1/GCY-10 receptor guanylyl cyclase. It is useful as a compact reference for its enzymatic activity, expression pattern, pathway position, and mutant phenotypes.
ODR-1 catalyzes the conversion of GTP to the second messenger cyclic GMP (cGMP), a reaction classified under EC 4.6.1.2 (ferkey2021chemosensorysignaltransduction pages 34-35, usuyama2012amodelof pages 2-3). Like other receptor-type guanylyl cyclases, the cyclase domain of ODR-1 requires dimerization to form an active catalytic site that coordinates magnesium and binds GTP for cyclization into cGMP (ferkey2021chemosensorysignaltransduction pages 34-35).
A distinguishing feature of ODR-1 is that it does not appear to function as a homodimer. Instead, ODR-1 forms an obligate heterodimer with DAF-11, another transmembrane guanylyl cyclase. Each protein individually lacks key catalytic residues necessary for full enzymatic activity, but when paired, the two subunits contribute complementary residues to reconstitute a functional active site (bargmann2006chemosensationinc. pages 10-12). This was demonstrated experimentally: fusion proteins of ODR-1 and DAF-11 intracellular domains, when co-expressed in ASEL neurons, were sufficient to restore cGMP production and calcium influx in response to pH stimuli, whereas neither alone could rescue function (ferkey2021chemosensorysignaltransduction pages 35-35). However, formal biochemical proof of heterodimerization in the native AWC cell context remains to be established (ferkey2021chemosensorysignaltransduction pages 35-35).
Critically, the cyclase domain rather than the extracellular domain mediates the primary function of ODR-1 in olfactory signaling. ODR-1 proteins with deleted or mutated extracellular domains can still rescue olfactory defects in odr-1 mutants, indicating that ODR-1 does not act as a classical ligand-activated receptor in AWC (bargmann2006chemosensationinc. pages 10-12). Instead, ODR-1 is thought to be regulated intracellularly, downstream of G-protein-coupled receptor (GPCR) signaling, via the Gα subunit ODR-3 (ferkey2021chemosensorysignaltransduction pages 35-35, bargmann2006chemosensationinc. pages 10-12).
ODR-1 is expressed in a defined subset of amphid chemosensory neurons. The canonical expression pattern includes the AWC and AWB olfactory neuron pairs, where its role in olfaction has been most thoroughly studied (bargmann2006chemosensationinc. pages 10-12). Additional expression has been reported in ASI, ASJ, and ASK sensory neurons (sojka2025anextensivegap pages 2-4, stuhr2024c.elegansdisplay pages 1-5). The odr-1 promoter is commonly used as a marker for AWC and AWB neurons in experimental studies (sojka2025anextensivegap pages 2-4). The LIM homeodomain transcription factor LIM-4 has been shown to induce odr-1 expression as part of AWB neuronal fate specification (stuhr2024c.elegansdisplay pages 1-5).
As a single-pass transmembrane rGC, ODR-1 is localized to the sensory cilia of chemosensory neurons. This is supported by functional evidence: ODR-1 function is required for maintaining proper AWC cilia morphology, and loss of odr-1 results in distorted AWC cilia (sun2025multipleregulatorsconstrain pages 1-2). Furthermore, ODR-1 function and cilia integrity are jointly required to maintain EGL-4/PKG in the cytoplasm prior to prolonged odor exposure, consistent with ODR-1 acting at the ciliary compartment where primary sensory transduction occurs (ferkey2021chemosensorysignaltransduction pages 18-19). The odr-1 promoter has been used to drive expression of GFP-tagged guanylyl cyclases to cilia and distal dendritic ends of AWC neurons (pandey2026alateralizedsensory pages 6-7).
