carA

Existing Annotations Review

GO Term	Evidence	Action	Reason
GO:0004930 G protein-coupled receptor activity	IBA GO_REF:0000033	ACCEPT	Summary: Phylogenetic inference that cAR1 is a G protein-coupled receptor is correct and central to its function. cAR1 is a canonical seven-transmembrane serpentine receptor that couples to heterotrimeric G proteins. Reason: cAR1 is a bona fide GPCR; direct evidence shows it catalyzes the heterotrimeric G-protein cycle upon cAMP binding. This is a core molecular function, though the more specific cAMP/chemoattractant receptor terms better capture the ligand. Supporting Evidence: PMID:11264536 occupied receptors, whether or not they are phosphorylated, catalyze the G-protein cycle
GO:0005886 plasma membrane	IBA GO_REF:0000033	ACCEPT	Summary: cAR1 is a multi-pass plasma-membrane receptor, confirmed by direct subcellular localization studies. Phylogenetic inference of plasma membrane localization is correct. Reason: The plasma membrane origin of cAR1-enriched fractions was confirmed by cell-surface biotinylation and immunoelectron microscopy; this is where cAR1 binds extracellular cAMP and signals. Supporting Evidence: PMID:9168471 Cell surface biotinylation and preembedding immunoelectron microscopy both confirmed the plasma membrane origin of this preparation
GO:0007189 adenylate cyclase-activating G protein-coupled receptor signaling pathway	IBA GO_REF:0000033	MODIFY	Summary: cAR1 activates adenylyl cyclase (ACA) via heterotrimeric G proteins as part of the cAMP relay. This IBA term is correct; a more specific child term for cAMP-receptor signaling exists and is used elsewhere in this record. Reason: The essence is correct, but the cAMP-receptor-specific child term GO:0140582 (used by multiple experimental annotations here) more precisely captures cAR1 signaling. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: PANTHER:PTN000560943 · PANTHER node for the Dictyostelium cAMP-receptor (cAR) family SUPPORTS SOURCE BUT NOT TARGET The adenylate-cyclase-activating signaling role is real for cAR1, but a cAMP-receptor-specific child term captures cAR1 more precisely than the generic GPCR parent dictyBase:DDB_G0273397 · Dictyostelium aggregation-stage cAR paralog SUPPORTS SOURCE BUT NOT TARGET Source paralog genuinely couples to adenylate cyclase; the term is correct but too general for cAR1 Proposed replacements: adenylate cyclase-activating G protein-coupled cAMP receptor signaling pathway Supporting Evidence: PMID:9578623 assessed the capacity of each to mediate chemotaxis, activation of adenylyl cyclase and actin polymerization
GO:0004888 transmembrane signaling receptor activity	IEA GO_REF:0000002	KEEP AS NON CORE	Summary: A correct but general parent of GPCR/cAMP receptor activity. cAR1 is a transmembrane signaling receptor, but more informative child terms apply. Reason: Accurate but non-specific; the core function is better represented by cAMP receptor activity and G protein-coupled chemoattractant receptor activity. Supporting Evidence: PMID:11264536 occupied receptors, whether or not they are phosphorylated, catalyze the G-protein cycle
GO:0004930 G protein-coupled receptor activity	IEA GO_REF:0000002	ACCEPT	Summary: InterPro2GO inference of GPCR activity, duplicating the IBA annotation and consistent with cAR1 being a serpentine GPCR. Reason: cAR1 is a canonical GPCR; this electronic annotation is correct and corroborated by direct evidence of G-protein activation. Supporting Evidence: PMID:11264536 occupied receptors, whether or not they are phosphorylated, catalyze the G-protein cycle
GO:0007165 signal transduction	IEA GO_REF:0000117	KEEP AS NON CORE	Summary: A very general process term. cAR1 is a signal transduction receptor, but far more specific pathway terms are available and used here. Reason: Correct but uninformative; retained as non-core because specific cAMP-receptor signaling terms better represent the function. Supporting Evidence: PMID:1849108 cAR1-mediated signal transduction controls the development of Dictyostelium
GO:0007166 cell surface receptor signaling pathway	IEA GO_REF:0000002	KEEP AS NON CORE	Summary: Correct general parent term. cAR1 is a cell-surface receptor that initiates signaling, but a more specific GPCR/cAMP-receptor term is preferable. Reason: Accurate but non-specific; specific cAMP receptor signaling terms are used as core. Supporting Evidence: PMID:1849108 cAR1, a G-protein-linked surface cAMP receptor, plays a central role in the development of Dictyostelium
