ct kf2 ctnct6 ctK lethals _________________________________________________________________ | | | | | | -0.04- | -0.16- | - ~0.07- | Genetic fine structure map of the cut locus
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
RNA-Seq data support additional isoforms with extended 3' UTRs of differing length, some of which appear to be stage and/or tissue specific.
Gene model reviewed during 5.45
Gene model reviewed during 5.48
Gene model reviewed during 6.19
8.2 (compiled cDNA)
None of the polypeptides share 100% sequence identity.
g1345461 contains only the homeodomain.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ct using the Feature Mapper tool.
Comment: reported as dorsal/lateral sensory complexes
ct is expressed in principal cells of the adult Malpighian tubules but not in intestinal stem cells. ct can be used as a marker for renal progenitor cells during metamorphosis. At the onset of metamorphosis (0hr APF) ct is expressed in a few clusters of esg-positive (esg marks midgut progenitor cells and renal progenitor cells) cells close to the midgut-hindgut border. At 0.5hr APF, 20-30 progenitors in 5-6 clusters express ct. By 1hr APF, midgut progenitor islands merge together and the ct-expressing progenitors align along the midgut-hindgut border in 1-3 rows. Starting at 3hr APF ct-expressing progenitors migrate across the midgut border and enter the renal tubules. ct-minus cells are engulfed and expelled into the pupal midgut. ct-expressing progenitors occupy the lower ureter region and differentiate into new principal cells.
ct is coexpressed with Dll in the majority of eo support cells for the dorsal organ, terminal organ, and ventral organ ganglia, as well as being weakly coexpressed in a few neurons of all three ganglia.
ct expression is downregulated in main body follicle cells at stage 8; from then on, its expression is limited to the anteriorly and posteriorly localized polar follicle cells.
ct expression in follicle cells increases at oogenesis stage S2 and remains high until stage S6. It remains low in most follicle cells from stages S7-10A but high ct levels persist in the border cells throughout their migration. At stage S10B ct levels increase in the main body follicle cells with significantly higher levels in the centripetal follicle cells.
Within a simple external sensory organ, the nuclei of the tormogen and trichogen cells express ct protein strongly, while the thecogen cells and neurons are not consistently labeled.
While the protein is detected in all myoblasts in the developing wing notum the expression is lower in the proximal region that overlaps vg expression and is high in the distal region where vg is not expressed.
The Malpighian tubule cells are alocated and evert from the embryonic hindgut during extended germband stage. From this stage on protein is detected in the tubule cells.
ct protein accumulation from larval through adult stages was studied by immunolocalization. ct protein is found in diverse tissues, including the wing and leg discs, muscle, ovarian follicle cells, and the central nervous system. In many tissues, ct protein is expressed in a subset of cells. In many cases, it is found in precursors, and persists in differentiated cells. In the third instar larval wing disc, ct protein is first detected in regions corresponding to the prospective notum, wing blade, and wing hinge. In the first 2 hours of puparium formation, ct protein expression is detected in the distal anterior wing margin where, by 6 hours, ct protein is detected in the chemosensory organ cells. At 24 hours of pupariat on, expression is also detected in macrochaetae and microchaetae of the notum. The prospective wing margin stains from third larval instar through 24 hours of pupa formation. Regions of the leg disc which will give rise to the tarsus and to pioneer neurons express ct protein from third larval instar through 3 hour pupae. Malpighian tubules, ovarian follicle cells from stage S2 to S14, larval adepithelial cells and adult muscles of the thorax, head and abdomen are among tissues which express ct protein. Structures of the adult head which express ct protein include the cortex of medulla and lobulla, and the neuropil. The interommatidial bristle precursors and cone cell precursors of 24 hour pupal eye discs, and adult cone cells also contain ct protein.
ct protein is expressed in all cells after heat shock in cths.P flies. Ectopically expressed ct protein leads to expression of endogenous ct protein in chordotonal organ precursors and the expression is maintained in their progeny. This leads to the morphologic and antigenic transformation of chordotonal organs into external sensory organs. In cuths.P embryos, expression is also seen in an expanded domain of tracheal histoblasts.
