EcR-B1, EcRB1, DmEcR, EcR-A, ecdysteroid receptor
alternatively spliced exon
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 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.
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 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.
GBrowse - Visual display of RNA-Seq signalsView Dmel\EcR in GBrowse 2
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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 GBrowse 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.
Source for identity of: EcR CG1765
Source for merge of EcR anon-WO0229075.1 was sequence comparison ( date:051113 ).
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).
The EcR-A isoform is not a signal transducer for programmed cell death in Crz-expressing ventral nerve cord neurons. EcR-B isoforms play significant roles in Crz-expressing ventral nerve cord neuron cell death.
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.
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.
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 is required for hatching, at each larval moult and for the initiation of metamorphosis.
Binding site selection procedure demonstrates that the EcR/usp heterodimer binds to the core recognition motif (consensus sequence consists of a perfect palindrome of the heptameric half-site sequence GAGGTCA that is separated by a single A/T base pair).
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.
DNA-blotting assay has identified a high affinity ecdysone receptor binding site within the ng1 and ng2 coding sequence. EMSA assay demonstrates the 93bp 'ng element' is able to bind an EcR/usp heterodimer and usp alone.
Expression throughout the onset of metamorphosis is not affected by Eip74EF mutations.
The EcR product binds to two sites, element I and element II, in the regulatory region of Sgs4. Element II appears to be of no importance for the expression of Sgs4 while element I is an ecdysone response element necessary, but not sufficient, for Sgs4 induction.
The in vitro characterisation of the EcR/usp binding site its ecdysone- dependent in vivo occupancy in different genetic backgrounds support the conclusion that the Fbp1 enhancer is a primary target of the EcR.
Neurons show qualitative and quantitative changes in EcR expression during their life history and these differences correlate with distinct patterns of ecdysteroid response.
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.
Transient cotransfection experiments in HeLa cells demonstrated that EcR must heterodimerize with usp (the homolog of the mammalian retinoid X receptor) for DNA binding and transactivation. EcR/usp gene product DNA binding activity is unaffected by ecdysteroid and 9-cis-retinoic acid.
EcR and usp native gene products co-localise on ecdysone-responsive loci. Physical associations in the presence and absence of ecdysone redefine the ecdysone receptor as a dynamic complex whose activity may be altered by combinatorial interactions among subunits and ligand.
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.