EcR-B1, EcRB1, DmEcR, EcR-A, ecdysteroid receptor
transcription factor - nuclear receptor - zinc finger - regulates molting cycles and oogenesis
Please see the JBrowse view of Dmel\EcR for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.46
Tissue-specific extension of 3' UTRs observed during later stages (FBrf0218523, FBrf0219848); all variants may not be annotated
6, 5, 4 (northern blot)
6.0 (northern blot)
878, 849, 669 (aa); 105, 80 (kD)
878 (aa); 105 (kD observed)
alternatively spliced exon
Heterodimer of USP and ECR (PubMed:8247157). Only the heterodimer is capable of high-affinity binding to ecdysone (PubMed:8247157). Interacts with trr in an ecdysone-dependent manner (PubMed:14603321). Upon ecdysone stimulation, interacts with Nup98 (PubMed:28366641).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\EcR using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: reference states 0-3 hr AEL
Comment: maternally deposited
Comment: reference states >=3 hr AEL
The temporal pattern of EcR RNA expression was carefully studied and related to times of ecdysone pulses. Peaks of the 5kb EcR-A RNA occur in mid-embryogenesis and early and late in pupation.
The temporal pattern of EcR RNA expression was carefully studied and related to times of ecdysone pulses. The strongest peak of EcR-B1 RNA expression occurs in late third instar larvae. Smaller peaks are observed during late embryonic, late first and second instar larval, and mid pupal stages.
The 6 kb EcR transcript is detected in all stages except for 0-3 hr embryos. Expression is most abundant in embryos and in late third instar larvae and early pupae, with highest levels seen in wandering third instar larvae.
Comment: isoform specific
Comment: isoform "B1"
Comment: isoform "B1"
At 0h APF, reticular neuropil associated glial cells (astrocyte-like cells) express "EcR-B1" (EcR-RB), but not "EcR-A" (EcR-RA, EcR-RD) <up>isoform identities obtained from UniProt</up>.
EcR staining is widespread in the adult brain.
EcR isoform "A" is uniformly distributed in egg chambers at all stages. Isoform "B1" is more highly expressed in follicle cells than germline cells and shows a fourfold enrichment in anterior follicle cells at early oogenesis stage S9. The enrichment is reduced by mid stage 9 and absent by stage 10.
EcR is expressed in approximately 20 antennal lobe projection neurons, 18 of which are located in a anterodorsal cluster.
JBrowse - Visual display of RNA-Seq signals
View Dmel\EcR in JBrowse2-55
2-55.8
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Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
monoclonal
Ortholog of B. mori juvenile-hormone-related gene (involved in JH biosynthesis, metabolism or signaling).
DNA-protein interactions: genome-wide binding profile assayed for EcR protein in Kc167 cells; see Chromatin_types_NKI collection report. Individual protein-binding experiments listed under "Samples" at GEO_GSE22069 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22069).
dsRNA has been made from templates generated with primers directed against this gene. RNAi of EcR reduces the primary dendrite outgrowth of ddaD and ddaE neurons, but causes only modest reduction of lateral branching and lateral branch outgrowth. RNAi also causes defects in muscle, alterations in the number of MD neurons, defects in dendrite morphogenesis and reproducible defects in da dendrite development.
ChEST reveals this is a target of Mef2.
Ecdysone signalling cell-autonomously downregulates PI3K activity in the fat body.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
EcR is not required for morphogenetic furrow formation in the developing eye.
The EcR/usp heterodimer DNA binding activity requires activation by a chaperone heterocomplex of six proteins including the products of Hsp83 and the Hsc70 genes. The gene products of Hsp83 and the Hsc70 genes are also required in vivo for EcR activity and EcR is the primary target of the chaperone complex.
Genetic interaction between EcRE261st and Sin3Ak07401 reported in FBrf0111507 is not evident when EcRC300Y is combined with Sin3A08269, suggesting that the original observed interaction could be due to background effects.
EcR function is required maternally for normal oogenesis.
EcR has a cell autonomous role in controlling neuronal remodelling.
EcR is required for hatching, at each larval moult and for the initiation of metamorphosis.
The EcR/usp heterodimer binds in vitro to direct repeats and these repeats can confer ecdysteroid responsiveness on minimal promoters in a cell transfection assay. The natural pseudopalindromic EcR/usp binding site in the Fbp1 enhancer is required to mediate a fat body-specific ecdysteroid response. The profound differences in structure between these two types of EcR/usp binding site do not dictate a spatial and temporal specificity of the transcriptional response they mediate.
Interaction of the DNA binding domain with a 20-hydroxyecdysone palindromic response element from the promoter region of Hsp27 has been studied.
Expression throughout the onset of metamorphosis is not affected by Eip74EF mutations.
Neurons show qualitative and quantitative changes in EcR expression during their life history and these differences correlate with distinct patterns of ecdysteroid response.
Ecdysteroid-regulated gene.
Postmeiotic differentiation defect.
The correlation of a unique pattern of ecdysone receptor isoform A expression in the CNS of the emerging adult with a particular steroid regulated cell death fate suggests that variations in the pattern of receptor isoform expression may serve as important switches during development.
The ecdysone receptor gene encodes three receptor isoforms with common DNA and hormone binding domains but different N-terminal regions. Different isoforms predominate at different developmental stages that are marked by a pulse of ecdysone.
EcR protein can function as a ligand-dependent transcription factor in mammalian cells.
Identification: EcR was identified in a screen for members of the steroid receptor superfamily.
The DNA binding properties of the ecdysone receptor protein have been defined. In vitro binding studies demonstrate that ecdysterone causes activation or repression of the receptor DNA binding domain via an irreversible change in conformation.
A novel bromoacetly ecdysteroid IV reacts with partially purified EcR rapidly and almost quantitatively.
Source for merge of: snt EcR
Source for merge of: EcR CG8347
Source for merge of: EcR lie
Source for merge of: EcR anon-WO0229075.1
Source for merge of EcR anon-WO0229075.1 was sequence comparison ( date:051113 ).
Source for identity of: EcR CG1765