ODR-1 is a central component of the cGMP-based olfactory signal transduction pathway in AWC neurons. The pathway operates as follows:
| Step Number | Component/Molecule | Gene Name | Molecular Function | Role in Pathway |
|---|---|---|---|---|
| 1 | Attractive odorant detected in AWC | not uniquely assigned | External chemical cue sensed by olfactory receptor machinery | Initiates AWC olfactory signaling that ultimately drives chemotaxis and adaptation; specific upstream receptors for many AWC odors remain incompletely defined (usuyama2012amodelof pages 2-3, bargmann2006chemosensationinc. pages 10-12) |
| 2 | Odor-responsive GPCR system | multiple candidate GPCRs | G protein-coupled receptor activity | Couples odor detection to intracellular signaling in AWC and activates heterotrimeric G-protein signaling upstream of ODR-3 and guanylyl cyclase regulation (usuyama2012amodelof pages 2-3, bargmann2006chemosensationinc. pages 10-12) |
| 3 | G-protein alpha subunit | odr-3 | Gα signaling transducer | Acts downstream of odor-sensing GPCRs and upstream of guanylyl cyclase; in AWC models, odor input alters ODR-3 signaling, which suppresses cyclase activity during stimulation and relieves suppression after odor removal (usuyama2012amodelof pages 2-3, bargmann2006chemosensationinc. pages 10-12, usuyama2012amodelof pages 1-2) |
| 4 | Receptor guanylyl cyclase complex | odr-1, daf-11 | Membrane guanylyl cyclase that converts GTP to cGMP | Core cyclase step in AWC; ODR-1 and DAF-11 likely function as a heterodimer, with the intracellular cyclase domain providing the essential signaling output rather than the extracellular domain (ferkey2021chemosensorysignaltransduction pages 35-35, bargmann2006chemosensationinc. pages 10-12) |
| 5 | cGMP second messenger | cGMP | Diffusible cyclic nucleotide messenger | Transduces cyclase activity into ion channel gating; cGMP levels are dynamically regulated during odor stimulation and recovery, helping encode ON/OFF response properties and adaptation state (usuyama2012amodelof pages 2-3, usuyama2012amodelof pages 1-2) |
| 6 | Cyclic nucleotide-gated channel | tax-2, tax-4 | cGMP-gated cation channel | Opens in response to cGMP and mediates the primary depolarizing sensory current in AWC, linking cyclase activity to electrical and calcium responses (bargmann2006chemosensationinc. pages 10-12, usuyama2012amodelof pages 2-3) |
| 7 | Calcium influx and amplification | Ca2+ influx; channel complex includes CNG and downstream VGCCs | Ionic signaling / second messenger | CNG channel opening permits calcium entry and membrane depolarization; odor removal triggers a transient calcium rise in AWC, with feedback control shaping response duration and gain (usuyama2012amodelof pages 1-2, usuyama2012amodelof pages 2-3) |
| 8 | Voltage-gated calcium channel amplification | unc-2 and other VGCC components | Voltage-gated Ca2+ entry | Acts downstream of the primary cGMP-gated event to amplify sensory depolarization and calcium signaling in olfactory neurons, contributing to full physiological output (ferkey2021chemosensorysignaltransduction pages 15-16, usuyama2012amodelof pages 2-3) |
| 9 | cGMP-dependent protein kinase adaptation arm | egl-4 | PKG serine/threonine kinase activated by cGMP | Mediates adaptation across timescales: rapidly tunes AWC response thresholds, later acts on cytoplasmic targets, and after prolonged odor exposure translocates to the nucleus; ODR-1 function is required to keep EGL-4 cytoplasmic before prolonged stimulation (ferkey2021chemosensorysignaltransduction pages 17-18, ferkey2021chemosensorysignaltransduction pages 18-19) |
| 10 | Nuclear feedback on gene expression | hpl-2, odr-1 | Chromatin-mediated transcriptional repression | After prolonged odor exposure, nuclear EGL-4 phosphorylates HPL-2, which represses transcription of odr-1, creating a negative-feedback loop that contributes to long-term olfactory adaptation/plasticity (ferkey2021chemosensorysignaltransduction pages 18-19) |
Table: This table summarizes the best-supported AWC olfactory signal transduction pathway centered on ODR-1, from odor detection through cGMP signaling and long-term adaptation. It is useful for mapping where ODR-1 acts enzymatically and how its output is integrated into calcium signaling and feedback regulation.