GO:0007186 G protein-coupled receptor signaling pathway	IEA GO_REF:0000002	KEEP AS NON CORE	Summary: cAR1 signals via a G protein-coupled receptor pathway, which is accurate. This term is a parent of the specific adenylate cyclase-activating cAMP receptor pathway used for the experimental annotations. Reason: Accurate but general; the specific GO:0140582 term better captures cAR1's core signaling role. Supporting Evidence: PMID:7949426 cAR1, coupled by a typical heterotrimeric G-protein to intracellular effectors
GO:0016020 membrane	IEA GO_REF:0000120	KEEP AS NON CORE	Summary: cAR1 is an integral membrane protein; this general term is correct but subsumed by the more specific plasma membrane annotation. Reason: Accurate but non-specific relative to the plasma membrane localization that is directly supported. Supporting Evidence: PMID:9168471 Cell surface biotinylation and preembedding immunoelectron microscopy both confirmed the plasma membrane origin of this preparation
GO:0030552 cAMP binding	IEA GO_REF:0000002	ACCEPT	Summary: cAR1 binds extracellular cAMP with nanomolar affinity; direct ligand binding is well established. This InterPro2GO annotation is correct. Reason: cAMP binding is the defining ligand-recognition activity of cAR1, supported by direct binding assays. Supporting Evidence: PMID:1648967 The affinity of the expressed cAR1 was similar to that of the endogenous receptors in aggregation stage cells
GO:0035589 G protein-coupled purinergic nucleotide receptor signaling pathway	IEA GO_REF:0000108	REMOVE	Summary: This electronically inferred term classifies cAR1 signaling as purinergic nucleotide receptor signaling. cAR1 is a cAMP receptor whose signaling is distinct from classical purinergic (P2X/P2Y) receptor pathways; this is an over-propagation from automated inter-ontology inference. Reason: cAR1 is not a purinergic (ATP/ADP/UTP) receptor; it recognizes the second-messenger-derived chemoattractant cAMP. Its signaling is captured accurately by the cAMP receptor / adenylate cyclase-activating cAMP receptor terms. This IEA (GO_REF:0000108, logical inference) mislabels the pathway and should be removed.
GO:1904776 regulation of protein localization to cell cortex	IGI PMID:40934557 The Ras association domain of DydA as a specific reporter of...	KEEP AS NON CORE	Summary: cAR1 (Car1/3) and G-protein signaling are required for chemoattractant- induced cortical/leading-edge translocation of a RasG biosensor, placing cAR1 upstream of cortical protein localization during chemotaxis. Reason: A valid downstream developmental/chemotactic consequence of cAR1 signaling rather than its core molecular function. Supporting Evidence: PMID:40934557 This localization required GPCR Car1/3 and G-protein signaling
GO:0010856 adenylate cyclase activator activity	IMP PMID:9578623 Switching of chemoattractant receptors programs development ...	KEEP AS NON CORE	Summary: cAR1 activates adenylyl cyclase (ACA) as part of the cAMP relay. The activation is receptor-mediated and G-protein-dependent (indirect) rather than cAR1 acting directly on the cyclase, so this MF is best treated as non-core. Reason: cAR1 mediates activation of adenylyl cyclase, but does so indirectly via heterotrimeric G proteins; the direct molecular function is receptor/cAMP binding. Retained as non-core. Supporting Evidence: PMID:9578623 assessed the capacity of each to mediate chemotaxis, activation of adenylyl cyclase and actin polymerization
GO:0030295 protein kinase activator activity	IMP PMID:8670837 Dual role of cAMP and involvement of both G-proteins and ras...	KEEP AS NON CORE	Summary: cAMP binding to cAR1 stimulates activation of the MAP kinase ERK2, but this occurs through a G-protein/Ras-dependent cascade, not by cAR1 directly binding and activating a kinase. Reason: The kinase activation is an indirect downstream effect of cAR1 signaling; the core molecular function is receptor/ligand binding. Retained as non-core. Supporting Evidence: PMID:8670837 Binding of extracellular cAMP to cAMP receptor 1, a G-protein coupled cell surface receptor, transiently stimulates phosphorylation, activation and nuclear translocation of ERK2
GO:0140295 pathogen-derived receptor ligand activity	IDA PMID:37866633 The Legionella autoinducer LAI-1 is delivered by outer membr...	REMOVE	Summary: This annotation assigns cAR1 a pathogen-derived receptor ligand activity. cAR1 is a host cell-surface receptor, not a pathogen-derived ligand, and the cited study (Legionella LAI-1 delivered via outer membrane vesicles, which inhibit Dictyostelium migration) does not mention cAR1 in its full text. Reason: The molecular function is biologically inverted for cAR1 (a receptor cannot have receptor-ligand activity), and the full text of PMID:37866633 does not implicate cAR1 as the ligand or receptor for LAI-1. This appears to be a curation/mapping error rather than a supportable function.
