l(4)17, ciD, CID, Gli, l(4)13
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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.
Gene model reviewed during 5.39
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.46
Multiphase exon postulated: exon reading frame differs in alternative transcripts.
4.6 (northern blot)
None of the polypeptides share 100% sequence identity.
155 (kD)
1282 (aa)
Interacts with RDX (PubMed:16740475). Interacts with cos (PubMed:9244298, PubMed:15691767). Interacts with slmb; the interaction is enhanced by phosphorylation by CkIalpha and dco (PubMed:16326393).
Polyubiquitinated by RDX in the presence of CUL3, which results in proteasomal degradation.
Phosphorylated on multiple sites by protein kinase A (PKA) and phosphorylation by PKA primes further phosphorylation by CK1 and GSK3. Phosphorylation is essential for its proteolytic processing. cos recruits multiple kinases to promote efficient phosphorylation of ci while Hh signaling inhibits phosphorylation by restricting the accessibility of ci to the kinases (PubMed:15691767). Phosphorylation by CkIalpha and dco enhances binding to Slmb, the F-box recognition component of the SCF(slmb) E3 ubiquitin-protein ligase required for ci processing (PubMed:16326393).
Transcriptional repressor ciR, a C-terminally truncated form, is generated from the full-length ci (ciFL/ci-155) through proteolytic processing. Hh suppresses the formation of ci75 and promotes the conversion of ci155 into a transcriptional activator (ci155A).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ci using the Feature Mapper tool.
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: expressed in three broad stripes
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as dorsal epidermis anlage
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
The ci transcript is expressed in the anterior compartment of each segment during embryogenesis.
ci is expressed ubiquitously in early embryos. Expression later resolves into 15 stripes encompassing the anterior compartment of each segment. ci is also expressed in the anterior compartments of imaginal discs. In engrailed mutants, ci expression is derepressed in the posterior compartments, suggesting that ci expression is normally repressed by en in these cells.
ci is uniformly expressed throughout the cellular blastoderm and at gastrulation. At germband extension, expression resolves into 15 broad stripes that encompass the anterior 3/4 of each segment. ci transcripts are also found in the hindgut and foregut. Expression peaks at 5-8hrs of embryonic development.
Strong ci protein accumulation is observed at the morphogenetic furrow.
ci is specifically expressed in all cells of the anterior compartment and is most abundant in a band of four to seven cells that are one to two cells from the anterior side of the AP border.
ci protein is present in both the posterior optic lobe and adjacent anterior optic lobe cells in mid stage 11 embryos. It is also expressed broadly in tracheal pits.
ci protein is expressed at similar levels in wing and haltere discs.
ci protein is localized to the anterior compartment of the wing disc.
Immunoreactivity to ci protein detected throughout the anterior compartment of the wing disc, and is most pronounced along the anterior/posterior compartment boundary
The full length ci protein is detected primarily near the anterior/posterior compartment boundary in the anterior compartment, with lower levels detected elsewhere as determined by an antibody that is specific for the full length protein. Cellular fractionation indicates that full length ci protein is cytoplasmic.
Comment: expressed in two broad stripes
GBrowse - Visual display of RNA-Seq signals
View Dmel\ci in GBrowse 2Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
monoclonal
monoclonal antibody
polyclonal antibody
Source for identity of: ci CG2125
The stability of endogenous ci protein is regulated by the ubiquitin-proteasome system and not lysosome-mediated protein degradation.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of ci causes a loss of dorsal class I da neurons without affecting the ventral class I neuron vpda and an overall reduction of dorsal md neurons. ci RNAi causes embryonic lethality at high concentrations of dsRNA. RNAi also causes defects in muscle, defects in the epidermis, alterations in the number of MD neurons and defects in dendrite morphogenesis.
ChEST reveals this is a target of Mef2.
