che-2

Existing Annotations Review

GO Term	Evidence	Action	Reason
GO:0060271 cilium assembly	IBA GO_REF:0000033	ACCEPT	Summary: CHE-2 is essential for cilium assembly. PMID:10518500 demonstrates that che-2 mutants have extremely short cilia with abnormal posterior projection, and that cilium extension fails during development in these mutants. The IBA annotation based on phylogenetic inference from the IFT80 orthology group is well-supported by direct experimental evidence. Reason: Core function strongly supported by literature. PMID:10518500 shows che-2 mutants have severely defective cilia that remain short throughout development. Expression of che-2 can rescue cilium morphology even at adult stage, demonstrating its essential role in cilium assembly. Supporting Evidence: PMID:10518500 These mutants have extremely short cilia with an abnormal posterior projection, and show defects in behaviors that are mediated by ciliated sensory neurons. PMID:10518500 Using green fluorescent protein, we found that the extension of cilia in wild-type animals took place at the late embryonic stage, whereas the cilia of che-2 mutant animals remained always short during development. file:worm/che-2/che-2-deep-research-falcon.md model: Edison Scientific Literature
GO:0005929 cilium	IBA GO_REF:0000033	ACCEPT	Summary: CHE-2 localizes to cilia as demonstrated by GFP tagging experiments in PMID:10518500. This IBA annotation is phylogenetically inferred and consistent with experimental localization data showing CHE-2::GFP in sensory cilia. Reason: Localization to cilium is directly demonstrated experimentally. CHE-2-tagged GFP localizes to cilia of almost all ciliated sensory neurons (PMID:10518500). Supporting Evidence: PMID:10518500 CHE-2-tagged green fluorescent protein is localized at the cilia of almost all the ciliated sensory neurons.
GO:0030992 intraciliary transport particle B	IBA GO_REF:0000033	ACCEPT	Summary: CHE-2/IFT80 is a well-established component of the IFT-B complex. This is supported by ComplexPortal annotation (CPX-1290) and extensive literature on IFT-B composition. PMID:22922713 provides detailed mechanistic evidence showing that IFT-B components including CHE-2 orthologs move together during anterograde transport. Reason: Core structural function as IFT-B component is well-established through phylogenetic conservation and direct biochemical evidence. UniProt entry references ComplexPortal CPX-1290 (Intraflagellar transport complex B). The WD40 domain architecture of CHE-2 is characteristic of IFT-B components. Supporting Evidence: PMID:22922713 Similar to OSM-6, in dyf-2(jhu616), all other IFT-B components examined also showed active anterograde movements, but lost most of the retrograde IFT movements and accumulate at the ciliary tip
GO:0005929 cilium	IEA GO_REF:0000044	ACCEPT	Summary: IEA annotation based on UniProt subcellular location vocabulary mapping. This is consistent with but less specific than the IBA annotation for the same term. Reason: Redundant with IBA annotation but acceptable as independent evidence line. The UniProt entry explicitly states subcellular location as cilium. Supporting Evidence: UniProt:G5EGF0 SUBCELLULAR LOCATION: Cell projection, cilium
GO:0005929 cilium	NAS PMID:28479320 Dynein-Driven Retrograde Intraflagellar Transport Is Triphas...	ACCEPT	Summary: NAS annotation from ComplexPortal referencing a study on dynein-driven retrograde IFT. The paper discusses IFT-B components including CHE-2 orthologs in the context of ciliary transport. Reason: Consistent with other cilium localization annotations. While NAS is weaker evidence than IDA, it is supported by the broader literature context. Supporting Evidence: PMID:28479320 Disruption of the dynein-2 tail domain, light intermediate chain, or intraflagellar transport (IFT)-B complex abolishes dynein-2's ciliary localization, revealing their important roles in ciliary entry of dynein-2
GO:0042073 intraciliary transport	NAS PMID:28479320 Dynein-Driven Retrograde Intraflagellar Transport Is Triphas...	MODIFY	Summary: CHE-2 as an IFT-B component participates in intraciliary transport. PMID:28479320 focuses on retrograde IFT but discusses the overall IFT machinery including IFT-B. PMID:22922713 provides more detailed evidence of CHE-2 orthologs' IFT movement. Reason: The annotation is correct but could be more specific. CHE-2/IFT80 is primarily involved in anterograde transport as part of the IFT-B complex. Consider using GO:0035720 (intraciliary anterograde transport) for greater specificity. Proposed replacements: intraciliary anterograde transport Supporting Evidence: PMID:22922713 Similar to OSM-6, in dyf-2(jhu616), all other IFT-B components examined also showed active anterograde movements, but lost most of the retrograde IFT movements and accumulate at the ciliary tip
GO:0060271 cilium assembly	NAS PMID:28479320 Dynein-Driven Retrograde Intraflagellar Transport Is Triphas...	ACCEPT	Summary: NAS annotation for cilium assembly from ComplexPortal. Redundant with IBA and IMP annotations for the same term but acceptable as additional evidence source. Reason: Consistent with IBA and IMP annotations. Cilium assembly is a core function of CHE-2. Supporting Evidence: PMID:10518500 Hence, the abnormal posterior projection is due to the inability of cilia to extend, rather than degeneration of cilia once correctly formed
GO:0003674 molecular_function	ND GO_REF:0000015	ACCEPT	Summary: ND (No biological Data) annotation indicates no specific molecular function has been experimentally determined. While CHE-2 is a structural component of IFT-B, it does not appear to have enzymatic activity - its function is primarily as a scaffold/adaptor. Reason: Appropriate use of ND. CHE-2 has no known enzymatic or catalytic activity; it functions as a structural component of the IFT-B complex through protein-protein interactions mediated by its WD40 repeats. Supporting Evidence: PMID:10518500 The che-2 gene encodes a new member of the WD40 protein family, suggesting that it acts in protein-protein interaction.
