DmUSP, CF1, EG:22E5.1 , dUSP, NR2B4
Gene model reviewed during 5.43
Shares 5' UTR with downstream gene.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.46
Gene model reviewed during 5.55
Heterodimer of USP and ECR. Only the heterodimer is capable of high-affinity binding to ecdysone.
Composed of three domains: a modulating N-terminal domain, a DNA-binding domain and a C-terminal ligand-binding domain.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\usp using the Feature Mapper tool.
usp transcripts are detected at all stages tested on northern blots with the highest levels in late wandering third instar larvae and the lowest levels in early first and third instar larvae.
usp transcripts accumulate in the oocyte and nurse cells starting in oocyte stage S8 and reaching a maximum in stage S10. By stage S12, they are confined to the degenerating nurse cells. usp transcripts are uniformly distributed in early embryos and remain so through germ band elongation. During germ band retraction, transcript levels become higher in the ventral nervous system and in the developing midgut.
usp transcripts are expressed throughout the life cycle with the highest levels in embryos and adults.
usp protein is detected at all embryonic stages and in first instar larvae on western blots. It decreases to low levels in 2nd and early third instar larvae and increases again in late third instar larvae and pupae. usp protein is detected by immunolocalization in late third instar larvae. It is present in wing disc, salivary gland, fat body, ring gland, CNS, leg disc and antennal disc.
During oogenesis, usp protein is detected in germ-line nurse cells and in the somatic follicular epithelium.
GBrowse - Visual display of RNA-Seq signalsView Dmel\usp in GBrowse 2
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.
Ortholog of B. mori juvenile-hormone-related gene (involved in JH biosynthesis, metabolism or signaling).
dsRNA has been made from templates generated with primers directed against this gene. RNAi of usp 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.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
usp has no apparent function in mid-third instar larvae, but is required in late third instar larvae for the appropriate developmental and transcriptional responses to the ecdysone pulse that triggers puparium formation.
usp is required in the anterior of the ovary for normal terminal filament differentiation.
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 function of a bacterially expressed usp protein is studied and results demonstrate the suitability of this technology for functional studies of insect nuclear receptors.
Cotransfection studies show that heterodimers of usp and human thyroid hormone receptor β (T3Rβ) can transactivate the human apolopoprotein A-II (apoA-II) promoter.
usp protein binds juvenile hormone III and juvenile hormone III acid with specificity, adopting a different final conformation state for each ligand.
usp is required for normal morphogenetic furrow movement and ommatidial cluster formation.
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 is 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.
Clonal analysis with usp mutations in adult flies reveals a range of imaginal disc phenotypes.
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.
usp expression undergoes numerous and frequent changes during embryonic, larval and adult development.
The equilibrium dissociation constant of the usp protein to its response element on the Cp15 promoter is determined and compared to the binding activities of other nuclear hormone receptors to their cognate elements.
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.
Distribution of usp product during oogenesis, and in vitro binding properties of bacterially produced usp product both to an optimal binding site and to the Cp15 promoter have been studied. USP may operate as a heterodimer in vivo, though identity of the partner remains to be determined.
Evolutionary history for nuclear receptor genes, in which gene duplication events and swapping between domains of different origins took place, is studied.
usp is a Drosophila partner of EcR. Together usp and EcR bind DNA in a highly cooperative pattern. Cotransfection of both usp and EcR is required to render cultured mammalian cells ecdysone responsive.
usp product is a retinoid X receptor homologue, this suggests that similar chemical cues underlie morphogenetic signalling in vertebrate and invertebrate systems.
Molecular cloning and characterization has shown usp to be a novel member of the zinc finger protein superfamily.
Mutants are recessive lethals. usp1/usp1 or usp1/γ progeny of usp1/+ mothers die during the first larval instar or in the molt to the second instar. Those that die during the molt to the second instar sometimes have incompletely molted the first instar set of larval spiracles and thus have two sets of spiracles (FBrf0042629; FBrf0055872). usp1/Y embryos derived from usp1/usp1 germ cells die just prior to or just after hatching with an oval scar on the ventral surface of the posterior eighth abdominal or ninth abdominal segment. The spiracles of these animals appear normal as does the rest of the cuticle and the ventral nervous system. Paternally supplied usp+ completely rescues this phenotype and allows survival to adulthood (FBrf0042629; FBrf0055872). Use of a conditional expression system for rescue of the first/second instar lethal phase results in survival into the third instar and early pupal periods, with no animals surviving beyond pupal stage P4 (FBrf0055872). usp1/0//usp+ gynandromorphs do not survive suggesting that the gene is required in multiple parts of the body and not just in the terminal regions. γ-ray induced usp1/usp1 clones survive in the female germ-line, abdomen, thorax and head, showing that usp is not a general cell lethal. Clones in the head are associated with defects in rhabdomere and ommatidial morphology (FBrf0055872). Expression of a usp cDNA at high levels throughout development rescues the usp- phenotype and has no deleterious effect on usp+ animals, suggesting that any necessary spatial or temporal regulation of usp action occurs by regulation of some other factor such as a ligand.
Encodes a protein that binds the promoter region of Cp15.