In the 5-6 hour embryo, ct protein is expressed in sensory precursor cells, which will give rise to the external sensory organs. ct protein appears in many putative external sensory organ precursors in 5-10 hour embryos, starting with the position of the double innervated sensillum trichoideum and sensillum campaniformium (des2 and v\'es2) in abdominal segments, and the basiconical sensilla (les3, v\'es3) in the thoracic segments. In most external sensory organs at late embryogenesis, the trichogen and tormogen label more intensely for ct protein than the neuron and thecogen. Some CNS cells, the Malpighian tubules, and cells surrounding the anterior and posterior spiracles express ct protein starting at 5-7 hours of embryogensis.
On a Western blot, the 280 kD ct protein is first detected in 6-9 hour embryos, and persists through the rest of embryogenesis.
On a Western blot, the 320 kD ct protein is first detected in 6-9 hour embryos, and persists through the rest of embryogenesis.
All external sensory organs of the embryo, including the antenno-maxillary complex and the external sensory organs in the spiracles, express ct protein. Staining is visible before morphological differentiation of cells of the external sensory organs at stage 11-12 of embryogenesis. Additional tissues which express the ct protein include some neurons with multiple dendritic arborizations, and cells lining the Malpighian tubules.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ct in GBrowse 2
The interval between ct and cm or ct and sn is that between ct6 and either cm or sn. ctkf-2 (the most distal locus in this study) maps 0.04 units to the left of ct6. ctn maps 0.007 units to the left of ct6, and ctK maps 0.16 units to the right of ct6. The lethal ct alleles used in this study map as a cluster approximately 0.07 units to the right of ctK.
Please 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.
Source for merge of ct BcDNA:GH10590 was a shared cDNA ( date:030728 ).
ct is among the most mutable X-linked genes; several large-scale mutagenesis experiments have yielded many alleles, the majority of which are lost. The majority of induced ct alleles are lethal, or associated with chromosome rearrangements, or both. A derivative of ct6 (termed Uc: Unstable chromosome) studied by Lim (1979) and ctMR2 derived from a hybrid dysgenic cross involving MR-h12 on chromosome 2 by Gerasimova (1981) are highly unstable. The instability is manifest as increased incidence of lethal mutations, many of which are associated with chromosome aberrations broken in 6F (Lim), high reversion frequencies often accompanied by mutation at other loci.
ct is required for follicle-cell proliferation and maintenance of the mitotic cycle.
The level of ct expressed by different da sensory neurons regulates class-specific dendrite morphogenesis.
Analysis of ct mutants suggests that germline cell cytokineses are normal in mutant females.
ct function is critical for maintaining the structural integrity of germline-derived cells and their arrangement within an egg chamber.
ct acts to maintain margin wg expression, providing a potential explanation of the ct mutant phenotype. N, but not wg signalling, is autonomously required for ct expression. wg is required indirectly for ct expression, results suggest this requirement is due to the regulation by wg of Dl and Ser expression in cells flanking the ct and wg expression domains. Dl and Ser play a dual role in the regulation of ct and wg expression.
Ectopic expression of ct, Hsap\CUTL1, and Mmus\Cutl1 similarly affects embryonic sensory organ development and can rescue a wing scalloping mutant phenotype associated with loss of ct expression along the prospective wing margin. These results suggest the function of ct is evolutionarily conserved.
The FLP/FRT recombinase system has been used to determine that ct is required for the proper differentiation of md neurons.
A group of ct regulatory elements have been identified that drive Ecol\lacZ reporter gene expression in all of the embryonic tissues and the adult peripheral nervous system. Results demonstrate that ct has separate enhancers for the adult and larval peripheral nervous systems and for different groups of adult external sensory organs.
Ectopic ct expression has at least two effects, an excessive cell death and a maldifferentiation of photoreceptor precursors.
