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WormBase Tree Display for Gene: WBGene00001486

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Name Class

WBGene00001486EvidencePerson_evidenceWBPerson51
WBPerson2183
SMapS_parentSequenceF59G1
IdentityVersion1
NameCGC_namefrh-1Person_evidenceWBPerson730
Sequence_nameF59G1.7
Molecular_nameF59G1.7
F59G1.7.1
CE19476
Other_nameCELE_F59G1.7Accession_evidenceNDBBX284602
Public_namefrh-1
DB_infoDatabase (13)
SpeciesCaenorhabditis elegans
HistoryVersion_change107 Apr 2004 11:29:24WBPerson1971EventImportedInitial conversion from geneace
StatusLive
Gene_infoBiotypeSO:0001217
Gene_classfrh
Allele (19)
StrainWBStrain00035730
RNASeq_FPKM (74)
GO_annotation (29)
Contained_in_operonCEOP2232
Ortholog (30)
Structured_descriptionConcise_descriptionfrh-1 encodes the C. elegans frataxin ortholog; by homology, FRH-1 is predicted to be a mitochondrial protein required for biogenesis of iron-sulfur clusters, co-factors necessary for proper function of electron transport chain proteins; in C. elegans, loss of frh-1 activity via RNAi results in small body size, pale coloration, reduced motility, decreased pharyngeal pumping and defecation, reduced egg-laying and fertility, hypersensitivity to oxidative stress, and altered adult lifespan; an frh-1::gfp promoter fusion is expressed in neurons, the pharynx, gut, spermatheca and body wall muscle; in the pharynx, FRH-1 localizes to the mitochondria.Paper_evidenceWBPaper00025031
WBPaper00028282
Curator_confirmedWBPerson1843
WBPerson1823
WBPerson567
Date_last_updated17 Aug 2009 00:00:00
Automated_descriptionPredicted to enable several functions, including 2 iron, 2 sulfur cluster binding activity; ferroxidase activity; and iron ion binding activity. Involved in determination of adult lifespan; response to hydrogen peroxide; and response to superoxide. Located in mitochondrion. Expressed in amphid neurons; body wall musculature; pharyngeal muscle cell; and spermatheca. Used to study Friedreich ataxia. Human ortholog(s) of this gene implicated in Friedreich ataxia 1 and type 2 diabetes mellitus. Is an ortholog of human FXN (frataxin).Paper_evidenceWBPaper00065943
Curator_confirmedWBPerson324
WBPerson37462
Inferred_automaticallyThis description was generated automatically by a script based on data from the WS291 version of WormBase
Date_last_updated29 Nov 2023 00:00:00
Disease_infoExperimental_modelDOID:12705Homo sapiensPaper_evidenceWBPaper00028282
WBPaper00041842
Accession_evidenceOMIM229300
Curator_confirmedWBPerson324
Date_last_updated02 Oct 2013 00:00:00
Potential_modelDOID:3068Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:3951)
DOID:0111218Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:3951)
DOID:9352Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:3951)
DOID:12705Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:3951)
Disease_relevanceIn humans, deficiency of the mitochondrial protein frataxin (FXN) causes Friedreich ataxia (FRDA), an autosomal recessive neurological disorder.Homo sapiensAccession_evidenceOMIM229300
606829
Curator_confirmedWBPerson324
Models_disease_in_annotationWBDOannot00000235
WBDOannot00000628
Molecular_infoCorresponding_CDSF59G1.7
Corresponding_transcriptF59G1.7.1
Other_sequence (12)
Associated_featureWBsf657644
WBsf221365
Experimental_infoRNAi_result (71)
Expr_patternExpr4755
Expr4756
Expr4757
Expr1028907
Expr1030887
Expr1152978
Expr2011879
Expr2030117
Drives_constructWBCnstr00012222
WBCnstr00012223
WBCnstr00012224
Construct_productWBCnstr00012222
WBCnstr00012223
WBCnstr00012224
Microarray_results (20)
Expression_cluster (87)
Interaction (115)
Map_infoMapIIPosition-0.852617Error0.000682
PositivePositive_cloneF59G1Inferred_automaticallyFrom CDS info
From sequence, transcript, pseudogene data
Mapping_dataMulti_point4326
Pseudo_map_position
Reference (22)
RemarkMap position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC.CGC_data_submission
MethodGene