GO:0140676 oscillatory cAMP signaling	IDA PMID:37921687 Collective signalling drives rapid jumping between cell stat...	ACCEPT	Summary: cAR1 is the receptor that detects the collective, oscillatory cAMP signals that coordinate the developmental gene-expression jump during aggregation. Oscillatory cAMP signaling is a central role of cAR1. Reason: cAR1 mediates the cell's response to collective oscillations of cAMP; this oscillatory cAMP signaling is a core aspect of cAR1 function during aggregation. Supporting Evidence: PMID:37921687 the jump coincides with the onset of collective oscillations of cAMP
GO:0140582 adenylate cyclase-activating G protein-coupled cAMP receptor signaling pathway	IMP PMID:8280098 Phospholipase C in Dictyostelium discoideum. Identification ...	ACCEPT	Summary: Genetic evidence links cAR1 and its G proteins to cAMP-regulated signaling (here, dual regulation of phospholipase C), consistent with cAR1 operating the G protein-coupled cAMP receptor signaling pathway. Reason: cAR1 is a core component of the surface cAMP receptor / G-protein signaling module; the paper directly implicates cAR1 with a G protein in cAMP signal transduction. Supporting Evidence: PMID:8280098 The inhibitory pathway is composed of the surface receptor cAR1 and the G-protein G1
GO:0070371 ERK1 and ERK2 cascade	IMP PMID:8670837 Dual role of cAMP and involvement of both G-proteins and ras...	ACCEPT	Summary: cAMP binding to cAR1 transiently activates ERK2 in a G-protein-dependent manner, placing cAR1 upstream of the ERK cascade during chemotactic signaling. Reason: Directly supported by the finding that cAR1 activation stimulates ERK2 phosphorylation, activation and nuclear translocation, a genuine downstream signaling role. Supporting Evidence: PMID:8670837 Binding of extracellular cAMP to cAMP receptor 1, a G-protein coupled cell surface receptor, transiently stimulates phosphorylation, activation and nuclear translocation of ERK2
GO:0030695 GTPase regulator activity	IDA PMID:21103944 Chemoattractant-mediated Rap1 activation requires GPCR/G pro...	KEEP AS NON CORE	Summary: As a GPCR, cAR1 acts as a guanine-nucleotide exchange factor for heterotrimeric G proteins and is required for chemoattractant-mediated activation of the small GTPase Rap1. Its GTPase-regulator role is receptor- driven and largely mediated through the heterotrimeric G proteins. Reason: cAR1 regulates GTPase cycling indirectly as part of its GPCR function; the core molecular activity is receptor/cAMP binding. Retained as non-core. Supporting Evidence: PMID:21103944 The rapid Rap1 activation upon cAMP chemoattractant stimulation was absent in cells lacking chemoattractant cAMP receptors cAR1/cAR3
GO:0140582 adenylate cyclase-activating G protein-coupled cAMP receptor signaling pathway	IDA PMID:8999903 Random mutagenesis of the cAMP chemoattractant receptor, cAR...	ACCEPT	Summary: Mutagenesis of cAR1 directly demonstrates its role in transducing extracellular cAMP signals via G-protein-dependent (and independent) mechanisms, the core cAMP receptor signaling pathway. Reason: Direct experimental evidence that cAR1 mediates cAMP signal transduction; a core process for this receptor. Supporting Evidence: PMID:8999903 The cAMP chemoattractant receptor, cAR1, of Dictyostelium transduces extracellular cAMP signals via G protein-dependent and G protein-independent mechanisms
GO:0005829 cytosol	IDA PMID:21541374 Quantification of GPCR internalization by single-molecule mi...	KEEP AS NON CORE	Summary: Single-molecule imaging shows the fraction of cytosolic cAR1 increases after persistent agonist stimulation, reflecting phosphorylation-dependent receptor internalization rather than a steady-state cytosolic pool. Reason: The cytosolic signal represents internalized receptor during desensitization, not the site of the receptor's core signaling function (the plasma membrane). Retained as non-core. Supporting Evidence: PMID:21541374 the fraction of cytosolic receptors increases after persistent agonist stimulation