The Mutator Strain (MS) is characterised by a high frequency of spontaneous mutations and their reversions. Spontaneous reversions of ct and f gypsy mutations are shown to be due to precise excisions of the element.
A group of cells that express ct lies between the dorsal and ventral rows of margin bristle precursors, and may act as barrier cells between the compartments. This group of cells is divided into dorsal and ventral by the additional expression of ap in the dorsal cells only.
Wing phenotype of cut mutations correlates with expression in prospective wing margin.
The ct wing phenotype is caused by activation of the wing margin enhancer at pupariation, the su(Hw) gene product is only active when the enhancer is active, thereby blocking the enhancer by binding to gypsy. Enhancer blocking by su(Hw) protein is reversible.
Muscle phenotype of mutants studied using polarised light microscopy and antibody staining to detect Mhc-lacZ reporter gene expression in muscles.
One of the homeodomain loci identified in a screen for genes encoding DNA binding proteins capable of binding to a consensus Engrailed binding site.
Mutations in the ct gene transform sense organs from external sensory receptors to chordotonal organs. The ct gene influences axonal projections of the transformed receptors, additional genes could be involved in this specification.
Seven new lethal alleles that arose either on a Uc chromosome or on a chromosome that had been associated with Uc were molecularly mapped: all were found to be associated to a gypsy transposable element insertion.
Wing margin mutations, such as N, Ser, sd and sc, interact synergistically with ct and ap, Bx and Ly act additively.
Mutations at the ct locus cause a morphological transformation of the Malpighian tubules to a bladder like structure, with stacks of epithelial cells in its wall. cad and ct are independent of each other with respect to Malpighian tubule regulation: both pathways require Kr.
A number of cut mutations were induced by non-precise excision of a silent P-element insertion, which resulted in deletions of the regulatory region of cut. A reversion of one of these mutations was found to be caused by the insertion of a Stalker element near the deletion that suppresses the deficiency at the regulatory region of the cut gene.
The deduced amino acid sequence of human CCAAT dispacement protein (Hsap\CUTL1) reveals high homology to ct with respect to the presence of a unique homeodomain and 'cut repeats'. ct participates in determining cell fates in several tissues, the predicted similarity suggests a broad role for Hsap\CUTL1 in mammalian development.
Ubiquitous ct expression in embryos results specifically in the morphological and antigenic transformation of ch sense organs into es organs. ct is necessary and sufficient for the specification of es identity in the sensory organ precursor cells and their progeny. Specificity also involves the ASC and da.
ct-expressing cells flanking the margin stripe are precursors of the chemosensory organs. An enhancer of ct, located 80kb upstream of the ct gene promoter, confers expression in the mechanoreceptors and noninnervated bristles from a heterologous promoter.
The complementation behaviour and protein distribution of cut mutants has been studied to define the regulatory regions of ct. Results suggest that cut is necessary for cell type specification and morphogenesis in variety of tissues. The regulatory region of cut contains at least four separate units with different tissue specific functions.
The incorrect specification of es organ identity in ct mutants results from either the lack of ct protein in some or all es cells or lack of nuclear localization of ct.
Three phenotypic revertants of a gypsy induced mutation reveal that jockey insertions relieve the gypsy induced phenotype at ct by interfering with a region which is required for the transcriptional competence of gypsy.
Within the ct locus nucleotide position -118 may be considered a hotspot for gypsy element insertions, nucleotide position -123 for roo element insertions and nucleotide position -116 for Burdock insertions.
A screen for X-linked genes that affect embryo morphology revealed ct.
ct has been molecularly characterized.
