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General Information
Symbol
Dmel\ct
Species
D. melanogaster
Name
cut
Annotation Symbol
CG11387
Feature Type
FlyBase ID
FBgn0004198
Gene Model Status
Stock Availability
Gene Snapshot
cut (ct) encodes a homeoprotein that functions as a transcriptional factor in many different cells such as wing disc, muscle, oocyte and sense organ cells. It is a regulator of type-specific neuronal identity in the peripheral nervous system. ct is expressed at variable levels in the dendritic arborization (DA) neurons and these levels control the different dendritic morphologies specific for each class of DA neurons. [Date last reviewed: 2019-03-07]
Also Known As

kf, kinked-femur

Key Links
Genomic Location
Cytogenetic map
Sequence location
X:7,608,428..7,678,859 [+]
Recombination map

1-20

RefSeq locus
NC_004354 REGION:7608428..7678859
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
GO Summary Ribbons
Gene Ontology (GO) Annotations (23 terms)
Molecular Function (3 terms)
Terms Based on Experimental Evidence (1 term)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN001019067
(assigned by GO_Central )
Biological Process (18 terms)
Terms Based on Experimental Evidence (12 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (8 terms)
CV Term
Evidence
References
Cellular Component (2 terms)
Terms Based on Experimental Evidence (1 term)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000361901
(assigned by GO_Central )
inferred from biological aspect of ancestor with PANTHER:PTN001019067
(assigned by GO_Central )
Protein Family (UniProt)
Belongs to the CUT homeobox family. (P10180)
Summaries
Gene Group (FlyBase)
CUT HOMEOBOX TRANSCRIPTION FACTORS -
CUT homeobox transcription factors are sequence-specific DNA binding proteins that regulate transcription. The CUT proteins have a homeodomain and one or more copies of the 75 amino acid DNA-binding CUT domain. (Adapted from FBrf0232555 and PMID:18797923).
Protein Function (UniProtKB)
Regulator of cell fate decisions in multiple lineages. Specifically, functions as a determination factor that specifies sensory organ identity in precursor cells. Probably also involved in cell type specification of Malpighian tubules. In absence of cut gene external sensory organs are transformed into chordotonal organs.
(UniProt, P10180)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
ct: cut
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, Proc. Nat. Acad. Sci. USA 25: 299-308; 1940, J. Genet. 41: 75-139 (fig.)] 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, Mol. Gen. Genet. 103: 363-79). 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 Garc'a-Bellido, 1975, Wilhelm Roux's Arch. Entwicklungsmech. Org. 178: 233-45). Lethal alleles fall into three groups, based on their complementation characteristics: cutless, group I, and group II. Lethal alleles ctC145, ctJA124, and ctl49 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, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307). 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 discernable 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, Cell 51: 293-307 (fig.).] 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, Nature 333: 629-35). 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, Aust. J. Biol. Sci. 26: 903-09). 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.
           
                                                               ct
kf2   ctnct6                           ctK                lethals
_________________________________________________________________

|       | |                             |                       |
|  -0.04- |           -0.16-            |     - ~0.07-          |
         Genetic fine structure map of the cut locus

           
ct71g
ctJC20
ctk
Classified as a group-I lethal because homozygotes show reduced viability, and only 10% of fewer heterozygotes with other lethal alleles survive; survivors have weakly cut wings, as well as fine bristles, and enlarged and deformed humeral callus, not seen in other cut-wing mutants.
ctcl: cut-cutless
Acts as a lethal allele in combination with deficiencies for ct; phenotype normal in combination with viable ct alleles. Homozygotes have reduced viability and show thoracic protuberances (Schalet). Heterozygotes of ctcl with lethal alleles of ct die or eclose in small numbers; an exception is ctcl/ctHA46, which exhibits normal survival.
ctlS1 (A. Schalet)
Lethal; a member of cut Lethal II group, maps proximal to ctC145 (Jack, 1985). Not suppressed by su(Hw)2 (Schalet). ctlS1/+ males, frequently show thoracic protuberances (Schalet).
ctlS2 (A. Schalet)
Almost complete lethal; survival less than 1%. Not suppressed by su(Hw)2; cut-cutless type of mutant in that ctlS2 fails to complement lethal alleles, e.g. ctlS1, but complements kf2, ct6 and ctS. Rare surviving males and females are fertile with normal wings, but usually show thoracic protuberances in the region of the presutural and notoplural bristles as are also seen in heterozygotes of ctlS1, Df(1)ctJ4 or Df(1)ctJ6.
kf2
Summary (Interactive Fly)
Gene Model and Products
Number of Transcripts
3
Number of Unique Polypeptides
3