GO:0090325 regulation of locomotion involved in locomotory behavior	IGI PMID:26434723 The Importance of cGMP Signaling in Sensory Cilia for Body S...	KEEP AS NON CORE	Summary: This annotation relates to body size regulation through cGMP signaling in sensory cilia. The study shows that cilium structure mutants (including che-2) have small body size and locomotion defects due to disrupted sensory signaling. Reason: This is a downstream consequence of cilium structure defects rather than a direct function of CHE-2. The effect on locomotion is indirect, mediated through disrupted sensory perception in defective cilia. Not a core function. Supporting Evidence: PMID:26434723 The body size of Caenorhabditis elegans is thought to be controlled by sensory inputs because many mutants with sensory cilium structure defects exhibit small body size.
GO:0090326 positive regulation of locomotion involved in locomotory behavior	IMP PMID:26434723 The Importance of cGMP Signaling in Sensory Cilia for Body S...	KEEP AS NON CORE	Summary: IMP annotation for locomotion regulation based on che-2 mutant phenotype. The small body size and reduced locomotion in che-2 mutants is secondary to cilium structure defects affecting sensory perception. Reason: Pleiotropic effect of cilium defects. CHE-2's primary role is in cilium assembly and IFT; the locomotory phenotype is an indirect consequence of sensory defects. Supporting Evidence: PMID:26434723 the defects in the sensory cilium structure may disturb the balanced control of the cGMP level
GO:0040014 regulation of multicellular organism growth	IGI PMID:26434723 The Importance of cGMP Signaling in Sensory Cilia for Body S...	KEEP AS NON CORE	Summary: Body size regulation is affected in che-2 mutants due to disrupted cGMP signaling in defective sensory cilia. This is a downstream phenotype of the cilium structure defect. Reason: Secondary phenotype resulting from defective sensory cilia. The primary function of CHE-2 is cilium assembly, not growth regulation per se. Supporting Evidence: PMID:26434723 many mutants with sensory cilium structure defects exhibit small body size
GO:0040018 positive regulation of multicellular organism growth	IMP PMID:26434723 The Importance of cGMP Signaling in Sensory Cilia for Body S...	KEEP AS NON CORE	Summary: IMP annotation based on small body size phenotype of che-2 mutants. The reduced body size is a consequence of disrupted sensory signaling through defective cilia. Reason: Indirect effect of cilium structure defects on sensory-mediated growth regulation. Not a direct molecular function of CHE-2. Supporting Evidence: PMID:26434723 the cGMP level is precisely controlled by GCY-12 and PDE-2 to determine body size through EGL-4, and the defects in the sensory cilium structure may disturb the balanced control of the cGMP level
GO:0006935 chemotaxis	IMP PMID:7828815 Multiple chemosensory defects in daf-11 and daf-21 mutants o...	KEEP AS NON CORE	Summary: che-2 mutants exhibit chemotaxis defects. This study (PMID:7828815) focuses on daf-11 and daf-21 mutants but references che-2 as a cilium structure mutant with chemosensory defects. PMID:10208543 provides more direct evidence. Reason: Chemotaxis defect is a consequence of abnormal cilium structure in sensory neurons. CHE-2 enables chemotaxis indirectly by being required for proper cilium assembly in chemosensory neurons. Supporting Evidence: PMID:10518500 These mutants have extremely short cilia with an abnormal posterior projection, and show defects in behaviors that are mediated by ciliated sensory neurons.