The AWC olfactory neuron is an "OFF" neuron—it is tonically active in the absence of odor and is silenced by odor application. Upon odor removal, a transient increase in intracellular calcium occurs, the magnitude of which correlates with the duration of prior odor exposure (usuyama2012amodelof pages 1-2). Mathematical modeling of this pathway proposes that during odor stimulation, ODR-3 Gα suppresses guanylyl cyclase activity (reducing cGMP), and upon odor removal, the suppression ceases and cGMP synthesis is restored, opening CNG channels and triggering calcium influx (usuyama2012amodelof pages 2-3, usuyama2012amodelof pages 1-2). The model incorporates calcium-dependent negative feedback through guanylate cyclase-activating proteins (GCAPs/NCS-1) that regulate ODR-1 cyclase activity, ensuring transient calcium responses (usuyama2012amodelof pages 2-3).
Loss of odr-1 function results in defective chemotaxis to AWC-sensed odorants including benzaldehyde, isoamyl alcohol, and butanone, as well as defective AWB-mediated avoidance of repellents such as 2-nonanone (bargmann2006chemosensationinc. pages 10-12, khan2022molecularandneuronal pages 35-41). Importantly, odr-1 mutants retain normal dauer formation, distinguishing ODR-1 from DAF-11, which is required for both olfaction and dauer signaling (bargmann2006chemosensationinc. pages 10-12).
ODR-1 plays an essential role in olfactory adaptation through the cGMP-dependent protein kinase EGL-4. Adaptation in AWC occurs over multiple timescales: at short timescales (seconds), EGL-4 sets the threshold for calcium responsiveness needed for odor sensation in a gradient; at intermediate timescales (tens of minutes), EGL-4 phosphorylates cytoplasmic targets including the TAX-2 CNG channel subunit; after prolonged odor exposure (>60–80 minutes), EGL-4 translocates to the AWC nucleus (ferkey2021chemosensorysignaltransduction pages 17-18, ferkey2021chemosensorysignaltransduction pages 18-19).
ODR-1 function is specifically required to maintain EGL-4 in the cytoplasm until odor exposure triggers nuclear translocation. Furthermore, aberrantly high cGMP levels (due to loss of phosphodiesterases) block EGL-4 nuclear entry, indicating that precisely regulated cGMP dynamics—dependent on ODR-1—are critical for adaptation (ferkey2021chemosensorysignaltransduction pages 18-19). Once in the nucleus, EGL-4 phosphorylates the heterochromatin-binding factor HPL-2, which in turn downregulates transcription of the odr-1 gene itself, creating a negative feedback loop that contributes to long-term olfactory adaptation (ferkey2021chemosensorysignaltransduction pages 18-19). This mechanism may underlie heritable changes in AWC-mediated behaviors across generations.
A striking finding is that cGMP produced by ODR-1 in neurons such as AWB, AWC, and ASI can travel through gap junctions (innexin channels) to the ASH nociceptive neurons, where it acts non-cell-autonomously to dampen aversive signaling (sojka2025anextensivegap pages 1-2). Specifically, upon food deprivation, ODR-1-generated cGMP moves through an extensive gap junction neural network to reach ASH, where it binds to EGL-4 and stimulates phosphorylation and activation of RGS-2 and RGS-3, which in turn downregulate Gα (ODR-3/GPA-3) signaling and reduce behavioral sensitivity to nociceptive stimuli (sojka2025anextensivegap pages 1-2). Loss-of-function mutations in odr-1 result in hypersensitivity to ASH-detected chemical stimuli such as quinine, consistent with loss of this dampening mechanism (sojka2025anextensivegap pages 2-4, sojka2025anextensivegap pages 1-2). Similarly, cGMP produced by ODR-1 in ASK neurons has been shown to modulate the rising phase of ASH nociceptive calcium responses to copper ions through gap junction-mediated transport (wu2022positiveinteractionbetween pages 2-4).