GO:0031252 cell leading edge	IDA PMID:18469015 A spatially restricted increase in receptor mobility is invo...	ACCEPT	Summary: Single-molecule microscopy shows an agonist-induced increase in cAR1 mobility at the leading edge of chemotaxing cells, contributing to directional sensing. cAR1 is active at the leading edge. Reason: Directly supported localization of active cAR1 to the leading edge during chemotaxis, a functionally important site. Supporting Evidence: PMID:18469015 an agonist-induced increase in the mobile fraction of cAMP-receptor at the leading edge of chemotacting Dictyostelium discoideum cells
GO:0031152 aggregation involved in sorocarp development	IMP PMID:15507682 A rapid and efficient method to generate multiple gene disru...	ACCEPT	Summary: cAR1 is essential for the aggregation stage of Dictyostelium development; cAR1 nulls fail to aggregate. Aggregation is a core biological process for cAR1. Reason: cAR1-mediated cAMP signaling drives the chemotactic aggregation of starving cells into a multicellular mound; loss of cAR1 arrests development in early aggregation. Supporting Evidence: PMID:1849108 fail to bind or sense cAMP and arrest in early development
GO:0031152 aggregation involved in sorocarp development	IMP PMID:17630977 Regulation of G protein-coupled cAMP receptor activation by ...	ACCEPT	Summary: cAR1 is essential for multicellular development; constitutively active Ile-104 mutants block development, confirming cAR1's role in aggregation-stage development. Reason: Directly supported requirement of properly regulated cAR1 for the aggregation/development program. Supporting Evidence: PMID:17630977 cAR1, a G protein-coupled cAMP receptor, is essential for multicellular development of Dictyostelium
GO:0031152 aggregation involved in sorocarp development	IEP PMID:25887420 Leaps and lulls in the developmental transcriptome of Dictyo...	KEEP AS NON CORE	Summary: cAR1/carA is expressed during the aggregation phase when starving cells communicate via extracellular cAMP. Expression-pattern evidence is consistent with, but weaker than, the mutant-based support for a role in aggregation. Reason: IEP (expression) evidence corroborates the aggregation role established by mutant studies; retained as non-core given the weaker evidence type. Supporting Evidence: PMID:25887420 communicate via extracellular cAMP, aggregate by tens of thousands and develop into multicellular organisms
GO:0097696 cell surface receptor signaling pathway via STAT	IMP PMID:9670017 Developmentally and spatially regulated activation of a Dict...	ACCEPT	Summary: Extracellular cAMP acting through cAR1 rapidly induces tyrosine phosphorylation and nuclear translocation of Dd-STAT, a G protein-independent signaling output of the receptor. Reason: Directly supported role of cAR1 in mediating STAT (Dd-STAT) activation, a genuine signaling pathway downstream of the receptor. Supporting Evidence: PMID:9670017 The tyrosine phosphorylation and nuclear localization of Dd-STAT are induced very rapidly by extracellular cAMP through the serpentine cAMP receptor cAR1
GO:0005886 plasma membrane	TAS PMID:15473840 Chemoattractant signaling in dictyostelium discoideum.	ACCEPT	Summary: cAR1 is a plasma-membrane chemoattractant receptor; this is a well-established, traceable statement in the chemoattractant-signaling literature. Reason: Plasma membrane is the functional location of cAR1, corroborated by direct biochemical/microscopy evidence. Supporting Evidence: PMID:9168471 Cell surface biotinylation and preembedding immunoelectron microscopy both confirmed the plasma membrane origin of this preparation