GO:0060271 cilium assembly	IGI PMID:1732156 Genetic analysis of chemosensory control of dauer formation ...	ACCEPT	Summary: IGI annotation based on genetic interaction studies of dauer formation. This paper places che-2 in the cilium-structure gene class that is epistatic to daf-11 for dauer formation, supporting its role in cilium assembly. Reason: Supports the core function of CHE-2 in cilium assembly. The genetic epistasis analysis places che-2 among genes required for cilium structure. Supporting Evidence: PMID:1732156 Dauer-defective mutations in nine genes cause structurally defective chemosensory cilia, thereby blocking chemosensation
GO:0040024 dauer larval development	IGI PMID:11677050 DAF-7/TGF-beta expression required for the normal larval dev...	KEEP AS NON CORE	Summary: che-2 mutants affect dauer formation through their role in cilium structure. The study places che-2 in the genetic pathway between daf-11 and daf-7 for dauer control. Reason: Dauer development phenotype is secondary to cilium structure defects. che-2 mutants affect dauer formation because sensory cilia are required for environmental sensing that triggers dauer entry. Not a direct function of CHE-2. Supporting Evidence: PMID:11677050 cilium-related genes che-2 and che-3 are placed between daf-11 and daf-7, in the genetic pathway controlling dauer formation
GO:0036064 ciliary basal body	IDA PMID:22922713 The BBSome controls IFT assembly and turnaround in cilia.	ACCEPT	Summary: IDA annotation for localization to ciliary basal body. PMID:22922713 shows that IFT-B components accumulate at the ciliary base in certain mutant backgrounds, and that the BBSome assembles IFT complexes at the ciliary base. Reason: CHE-2/IFT80 as an IFT-B component is assembled at the ciliary basal body before transport into the cilium. The ciliary base is where IFT particles are organized. Supporting Evidence: PMID:22922713 the BBSome (refs 3, 4), a group of conserved proteins affected in human Bardet-Biedl syndrome(5) (BBS), assembles IFT complexes at the ciliary base, then binds to the anterograde IFT particle
GO:0097730 non-motile cilium	IDA PMID:10518500 A novel WD40 protein, CHE-2, acts cell-autonomously in the f...	ACCEPT	Summary: C. elegans sensory cilia are non-motile (primary) cilia. CHE-2::GFP localizes to these sensory cilia as directly demonstrated in PMID:10518500. Reason: Appropriate specific localization annotation. C. elegans sensory neurons have non-motile cilia, and CHE-2 localizes to these structures. Supporting Evidence: PMID:10518500 CHE-2-tagged green fluorescent protein is localized at the cilia of almost all the ciliated sensory neurons.
GO:0030512 negative regulation of transforming growth factor beta receptor signaling pathway	IGI PMID:11677050 DAF-7/TGF-beta expression required for the normal larval dev...	MARK AS OVER ANNOTATED	Summary: This annotation relates to the role of che-2 in the dauer pathway where it affects DAF-7/TGF-beta expression. The genetic analysis places che-2 between daf-11 and daf-7 in regulating TGF-beta signaling for dauer formation. Reason: This is an indirect effect mediated through cilium structure defects affecting sensory perception of environmental cues that regulate TGF-beta signaling. CHE-2 does not directly regulate TGF-beta signaling; it enables the sensory apparatus that perceives signals controlling this pathway. Supporting Evidence: PMID:11677050 cilium-related genes che-2 and che-3 are placed between daf-11 and daf-7, in the genetic pathway controlling dauer formation
GO:0006935 chemotaxis	IMP PMID:10208543 Sensing of cadmium and copper ions by externally exposed ADL...	KEEP AS NON CORE	Summary: che-2 mutants lack avoidance behavior to Cd2+ and Cu2+. The study shows that mutants with structural defects in ciliated neurons, including che-2, do not show chemotactic avoidance responses. Reason: Chemotaxis defect is downstream of cilium structure defect. CHE-2 is required for cilium assembly in chemosensory neurons; without proper cilia, these neurons cannot function in chemotaxis. Supporting Evidence: PMID:10208543 Mutants that have structural defects in ciliated neurons (che-2 and osm-3) as well as worms with three laser-operated neurons (ADL, ASE, and ASH), showed no avoidance behavior from Cd2+ and Cu2+
GO:0060271 cilium assembly	IMP PMID:10518500 A novel WD40 protein, CHE-2, acts cell-autonomously in the f...	ACCEPT	Summary: IMP annotation directly demonstrating CHE-2 requirement for cilium assembly. This is the primary reference establishing CHE-2 function, showing that mutants have truncated cilia and that rescue restores cilium morphology. Reason: Core function with strong experimental support. This is the definitive paper on CHE-2 function demonstrating its essential role in cilium formation. Supporting Evidence: PMID:10518500 Expression of che-2 in a subset of sensory neurons of a che-2 mutant by using a heterologous promoter resulted in restoration of the functions and cilium morphology of only the che-2-expressing neurons. PMID:10518500 Expression of che-2 in a che-2 mutant under a heat shock promoter showed that the extension of cilia, surprisingly, can occur even at the adult stage, and that such cilia can function apparently normally in behavior.
GO:0035720 intraciliary anterograde transport	IBA GO_REF:0000033	NEW	Summary: CHE-2/IFT80 is a core IFT-B component specifically involved in anterograde transport. PMID:22922713 shows IFT-B components move in the anterograde direction. Reason: More specific than GO:0042073 (intraciliary transport). IFT-B is specifically the anterograde transport machinery while IFT-A is retrograde. This term better captures CHE-2's molecular function. Supporting Evidence: PMID:22922713 Similar to OSM-6, in dyf-2(jhu616), all other IFT-B components examined also showed active anterograde movements, but lost most of the retrograde IFT movements and accumulate at the ciliary tip