One of 42 Drosophila genes identified as being most likely to reveal molecular and cellular mechanisms of nervous system development or plasticity relevant to human Mental Retardation disorders.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Proteolysis of ci requires phosphorylation by PKA.
ci null alleles are partially functionally complemented by Hsap\GLI, which rescues viability to late third instar, but produces larvae with grossly enlarged wing discs. ci null alleles are also partially functionally complemented by a combination of Hsap\GLI and Hsap\GLI3, rescuing to pupal or late third instar larvae and producing wild-type wing discs.
Using the yeast two-hybrid method and an in vitro binding assay it is demonstrated that Su(fu), ci and fu can interact directly to form a trimolecular complex, with Su(fu) binding to both its partners simultaneously. In the absence of hh signalling results propose that Su(fu) inhibits ci by binding to it and that, upon reception of the hh signal, fu is activated and counteracts Su(fu), leading to the activation of ci.
Characterisation of ci protein reveals it exists in at least two forms, one full-length and the other truncated, these forms differ in activity and subcellular location. The N-terminal domain has nuclear localisation and DNA binding activities that are impotent in the full-length protein. Processing of the full length protein is inhibited by hh, an observation that represents the first direct evidence that ci transduces the hh signal.
Each primordia of the genital disc (female genital, male genital and anal primordia) is divided into anterior and posterior compartments. Genes known to be expressed in compartment-specific manner in discs are expressed in analogous patterns in each primordia.
Genetic combinations with mutants of nub cause additive phenotypes.
hh elicits signal transduction via a complex that includes the products of the fu, ci and cos genes. The complex binds with high affinity to microtubules in the absence of hh protein, but not when hh is present. The complex may facilitate signalling from hh by governing access of the ci product to the nucleus.
The pattern of expression of ci in the larval and adult abdomen has been analysed.
Cells in anterior compartments lacking ci express hh and adopt a posterior fate without expressing en. Increased levels of ci can induce the expression of dpp independent of hh. Expression of ci in anterior cells controls limb development by restricting hh secretion to posterior cells and by conferring competence to respond to hh by mediating transduction of the hh signal.
The expression pattern of a number of genes in the larval genital discs, including ci, has been studied to determine the segment-parasegment organisation of the genital discs.
ara-caup expression at patches on the wing, located one at each side of the DV compartment border, is mediated by the hh signal through its induction of high levels of ci protein in anterior cells near to the AP compartment border. High levels of ci activate dpp expression and together ci and dpp positively control ara-caup expression.
The distribution of the ci protein during development is examined and epistasis analysis is used to position ci in the wg and hh signalling pathways. fu and hh modulate the post-transcriptional regulation of ci protein. ci is epistatic to ptc in the maintenance of wg expression and the formation of naked cuticle.
Proper regulation of both the ci RNA and protein appears to be critical for normal development.
Segment polarity mutations cause stripes of abnormal patterning within sectors of the leg disc, which may be mediated by regional perturbations in growth.
Assayed in an analysis of chromosome 4 using pulsed field gel electrophoresis.
Ectopic uniform wg expression results in change in ci expression: ci expressed in those cells that are not expressing en (as in wild type), but since the en stripe is broader the ci stripe is thinner.
Mutations in ci cause pleiotropic phenotypes in embryonic patterns and affect several longitudinal veins.
Late ptc transcription patterns depend upon selective repression by ciD.
ve, vn, ci, cg, svs, ast, H, Vno and vvl belong to the vein phenotypic group (Puro, 1982, Droso. Info. Serv. 58:205--208 ) within the 'lack-of-vein' mutant class. Loss-of-function alleles at these loci remove stretches of veins in two or more longitudinal veins. Double mutations within members of this group remove all veins, have smaller, slightly lanceolate wings, no sensilla and extra chaetae.
ci has a specific role in the control of cell fates during neurogenesis.
The expression of ci+ can be altered in direction of ci by certain chromosome rearrangements that have one break in vicinity of ci locus. Rearranged fourth chromosomes carrying a mutant allele of ci, R(ci), may also show altered expression of gene (Stern and Kodani, 1955). R(ci) and R(ci+) terminology not retained here; interaction with ci included in descriptions of aberrations involving chromosome 4.