The AWC neuron pair exhibits stochastic left-right asymmetry, with one neuron adopting AWCON fate and the other AWCOFF fate, defined by differential chemoreceptor expression. ODR-1 is part of the cGMP signaling pathway (along with DAF-11, ODR-3, and EGL-4) that is essential for maintaining AWCON and AWCOFF identities throughout the animal's life (alqadah2016stochasticleft–rightneuronal pages 4-4). Recent work has further demonstrated that receptor guanylyl cyclases in AWC mediate lateralized context-dependent olfactory plasticity: while ODR-1 is necessary for hexanol attraction under baseline conditions, a related guanylyl cyclase GCY-12 mediates context-dependent plasticity specifically in AWCOFF neurons through asymmetric molecular mechanisms (pandey2026alateralizedsensory pages 1-3, pandey2026alateralizedsensory pages 3-4).
A forward genetic screen identified ODR-1 as a regulator of DLK-1 (a conserved MAP3K) abundance in AWC sensory neurons. In odr-1 mutants, DLK-1 accumulates aberrantly throughout cilia and dendrites of AWC neurons, and AWC cilia display distorted morphology. These defects are ameliorated by loss of dlk-1 or its downstream transcription factor cebp-1, indicating a reciprocal antagonistic relationship between ODR-1 signaling and the DLK-1/CEBP-1 stress-signaling axis in maintaining ciliary structure (sun2025multipleregulatorsconstrain pages 1-2).
This study expanded the known network of innexin gap junctions that facilitate ODR-1-dependent cGMP transport to ASH neurons. Six additional innexins (INX-7, INX-15, INX-16, INX-17, UNC-7, and UNC-9) were identified as having overlapping and distinct roles within this regulatory network, underscoring the extensive non-cell-autonomous signaling circuit through which ODR-1-derived cGMP tunes sensory thresholds (sojka2025anextensivegap pages 2-4).
ODR-1 signaling in AWB and AWC sensory neurons was shown to mediate antipathy behavior toward certain diets, indicating that ODR-1's role extends beyond classical olfactory chemotaxis to food preference decisions that integrate nutritional needs with dietary lipid availability (stuhr2024c.elegansdisplay pages 1-5).
In a PNAS study, the authors demonstrated that symmetric behavioral plasticity in AWC neurons arises from asymmetric molecular mechanisms. While ODR-1 is required for baseline odorant attraction, GCY-12 drives context-dependent plasticity specifically in AWCOFF, revealing how multiple guanylyl cyclases partition signaling roles across lateralized neurons (pandey2026alateralizedsensory pages 1-3, pandey2026alateralizedsensory pages 3-4).
ODR-1/GCY-10 is a receptor-type guanylyl cyclase that functions as the primary cGMP-generating enzyme in the AWC and AWB olfactory neurons of C. elegans. It catalyzes the conversion of GTP to cGMP as an obligate heterodimer with DAF-11, with each subunit contributing essential but incomplete catalytic residues to the active site. Unlike many mammalian rGCs, ODR-1 is not activated by extracellular ligand binding to its ECD; rather, it is regulated intracellularly downstream of G-protein signaling. ODR-1 functions at sensory cilia, where it participates in the core olfactory transduction cascade (GPCR → ODR-3 Gα → ODR-1/DAF-11 → cGMP → TAX-2/TAX-4 CNG channels → Ca²⁺ influx). Beyond primary sensory transduction, ODR-1 is integral to olfactory adaptation through EGL-4-mediated feedback and to non-cell-autonomous modulation of nociception via gap junction-mediated cGMP transport. Recent studies have additionally revealed roles for ODR-1 in maintaining cilia structural integrity, regulating DLK-1 signaling, mediating food preference behaviors, and supporting lateralized signaling within the AWC neuron pair.
References
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