GO:0005886 plasma membrane	IDA PMID:9168471 Identification of detergent-resistant plasma membrane microd...	ACCEPT	Summary: cAR1 is enriched in detergent-resistant plasma-membrane microdomains; the plasma membrane origin was directly confirmed by surface biotinylation and immunoelectron microscopy. Reason: Direct experimental confirmation of cAR1's plasma membrane localization, the site of its receptor function. Supporting Evidence: PMID:9168471 Cell surface biotinylation and preembedding immunoelectron microscopy both confirmed the plasma membrane origin of this preparation
GO:0005515 protein binding	IPI PMID:25143405 Arrestins function in cAR1 GPCR-mediated signaling and cAR1 ...	KEEP AS NON CORE	Summary: cAR1 physically interacts with arrestin domain-containing proteins (AdcC); activation of cAR1 recruits AdcC to the membrane and links the receptor to periodic ERK2 activation and internalization. The bare protein binding term is uninformative. Reason: The specific interaction (arrestin binding regulating cAR1 signaling and internalization) is informative, but the generic GO:0005515 term does not convey function; retained as non-core. A more specific arrestin-binding molecular function would be preferable. Supporting Evidence: PMID:25143405 activation of cAR1 promotes the transient membrane recruitment of AdcC and interaction with cAR1
GO:0005769 early endosome	IDA PMID:7628637 Localization of cyclic-AMP receptors with acidosomes in Dict...	KEEP AS NON CORE	Summary: Internalized cAR1 localizes with acidosomes, which the authors argue are analogous to early/recycling endosomes and may be a site for recycling of internalized receptors. Reason: Endosomal localization reflects receptor trafficking/recycling after internalization rather than the core plasma-membrane signaling function. Retained as non-core. Supporting Evidence: PMID:7628637 acidosomes contain abundant receptors for cyclic AMP (CAR1) and that it may be the site for recycling of internalized receptors
GO:0009986 cell surface	IDA PMID:15507682 A rapid and efficient method to generate multiple gene disru...	ACCEPT	Summary: cAR1 is a cell-surface cAMP receptor, consistent with its plasma-membrane localization and function in sensing extracellular cAMP. Reason: cAR1 acts at the cell surface where it binds extracellular cAMP; corroborated by its description as a surface cAMP receptor. Supporting Evidence: PMID:1849108 cAR1, a G-protein-linked surface cAMP receptor, plays a central role in the development of Dictyostelium
GO:0006935 chemotaxis	IMP PMID:15507682 A rapid and efficient method to generate multiple gene disru...	ACCEPT	Summary: cAR1 mediates chemotaxis toward cAMP, the defining behavioral response it controls during aggregation. Reason: cAR1 is required for directed migration up cAMP gradients; chemotaxis is a core biological process for the receptor. Supporting Evidence: PMID:9578623 assessed the capacity of each to mediate chemotaxis, activation of adenylyl cyclase and actin polymerization
GO:0006935 chemotaxis	IGI PMID:9578623 Switching of chemoattractant receptors programs development ...	ACCEPT	Summary: Genetic complementation of car1-/car3- cells with cAR1 restores chemotaxis, confirming cAR1's role in chemotactic responses to cAMP. Reason: cAR1 mediates chemotaxis to cAMP; a core biological process directly tested by receptor expression assays. Supporting Evidence: PMID:9578623 assessed the capacity of each to mediate chemotaxis, activation of adenylyl cyclase and actin polymerization
GO:0023058 adaptation of signaling pathway	IMP PMID:23902692 Phosphorylation of chemoattractant receptors regulates chemo...	ACCEPT	Summary: Agonist-induced phosphorylation of cAR1 is required for adaptation of adenylyl cyclase responses and for proper long-range oscillatory cAMP wave production, a signaling-adaptation function. Reason: Non-phosphorylatable cAR1 mutants fail to adapt adenylyl cyclase and lose directional chemotaxis, directly demonstrating cAR1's role in signaling adaptation. Supporting Evidence: PMID:23902692 receptor phosphorylation is required to regulate adenylyl cyclase adaptation, long-range oscillatory cAMP wave production and cytoskeletal actin response