The suffix short repeat, carrying polyadenylation signals and polyadenylation sites, forms the last exon of ct. The suffix sequence is directly involved in the formation of the last splicing site and the 3' end maturation of ct mRNA.
ct mutants display posterior defects in spiracles, no Keilins organs and abnormal maxillary complex.
ct mutations fall into three nonoverlapping phenotypic classes: kinked femur, cut wings and lethal. Kinked-femur mutants are small with slightly dark, dull, red eye color; femurs kinked; wings seldom expand following eclosion, or when they do expand they are opaque and abnormal in shape; flies seem unable to move normally and die on the food soon after eclosion. Cut-wing mutants variably affect wing shape and head capsule development; phenotypic effects include incised wing margins with the tips usually cut to points, missing or ventrally displaced vibrissae, deformed antennae, e.g., flattened and embedded with aristae concave forward, smaller kidney-shaped eyes, warped abdominal bands and fine bristles. Most lethal alleles survive as clones of homozygous epidermal cells (Demerec). Developmental study of ct6 by Waddington (1939; Waddington, 1940) shows wing bud narrower than wild type as early as just after eversion of wing in early pupa. Cell death observed in prepupal wing bud (D. Fristrom, 1969). Clones of ct6 cells in internal areas of wing blade normal in size; marginal clones much reduced in size indicating cell death. Homozygous clones in either dorsal or ventral membrane must reach margin in order to produce incision, 100/127 marginal clones unassociated with gaps; when gaps are produced, they affect both wing surfaces even though clone confined to a single surface. Both dorsal and ventral chaetal elements at the edges of such gaps may show the markers of such clones (Santamaria and Garcia-Bellido, 1975). Lethal alleles fall into three groups, based on their complementation characteristics: cutless, group I and group II. Lethal alleles ctC145, ctJA124, and ct149 exhibit polyphasic lethality from late embryo to pharate adult (Johnson and Judd, 1979). Lethal embryos characterized by posterior defects in spiracles; no Keilin's organs and abnormal maxillary complex (Wieschaus, Nusslein-Volhard, and Jurgens, 1984). Group II and to a slightly lesser degree group I lethals fail to differentiate external sensory neurons in the peripheral nervous system; the presumptive external sensory neurons of the embryonic peripheral nervous system and their support cells are transformed into chordotonal neurons with their support cells; the transformed organs are chordotonal both in morphology and antigenic specificity. Same effect seen in the adult sensory organs in mosaics; embryonic effect differs from that seen in adults in that embryos lack peripheral sensory structures, e.g., Keilin's organs, whereas such structures persist, though reduced in size, in adult tissue. The numbers and positions of peripheral neurons is normal. CNS structure and function appear normal. No discernible effect of absence of ct function in the maternal germ line. Effect of ct mutations on PNS differentiation cell autonomous. (Bodmer, Barbel, Sheperd, Jack, Jan and Jan, 1987). Antibodies to ct protein specifically bind to nuclei of presumptive external sensory organ cells including those of the antennamaxillary organ and external sensory organs in spiracles, but not to nuclei of chordotonal organs; antibody staining also seen in some neurons with multiple dendritic arborizations and in cells lining the Malpighian tubules (Blochlinger, Bodmer, Jack, Jan and Jan, 1988). Kinked-femur, cut-wing and cutless alleles are mutually complementing: group I lethals complement kinked-femur but not cut-wing alleles; and group II lethals are noncomplementing; all combinations of lethal alleles are lethal. The different phenotypic classes of alleles occupy discrete and separate regions of the complex, with the order from left to right being, kinked femur, cut wing, group I lethals and group II lethals; cutless alleles have not been mapped. Kinked femur, cut, and group-I-lethal mutations are associated with chromosome aberrations or insertions of transposable elements, whereas group II lethals appear to be point mutations. ct6, ct68E (= ct67s?), ct78a and ctK suppressed by su(Hw)2; dvr2 enhances ct6 and inhibits its complete suppression by su(Hw)2; su(Hw)2/+ shows slight dominant suppression of wing phenotype of ctK (Lee, 1973). ct6 and ctK strongly enhanced by su(s); su(s) ctK lethal (Johnson) but rescued by su(Hw)2/+ (Craymer). ct6 the most commonly used allele.