Please see the JBrowse view of Dmel\ct for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Comments on Gene Model

Tissue-specific extension of 3' UTRs observed during later stages (FBrf0218523, FBrf0219848); all variants may not be annotated

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

Sequence Ontology: Class of Gene
Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0071068
10438
2175
FBtr0305134
10732
2165
FBtr0331733
11755
2174
Additional Transcript Data and Comments
Reported size (kB)

8.2 (compiled cDNA)

Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0071026
233.6
2175
5.31
FBpp0293664
233.4
2165
5.33
FBpp0304122
233.5
2174
5.31
Polypeptides with Identical Sequences

None of the polypeptides share 100% sequence identity.

Additional Polypeptide Data and Comments
Reported size (kDa)

320, 280 (kD observed)

2175 (aa); 240 (kD predicted)

Comments

g1345461 contains only the homeodomain.

ct protein positively regulates its own expression.

When the complete ct coding sequence is

expressed under the control of a heat shock promoter, 320 kD and 280 kD

bands are observed on a Western blot. The same two protein sizes are

detected in Western blots of wild type embryos.

External Data
Linkouts
Sequences Consistent with the Gene Model
Nucleotide / Polypeptide Records
 
Mapped Features

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.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Expression Data
Expression Summary Ribbons
Colored tiles in ribbon indicate that expression data has been curated by FlyBase for that anatomical location. Colorless tiles indicate that there is no curated data for that location.
For complete stage-specific expression data, view the modENCODE Development RNA-Seq section under High-Throughput Expression below.
Transcript Expression
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
Malpighian tubule

Comment: reference states >5-6 hr AEL

external sensory organ

Comment: reference states >5-6 hr AEL

northern blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Marker for
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
distribution deduced from reporter or direct label
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
v'esB neuron

Comment: reference states 10 hr AEL

vesB neuron

Comment: reference states 10 hr AEL

des2 neuron

Comment: reference states 5-6 hr AEL

les3 neuron

Comment: reference states 5-6 hr AEL

v'es2 neuron

Comment: reference states 5-6 hr AEL

v'es3 neuron

Comment: reference states 5-6 hr AEL

desC neuron

Comment: reference states 6-7 hr AEL

desD neuron

Comment: reference states 6-7 hr AEL

desB neuron

Comment: reference states 8 hr AEL

lesA neuron

Comment: reference states 8 hr AEL

lesB neuron

Comment: reference states 8 hr AEL

lesC neuron

Comment: reference states 8 hr AEL

v'esA neuron

Comment: reference states 8 hr AEL

vesC neuron

Comment: reference states 8 hr AEL

Malpighian tubule

Comment: reference states >5-6 hr AEL

external sensory organ

Comment: reference states >5-6 hr AEL

western blot
Stage
Tissue/Position (including subcellular localization)
Reference

Comment: reference states >6 hr AEL

Additional Descriptive Data

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 protein is expressed in a subset of neurons of the medulla anlage in third instar larva. In adults, ct is expressed in the medulla neurons Mi10b, Tm9, Tm3a and Tm3b.

ct expression was compared in the wing and haltere discs. ct xpression is lower along the D/V axis in the haltere than the wing and is completely absent in the posterior compartment of the haltere.

ct is expressed in all AMPs (adult muscle precursor 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.

ct is expressed in approximately 8 adPNs, 8 lPNs and all vPNs in adults.

ct protein labels all cells of developing microchaetae and macrochaetae.

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.

Marker for
Subcellular Localization
CV Term
Evidence
References
Expression Deduced from Reporters
Reporter: P{ctA3-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ct-GAL4.3}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ct-GAL4.14}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ctwHZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutA1-hs43}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutA2-hs43}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutB-hsp70-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutC-hsp70-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutD-hsp70-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutE-hsp70-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cutF-hsp70-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{cut-GAL4.B}
Stage
Tissue/Position (including subcellular localization)
Reference
wing margin

Comment: expression detected until 42 hr APF

High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\ct in GBrowse 2
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
FlyExpress - Embryonic expression images (BDGP data)
  • Stages(s) 7-8
  • Stages(s) 9-10
  • Stages(s) 11-12
  • Stages(s) 13-16
Alleles, Insertions, and Transgenic Constructs
Classical and Insertion Alleles ( 314 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 20 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of ct
Transgenic constructs containing regulatory region of ct
Deletions and Duplications ( 71 )
Disrupted in
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Sterility
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
joint & antenna | somatic clone
macrochaeta & wing
scutellum & macrochaeta
scutum & macrochaeta
wing (with ct6)
wing (with ctA)
wing & macrochaeta | posterior
Orthologs
Human Orthologs (via DIOPT v8.0)
Homo sapiens (Human) (6)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
11 of 15
Yes
Yes
10 of 15
No
Yes
 
1  
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Model Organism Orthologs (via DIOPT v8.0)
Mus musculus (laboratory mouse) (5)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
11 of 15
Yes
Yes
10 of 15
No
Yes
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Rattus norvegicus (Norway rat) (2)
9 of 13
Yes
Yes
8 of 13
No
Yes
Xenopus tropicalis (Western clawed frog) (4)
5 of 12
Yes
Yes
5 of 12
Yes
Yes
1 of 12
No
No
1 of 12
No
No
Danio rerio (Zebrafish) (9)
11 of 15
Yes
Yes
7 of 15
No
Yes
6 of 15
No
Yes
5 of 15
No
Yes
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Caenorhabditis elegans (Nematode, roundworm) (7)
10 of 15
Yes
Yes
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
Yes
Arabidopsis thaliana (thale-cress) (3)
2 of 9
Yes
Yes
1 of 9
No
Yes
1 of 9
No
Yes
Saccharomyces cerevisiae (Brewer's yeast) (1)
5 of 15
Yes
Yes
Schizosaccharomyces pombe (Fission yeast) (1)
4 of 12
Yes
Yes
Ortholog(s) in Drosophila Species (via OrthoDB v9.1) ( EOG091900PD )
Organism
Common Name
Gene
AAA Syntenic Ortholog
Multiple Dmel Genes in this Orthologous Group
Drosophila suzukii
Spotted wing Drosophila
Drosophila simulans
Drosophila sechellia
Drosophila erecta
Drosophila yakuba
Drosophila ananassae
Drosophila persimilis
Drosophila persimilis
Drosophila willistoni
Drosophila virilis
Drosophila mojavensis
Drosophila mojavensis
Drosophila grimshawi
Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG091500EK )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Musca domestica
House fly
Glossina morsitans
Tsetse fly
Lucilia cuprina
Australian sheep blowfly
Mayetiola destructor
Hessian fly
Aedes aegypti
Yellow fever mosquito
Anopheles gambiae
Malaria mosquito
Culex quinquefasciatus
Southern house mosquito
Orthologs in non-Dipteran Insects (via OrthoDB v9.1) ( EOG090W00BP )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Bombyx mori
Silkmoth
Danaus plexippus
Monarch butterfly
Heliconius melpomene
Postman butterfly
Apis florea
Little honeybee
Apis mellifera
Western honey bee
Bombus impatiens
Common eastern bumble bee
Bombus terrestris
Buff-tailed bumblebee
Linepithema humile
Argentine ant
Megachile rotundata
Alfalfa leafcutting bee
Nasonia vitripennis
Parasitic wasp
Dendroctonus ponderosae
Mountain pine beetle
Tribolium castaneum
Red flour beetle
Pediculus humanus
Human body louse
Rhodnius prolixus
Kissing bug
Cimex lectularius
Bed bug
Acyrthosiphon pisum
Pea aphid
Zootermopsis nevadensis
Nevada dampwood termite
Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( EOG090X00B6 )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strigamia maritima
European centipede
Ixodes scapularis
Black-legged tick
Stegodyphus mimosarum
African social velvet spider
Stegodyphus mimosarum
African social velvet spider
Tetranychus urticae
Two-spotted spider mite
Daphnia pulex
Water flea
Daphnia pulex
Water flea
Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( None identified )
No non-Arthropod Metazoa orthologies identified
Paralogs
Paralogs (via DIOPT v8.0)
Drosophila melanogaster (Fruit fly) (1)
1 of 10
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Model Summary Ribbon
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 3 )
Potential Models Based on Orthology ( 0 )
Human Ortholog
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Allele
Disease
Interaction
References
Disease Associations of Human Orthologs (via DIOPT v8.0 and OMIM)
Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
Functional Complementation Data
Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
Dmel gene
Ortholog showing functional complementation
Supporting References
Interactions
Summary of Physical Interactions
esyN Network Diagram
Show neighbor-neighbor interactions:
Select Layout:
Legend:
Protein
RNA
Selected Interactor(s)
Interactions Browser

Please see the Physical Interaction reports below for full details
protein-protein
Physical Interaction
Assay
References
RNA-protein
Physical Interaction
Assay
References
Summary of Genetic Interactions
esyN Network Diagram
esyN Network Key:
Suppression
Enhancement

Please look at the allele data for full details of the genetic interactions
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
suppressible
enhanceable
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
External Data
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Signaling Pathways (FlyBase)
Metabolic Pathways
External Data
Linkouts
Genomic Location and Detailed Mapping Data
Chromosome (arm)
X
Recombination map

1-20

Cytogenetic map
Sequence location
X:7,608,428..7,678,859 [+]
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
7B4-7B6
Limits computationally determined from genome sequence between P{EP}CBPEP1643&P{EP}EP1523EP1523 and P{EP}CHES-1-likeEP1453
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
7B3-7B4
(determined by in situ hybridisation)
7B-7B
(determined by in situ hybridisation)
7B1-7B2
(determined by in situ hybridisation)
7B3-7B3
(determined by in situ hybridisation)
7B1-7B4
(determined by in situ hybridisation)
Experimentally Determined Recombination Data
Notes

ct14-95-1D and ct20-135 map to the right of ct6.

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.

Stocks and Reagents
Stocks (97)
Genomic Clones (38)
cDNA Clones (38)
 

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.

cDNA clones, fully sequenced
BDGP DGC clones
Other clones
Drosophila Genomics Resource Center cDNA clones

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.

cDNA Clones, End Sequenced (ESTs)
BDGP DGC clones
RNAi and Array Information
Linkouts
DRSC - Results frm RNAi screens
GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
Antibody Information
Laboratory Generated Antibodies
Commercially Available Antibodies
 
Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
Other Information
Relationship to Other Genes
Source for database identify of
Source for database merge of

Source for merge of: ct CG11387

Source for merge of: ct BcDNA:GH10590

Additional comments

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.

Other Comments

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.

ct may function as a developmental switch between the achaete-scute complex and amos dependent multidendritic (md) neurons.

Analysis of ct mutants suggests that germline cell cytokineses are normal in mutant females.

Phenotypic analysis of double mutants implicates ct in the regulation of expression and/or function of Antp and pb, and documents a new role of ct in the control of segment identity.

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.

The combined effect of N and its target genes ct and wg regulate the expression of N ligands Dl and Ser which restrict N signalling to the wing dorsoventral boundary.

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.

Chi and mam regulate ct alleles lacking gypsy insertions. sd, mam and Chi cooperate synergistically to regulate ct expression.

wg and N cooperate to activate expression of ct, suggesting the wg and N pathways interact synergistically in the wing imaginal disc.

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.

The ct and ovo loci are hot spots for gypsy insertions.

Poxn expression is independent of ct but dependent on AS-C.

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.

A number of ct mutations associated with super-unstable mutations at the sn locus have been studied.

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.

Origin and Etymology
Discoverer
Etymology
Identification
External Crossreferences and Linkouts ( 189 )
Sequence Crossreferences
NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
UniProt/TrEMBL - Automatically annotated and unreviewed records of protein sequence and functional information
Other crossreferences
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
KEGG Genes - Molecular building blocks of life in the genomic space.
modMine - A data warehouse for the modENCODE project
Linkouts
BioGRID - A database of protein and genetic interactions.
DPiM - Drosophila Protein interaction map
DroID - A comprehensive database of gene and protein interactions.
DRSC - Results frm RNAi screens
Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyCyc Genes - Genes from a BioCyc PGDB for Dmel
FlyMine - An integrated database for Drosophila genomics
Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Synonyms and Secondary IDs (13)
Reported As
Symbol Synonym
BcDNA:GH10590
ct
(Aromolaran et al., 2020, Cavaliere et al., 2020, Keder et al., 2020, Yoong et al., 2020, Chen et al., 2019, Gaspar et al., 2019, Liu et al., 2019, Lo et al., 2019, Ramaekers et al., 2019, Shokri et al., 2019, Story et al., 2019, Yang and Chien, 2019, Ariss et al., 2018, Croset et al., 2018, Lavoy et al., 2018, Ong and Lin, 2018, Palliyil et al., 2018, Zhu et al., 2018, Pascual-Garcia et al., 2017, Transgenic RNAi Project members, 2017-, Guida et al., 2016, Kwon et al., 2016, Skottheim Honn et al., 2016, Slaninova et al., 2016, Baëza et al., 2015, Bartok et al., 2015, Dequéant et al., 2015, Duff et al., 2015, Javeed et al., 2015, Legent et al., 2015, Schertel et al., 2015, Zhang et al., 2015, Ashwal-Fluss et al., 2014, Bagley et al., 2014, Rhee et al., 2014, Smith and Shilatifard, 2014, White-Grindley et al., 2014, Babaoğlan et al., 2013, Iyer et al., 2013, Kyrchanova et al., 2013, Matzat et al., 2013, McNerney et al., 2013, Ruiz et al., 2013, Anderson et al., 2012, Brody et al., 2012, Golovnin et al., 2012, Manning et al., 2012, Plavicki et al., 2012, Tie et al., 2012, Wang and Sun, 2012, Zhai et al., 2012, Bellen et al., 2011, Kuzin et al., 2011, Matsui et al., 2011, Ramos et al., 2011, Slattery et al., 2011, Strand and Micchelli, 2011, Uddin et al., 2011, Weake et al., 2011, Zhai et al., 2011, Zheng et al., 2011, Buffin and Gho, 2010, Oliver et al., 2010, Popodi et al., 2010-, Suissa et al., 2010, Venken et al., 2010, Zhai et al., 2010, Akbari et al., 2009, Campbell et al., 2009, Christensen et al., 2009.2.28, Hödl and Basler, 2009, Long et al., 2009, Rajan et al., 2009, Wheeler et al., 2009, Brandt and Corces, 2008, Christensen et al., 2008.6.11, Christensen et al., 2008.12.28, Duong et al., 2008, Gause et al., 2008, Golovnin et al., 2008, Zartman et al., 2008, Beltran et al., 2007, Ebacher et al., 2007, Engström et al., 2007, Golovnin et al., 2007, Hatton-Ellis et al., 2007, Hattori et al., 2007, Hughes and Thomas, 2007, Jinushi-Nakao et al., 2007, Krattinger et al., 2007, Luque and Milan, 2007, Quinones-Coello, 2007, Quinones-Coello, 2007, Reiter et al., 2007, Vrailas-Mortimer et al., 2007, Capelson and Corces, 2006, Lei and Corces, 2006, Lovegrove et al., 2006, Lovegrove et al., 2006, Bolinger and Boekhoff-Falk, 2005, Capelson and Corces, 2005, Haddrill et al., 2005, Macdonald and Long, 2005, Merianda et al., 2005, Pérez et al., 2005, Pütz et al., 2005, Roegiers et al., 2005, Kamimura et al., 2004, Pai et al., 2004, Rollins et al., 2004, Wang and Struhl, 2004, Wang et al., 2004, Micchelli et al., 2003, Gause et al., 2001)
l(1)7Ba
l(1)7Bb
l(1)VE614
Name Synonyms
Cut
(Choubey et al., 2020, Harsh et al., 2020, Mo et al., 2020, Bernascone et al., 2019, Chai et al., 2019, Fic et al., 2019, Ng et al., 2019, Bellec et al., 2018, Kavaler et al., 2018, Kucherenko and Shcherbata, 2018, Zülbahar et al., 2018, Corty et al., 2016, Jin et al., 2016, Li and Jasper, 2016, Mukherjee et al., 2016, Saadin and Starz-Gaiano, 2016, Aparicio et al., 2015, Copf, 2015, Palmer et al., 2015, Ayeni et al., 2014, Charng et al., 2014, Claret et al., 2014, Domanitskaya et al., 2014, Ferreira et al., 2014, Karandikar et al., 2014, Macagno et al., 2014, Marr et al., 2014, Mishra et al., 2014, Oliveira et al., 2014, Zohar-Stoopel et al., 2014, Babaoğlan et al., 2013, Denholm et al., 2013, Fleming et al., 2013, Fox et al., 2013, Guichard et al., 2013, Huang et al., 2013, Jauffred et al., 2013, Khan et al., 2013, Kwon et al., 2013, Marianes and Spradling, 2013, Puram and Bonni, 2013, Sasamura et al., 2013, Upadhyay et al., 2013, van de Hoef et al., 2013, Yu et al., 2013, Barth et al., 2012, Giagtzoglou et al., 2012, Heck et al., 2012, Hödl and Basler, 2012, Singh and Mlodzik, 2012, Tursun, 2012, Wang and Sun, 2012, Wu et al., 2012, Xie et al., 2012, Yamamoto et al., 2012, Zhang et al., 2012, Benhra et al., 2011, Duan et al., 2011, Esteve et al., 2011, Hasegawa et al., 2011, Johnson et al., 2011, Kohwi et al., 2011, Lin et al., 2011, Mast et al., 2011, Pi et al., 2011, Popova et al., 2011, Poulton et al., 2011, Quijano et al., 2011, Rodriguez, 2011, Sun et al., 2011, Yan et al., 2011, Beam and Moberg, 2010, Bejarano et al., 2010, Benhra et al., 2010, Bernard et al., 2010, Cohen et al., 2010, Cordero and Cagan, 2010, Dutta et al., 2010, Egger-Adam and Katanaev, 2010, Fan et al., 2010, Fiuza et al., 2010, Genevet et al., 2010, Hamel et al., 2010, Kugler and Nagel, 2010, Li et al., 2010, Maurel-Zaffran et al., 2010, Mukhopadhyay et al., 2010, Pines et al., 2010, Quijano et al., 2010, Saj et al., 2010, Swanson et al., 2010, Usha and Shashidhara, 2010, Wu et al., 2010, Yu et al., 2010, Yu et al., 2010, Almudi et al., 2009, Andrews et al., 2009, Bhattacharya and Baker, 2009, Chen and Rasmuson-Lestander, 2009, Chen et al., 2009, Genevet et al., 2009, Mao and Freeman, 2009, McKay et al., 2009, Miller et al., 2009, Mirth et al., 2009, Mummery-Widmer et al., 2009, O'Keefe et al., 2009, Rajan et al., 2009, Roegiers et al., 2009, Shimono et al., 2009, Siddall et al., 2009, Steele et al., 2009, Yan et al., 2009, Acar et al., 2008, Bejarano et al., 2008, Braid and Verheyen, 2008, Canela-Xandri et al., 2008, Crozatier and Vincent, 2008, Eid et al., 2008, Jin et al., 2008, Kandachar et al., 2008, Katanaev et al., 2008, Lebreton et al., 2008, Mao et al., 2008, McNeill et al., 2008, O'Farrell and Kylsten, 2008, Schuldiner et al., 2008, Takaesu et al., 2008, Tian and Deng, 2008, Tien et al., 2008, Tran and Doe, 2008, Vaccari et al., 2008, Yu et al., 2008, Ambrus et al., 2007, Bhat, 2007, Buceta et al., 2007, Hatton-Ellis et al., 2007, Hattori et al., 2007, Herranz et al., 2007, Ida et al., 2007, Levine et al., 2007, Li et al., 2007, Luque and Milan, 2007, Nagaraj and Banerjee, 2007, Nurminsky, 2007, Sasaki et al., 2007, Silver et al., 2007, Sun and Deng, 2007, Yoshioka et al., 2007, Balakireva et al., 2006, Baril and Therrien, 2006, Childress et al., 2006, Gallagher and Knoblich, 2006, Glittenberg et al., 2006, Hutterer et al., 2006, Jaekel and Klein, 2006, Jordan et al., 2006, Lim and Tomlinson, 2006, Maqbool et al., 2006, O'Reilly et al., 2006, Roignant et al., 2006, Rusten et al., 2006, Seto et al., 2006, Tsuda et al., 2006, Vrailas and Moses, 2006, Vrailas et al., 2006, David et al., 2005, Lovato et al., 2005, Orgogozo and Grueber, 2005, Wei et al., 2005, