WormBase Tree Display for Gene: WBGene00000898
expand all nodes | collapse all nodes | view schema
| WBGene00000898 | SMap | S_parent | Sequence | Y55D5A | |||||
|---|---|---|---|---|---|---|---|---|---|
| Identity | Version | 1 | |||||||
| Name | CGC_name | daf-2 | Person_evidence | WBPerson521 | |||||
| Sequence_name | Y55D5A.5 | ||||||||
| Molecular_name (19) | |||||||||
| Other_name | CELE_Y55D5A.5 | Accession_evidence | NDB | BX284603 | |||||
| Public_name | daf-2 | ||||||||
| DB_info | Database (14) | ||||||||
| Species | Caenorhabditis elegans | ||||||||
| History | Version_change | 1 | 07 Apr 2004 11:29:21 | WBPerson1971 | Event | Imported | Initial conversion from geneace | ||
| Status | Live | ||||||||
| Gene_info | Biotype | SO:0001217 | |||||||
| Gene_class | daf | ||||||||
| Reference_allele | WBVar00143949 | ||||||||
| Allele (1322) | |||||||||
| Possibly_affected_by | WBVar02157253 | ||||||||
| WBVar02157255 | |||||||||
| WBVar02157256 | |||||||||
| WBVar02157257 | |||||||||
| WBVar02158490 | |||||||||
| WBVar02158840 | |||||||||
| Legacy_information | e1370ts : constitutive dauer formation at 25x; reversible by shift to 15x. ES3 (L3). NA19. | ||||||||
| See also e1032, e1286, e1365, e1368, e1370, e1391 | |||||||||
| [C.elegansII] e1370ts : constitutive dauer formation at 25C; reversible by shift to 15C. Increased lifespanat 20C; increased thermotolerance, UV resistance. Non-Srf. Synthetic lethal with daf-12. ES3 (L3). OA>40: e1032, e1286, e1365, sa230 (100%Daf-c at all temperatures), sa223 (sterile), m65 (nonconditional), etc. Most alleles (not e1370) hypersensitive to dauer pheromone. [Larsen et al. 1995; Malone and Thomas 1994; CF; JC] | |||||||||
| Strain (147) | |||||||||
| RNASeq_FPKM (74) | |||||||||
| GO_annotation (107) | |||||||||
| Ortholog (50) | |||||||||
| Paralog (34) | |||||||||
| Structured_description | Concise_description | daf-2 encodes a receptor tyrosine kinase that is the C. elegans insulin/IGF receptor ortholog; DAF-2 activity is required for a number of processes in C. elegans, including embryonic and larval development, formation of the developmentally arrested dauer larval stage (diapause), larval developmental timing, adult longevity, reproduction, fat storage, salt chemotaxis learning, and stress resistance, including response to high temperature, oxidative stress, and bacterial infection; DAF-2 signals through a conserved PI 3-kinase pathway to negatively regulate the activity of DAF-16, a Forkhead-related transcription factor, by inducing its phosphorylation and nuclear exclusion; in addition, DAF-2 negatively regulates the nuclear localization, and hence transcriptional activity, of SKN-1 in intestinal nuclei; amongst the 38 predicted insulin-like molecules in C. elegans, genetic and microarray analyses suggest that at least DAF-28, INS-1, and INS-7 are likely DAF-2 ligands; genetic mosaic and tissue-specific promoter studies indicate that daf-2 can function cell nonautonomously and within multiple cell types to influence dauer formation and adult lifespan, likely by regulating the production of secondary endocrine signals that coordinate growth and longevity throughout the animal; temporal analysis of daf-2 function indicates that daf-2 regulates lifespan, reproduction, and diapause independently, at distinct times during the animal's life cycle. | Paper_evidence (11) | ||||||
| Curator_confirmed | WBPerson1843 | ||||||||
| WBPerson567 | |||||||||
| Date_last_updated | 26 Jun 2011 00:00:00 | ||||||||
| Automated_description | Enables PTB domain binding activity; SH2 domain binding activity; and protein kinase binding activity. Involved in several processes, including dauer exit; regulation of developmental process; and regulation of macromolecule metabolic process. Acts upstream of with a negative effect on protein import into nucleus. Located in several cellular components, including cytoplasmic vesicle; neuronal cell body; and plasma membrane bounded cell projection. Expressed in several structures, including XXX cell; gonad; nerve ring; neurons; and vulva. Used to study Parkinson's disease and diabetes mellitus. Human ortholog(s) of this gene implicated in several diseases, including Alzheimer's disease; glucose metabolism disease (multiple); kidney cancer (multiple); and liver disease (multiple). Is an ortholog of human IGF1R (insulin like growth factor 1 receptor); INSR (insulin receptor); and INSRR (insulin receptor related receptor). | Paper_evidence | WBPaper00065943 | ||||||
| Curator_confirmed | WBPerson324 | ||||||||
| WBPerson37462 | |||||||||
| Inferred_automatically | This description was generated automatically by a script based on data from the WS291 version of WormBase | ||||||||
| Date_last_updated | 29 Nov 2023 00:00:00 | ||||||||
| Disease_info | Experimental_model | DOID:9351 | Homo sapiens | Paper_evidence | WBPaper00064218 | ||||
| Curator_confirmed | WBPerson324 | ||||||||
| Date_last_updated | 07 Nov 2022 00:00:00 | ||||||||
| DOID:14330 | Homo sapiens | Paper_evidence | WBPaper00045313 | ||||||
| Curator_confirmed | WBPerson324 | ||||||||
| Date_last_updated | 26 Jan 2015 00:00:00 | ||||||||
| Potential_model (37) | |||||||||
| Disease_relevance | Parkinson''s disease (PD) is an age-dependent neurodegenerative disease characterized by the accumulation of alpha-synuclein (alpha-syn) and the selective loss of dopamine (DA) neurons; studies in C. elegans models of alpha-syn proteotoxcity indicate that reduced IGF-1/insulin-like signaling (IIS) suppresses alpha-syn toxicity and DA neurodegeneration; specifically daf-2 mutant worms that overexpress human alpha-syn retain more wild-type DA neurons when compared to alpha-syn worms alone; mutants of daf-16/FOXO, a well-characterized downstream component of the IIS pathway enhanced neurodegeneration, and an intermediate level of neuroprotection was seen in daf-2; daf-16 double mutants overexpressing alpha-syn-GFP in DA neurons; further, RNA interference of glucose-6-phosphate isomerase (gpi-1/GPI), the glycolytic enzyme, enhanced alpha-syn-induced DA neurotoxicity, while it''s overexpression in DA neurons was neuroprotective; further studies in Drosophila and mice confirm that GPI is neuroprotective; these studies indicate that IIS signaling modulates alpha-syn induced DA neurodegeneration, across species. | Homo sapiens | Paper_evidence | WBPaper00045313 | |||||
| WBPaper00025083 | |||||||||
| WBPaper00031384 | |||||||||
| Curator_confirmed | WBPerson324 | ||||||||
| Date_last_updated | 26 Jan 2015 00:00:00 | ||||||||
| In glucose-fed wild-type animals, the exponential like decline was restored in the active state, indicating that insulin signaling may be involved in regulation of fractal scaling of C. elegans behavior. | Homo sapiens | Curator_confirmed | WBPerson324 | ||||||
| Models_disease_in_annotation | WBDOannot00000339 | ||||||||
| Models_disease_asserted | WBDOannot00001356 | ||||||||
| Molecular_info | Corresponding_CDS | Y55D5A.5a | |||||||
| Y55D5A.5c | |||||||||
| Y55D5A.5d | |||||||||
| Y55D5A.5e | |||||||||
| Y55D5A.5f | |||||||||
| Y55D5A.5g | |||||||||
| Corresponding_CDS_history | Y55D5A.5:wp187 | ||||||||
| Y55D5A.5a:wp229 | |||||||||
| Y55D5A.5b:wp229 | |||||||||
| Y55D5A.5b:wp247 | |||||||||
| Corresponding_transcript | Y55D5A.5b | ||||||||
| Y55D5A.5a.1 | |||||||||
| Y55D5A.5c.1 | |||||||||
| Y55D5A.5d.1 | |||||||||
| Y55D5A.5e.1 | |||||||||
| Y55D5A.5f.1 | |||||||||
| Y55D5A.5g.1 | |||||||||
| Other_sequence (112) | |||||||||
| Associated_feature (24) | |||||||||
| Experimental_info (11) | |||||||||
| Map_info | Map | III | Position | -8.03413 | Error | 0.111365 | |||
| Well_ordered | |||||||||
| Positive | Inside_rearr | nDf11 | |||||||
| Positive_clone | C44B11 | ||||||||
| H05C05 | |||||||||
| Y55D5A | Inferred_automatically | From sequence, transcript, pseudogene data | |||||||
| Negative | Outside_rearr | tDf9 | |||||||
| Mapping_data | 2_point | 273 | |||||||
| 411 | |||||||||
| 412 | |||||||||
| 7053 | |||||||||
| Multi_point (23) | |||||||||
| Pos_neg_data (12) | |||||||||
| Reference (1726) | |||||||||
| Picture | WBPicture0000013078 | ||||||||
| WBPicture0000013087 | |||||||||
| Method | Gene |