GO:0140582 adenylate cyclase-activating G protein-coupled cAMP receptor signaling pathway	IDA PMID:11264536 Receptor-mediated activation of heterotrimeric G-proteins in...	ACCEPT	Summary: FRET imaging in living cells shows chemoattractant (cAMP) binding to the receptor drives dissociation/reassociation of the heterotrimeric G protein, directly demonstrating the cAMP receptor signaling pathway. Reason: Direct in vivo evidence that cAR1 catalyzes the G-protein cycle upon cAMP binding; core to cAMP receptor signaling. Supporting Evidence: PMID:11264536 The G-protein heterotrimer rapidly dissociated and reassociated upon addition and removal of chemoattractant
GO:0140582 adenylate cyclase-activating G protein-coupled cAMP receptor signaling pathway	IMP PMID:7949426 Two cAMP receptors activate common signaling pathways in Dic...	ACCEPT	Summary: cAR1 is the primary receptor mediating cAMP responses (cAMP relay, cGMP synthesis) coupled through a heterotrimeric G protein; car1- cells have strongly reduced responses. Reason: Genetic evidence that cAR1 normally mediates cAMP-relay and other responses via a heterotrimeric G protein; core cAMP receptor signaling. Supporting Evidence: PMID:7949426 Dictyostelium cells respond to cAMP using one such receptor, cAR1, coupled by a typical heterotrimeric G-protein to intracellular effectors
GO:0140582 adenylate cyclase-activating G protein-coupled cAMP receptor signaling pathway	IGI PMID:7949426 Two cAMP receptors activate common signaling pathways in Dic...	ACCEPT	Summary: Double car1-/car3- deletion abolishes cAMP sensitivity, and cAR1 and cAR3 act redundantly through the same G protein, confirming cAR1's role in the cAMP receptor signaling pathway. Reason: Genetic interaction evidence that cAR1 (with cAR3) mediates cAMP signaling via a shared heterotrimeric G protein. Supporting Evidence: PMID:7949426 both interact with the same heterotrimeric G-protein to mediate these and other responses
GO:1903013 response to differentiation-inducing factor 1	HDA PMID:25518940 The Dictyostelium prestalk inducer differentiation-inducing ...	KEEP AS NON CORE	Summary: Phosphoproteomic analysis shows the cAMP receptor is rapidly dephosphorylated in response to DIF-1, reflecting cross-talk/antagonism between DIF-1 and cAMP signaling. Reason: cAR1's dephosphorylation in response to DIF-1 is a regulatory cross-talk response, not a core function of the receptor. Retained as non-core. Supporting Evidence: PMID:25518940 the rapid dephosphorylation of the cAMP receptor that we observe in response to DIF-1
GO:0001637 G protein-coupled chemoattractant receptor activity	IDA PMID:11264536 Receptor-mediated activation of heterotrimeric G-proteins in...	ACCEPT	Summary: cAR1 is the G protein-coupled receptor for the chemoattractant cAMP; occupied receptors directly catalyze the G-protein cycle as shown by live-cell FRET. This is a core molecular function. Reason: Directly supported chemoattractant GPCR activity coupling cAMP detection to heterotrimeric G-protein activation. Supporting Evidence: PMID:11264536 occupied receptors, whether or not they are phosphorylated, catalyze the G-protein cycle
GO:0001646 cAMP receptor activity	IDA PMID:9578623 Switching of chemoattractant receptors programs development ...	ACCEPT	Summary: cAR1 is the founding member of the Dictyostelium cAMP receptor family and functions as a cAMP receptor; direct expression/complementation assays confirm this activity. This is the core molecular function. Reason: Directly supported cAMP receptor activity; the defining function of cAR1. Supporting Evidence: PMID:9578623 The cAMP chemoattractant receptor family of Dictyostelium discoideum is composed of four receptors (cAR1-cAR4)
GO:0001646 cAMP receptor activity	IGI PMID:9578623 Switching of chemoattractant receptors programs development ...	ACCEPT	Summary: Complementation of receptor-null cells with cAR1 restores cAMP responses, genetically confirming cAR1 cAMP receptor activity. Reason: cAMP receptor activity is the core molecular function of cAR1; supported by genetic complementation. Supporting Evidence: PMID:9578623 The cAMP chemoattractant receptor family of Dictyostelium discoideum is composed of four receptors (cAR1-cAR4)
GO:0010225 response to UV-C	IDA PMID:25858552 Response of Dictyostelium discoideum to UV-C and involvement...	KEEP AS NON CORE	Summary: carA/car1 is among the developmentally regulated genes whose expression was examined during the UV-C response of Dictyostelium; this is a stress- response context rather than a core receptor function. Reason: cAR1 involvement here reflects developmental gene-expression changes under UV-C stress, not the receptor's core molecular role. Retained as non-core. Supporting Evidence: PMID:25858552 Expression of developmentally regulated genes yakA, car1, aca, csA, regA, ctnA, ctnB, gp24, hspD and dsn were analysed using semiquantitative RT-PCR
GO:0030552 cAMP binding	IDA PMID:15507682 A rapid and efficient method to generate multiple gene disru...	ACCEPT	Summary: cAR1 directly binds extracellular cAMP; ligand binding is the receptor's defining biochemical activity, well documented across many studies. Reason: cAMP binding is a core molecular function of cAR1, supported by direct binding measurements. Supporting Evidence: PMID:1648967 The affinity of the expressed cAR1 was similar to that of the endogenous receptors in aggregation stage cells
GO:0030552 cAMP binding	IDA PMID:1648967 Overexpression of the cAMP receptor 1 in growing Dictyosteli...	ACCEPT	Summary: Direct binding assays show cAR1 binds cAMP with nanomolar affinity (two affinity states, Kd ~30 and 300 nM), matching endogenous aggregation-stage receptors. Reason: Direct measurement of cAR1 cAMP binding affinity; a core molecular function. Supporting Evidence: PMID:1648967 two affinity states with Kd's of PMID:1648967 The affinity of the expressed cAR1 was similar to that of the endogenous receptors in aggregation stage cells
GO:0030552 cAMP binding	IMP PMID:17630977 Regulation of G protein-coupled cAMP receptor activation by ...	ACCEPT	Summary: Ile-104 substitutions in cAR1 dramatically alter the receptor's cAMP affinity, demonstrating that cAR1 binds cAMP and that this residue tunes ligand affinity. Reason: Mutational evidence directly implicating cAR1 in cAMP binding (affinity modulation); core molecular function. Supporting Evidence: PMID:17630977 all Ile(104) substitutions, except for the most conservative, dramatically elevated the receptor's cAMP affinity
GO:0030552 cAMP binding	IDA PMID:8999903 Random mutagenesis of the cAMP chemoattractant receptor, cAR...	ACCEPT	Summary: Random mutagenesis identified cAR1 mutants with altered cAMP binding (including conditional binding defects), directly demonstrating cAR1 cAMP binding activity. Reason: Direct biochemical evidence for cAR1 cAMP binding; core molecular function. Supporting Evidence: PMID:8999903 One class had a conditional defect in cAMP binding that was reversed by high salt
GO:0030552 cAMP binding	IMP PMID:9578623 Switching of chemoattractant receptors programs development ...	ACCEPT	Summary: cAR1 and related receptors sense different concentration ranges of cAMP; mutations altering ligand recognition confirm cAR1 cAMP binding activity. Reason: Mutational evidence that cAR1 binds cAMP; core molecular function. Supporting Evidence: PMID:9578623 various receptors and mutants sense different concentration ranges of cAMP
GO:1904643 response to curcumin	IDA PMID:26449461 Curcumin inhibits development and cell adhesion in Dictyoste...	KEEP AS NON CORE	Summary: Curcumin delays Dictyostelium chemotaxis, adhesion and development. This is a chemical/developmental response of the organism rather than a core cAR1 molecular function. Reason: cAR1's involvement reflects curcumin's inhibitory effect on cAMP-driven chemotaxis and development, a stimulus-response phenotype rather than a core receptor function. Retained as non-core. Supporting Evidence: PMID:26449461 This resulted in delayed chemotaxis, adhesion, and development of the organism
GO:1902168 response to catechin	IDA PMID:23516620 The green tea catechin epigallocatechin gallate (EGCG) block...	KEEP AS NON CORE	Summary: The green-tea catechin EGCG reduces random movement and chemotaxis of Dictyostelium and stalls development, a chemical-response phenotype affecting cAMP-driven chemotaxis. Reason: Reflects a stimulus-response (catechin) effect on chemotaxis/development rather than a core cAR1 molecular function. Retained as non-core. Supporting Evidence: PMID:23516620 EGCG reduces both random movement and chemotaxis of Dictyostelium amoebae
GO:0050764 regulation of phagocytosis	IMP PMID:17905919 Developmental commitment in Dictyostelium discoideum.	KEEP AS NON CORE	Summary: Extracellular cAMP pulses (sensed via cAR1) are sufficient to induce developmental commitment and the loss of phagocytosis in starving cells, placing cAR1 signaling upstream of phagocytosis regulation. Reason: Down-regulation of phagocytosis is a developmental consequence of cAMP and cAR1 signaling during commitment, not a core receptor function. Retained as non-core. Supporting Evidence: PMID:17905919 cAMP pulses are sufficient to induce both commitment and the loss of phagocytosis in starving cells
GO:0002029 desensitization of G protein-coupled receptor signaling pathway	IMP PMID:15574880 Constitutively active G protein-coupled receptor mutants blo...	ACCEPT	Summary: cAR1-mediated pathways undergo adaptation/desensitization; constitutively active DN mutants block development by turning on natural adaptation mechanisms, implicating cAR1 in GPCR desensitization. Reason: Directly supported role of cAR1 in adaptation/desensitization of its signaling; a genuine regulatory process for the receptor. Supporting Evidence: PMID:15574880 The activation of multiple pathways by cAR1 is transient because of poorly defined adaptation mechanisms
GO:0008277 regulation of G protein-coupled receptor signaling pathway	IDA PMID:11264536 Receptor-mediated activation of heterotrimeric G-proteins in...	KEEP AS NON CORE	Summary: Live-cell FRET shows that G-protein activation by occupied cAR1 reaches a steady state and does not decline even as responses adapt, informing how cAR1 GPCR signaling is regulated. Reason: Captures regulation of cAR1's own GPCR signaling (adaptation occurring downstream of the receptor); a regulatory aspect retained as non-core relative to the core receptor activity. Supporting Evidence: PMID:11264536 adaptation occurs at another point in the signaling pathway, and occupied receptors, whether or not they are phosphorylated, catalyze the G-protein cycle
GO:0031152 aggregation involved in sorocarp development	IMP PMID:1849108 Gene targeting of the aggregation stage cAMP receptor cAR1 i...	ACCEPT	Summary: Gene targeting shows cAR1-null mutants fail to bind/sense cAMP and arrest in early development, proving cAR1-mediated signaling controls the aggregation stage of development. Reason: Definitive genetic evidence that cAR1 is required for aggregation-stage development; a core biological process. Supporting Evidence: PMID:1849108 fail to bind or sense cAMP and arrest in early development PMID:1849108 cAR1-mediated signal transduction controls the development of Dictyostelium

Gene Description

Existing Annotations Review

Core Functions

cAR1 is the cell-surface cAMP receptor that binds extracellular cAMP, the chemoattractant coordinating aggregation. Acting as a seven-transmembrane GPCR at the plasma membrane, cAR1 detects cAMP to drive directed chemotaxis and the developmental aggregation program.

cAR1 directly binds the extracellular chemoattractant cAMP with nanomolar affinity at the plasma membrane; this ligand-binding activity is the biochemical basis for its receptor function and is tunable by mutations in the transmembrane core.

References

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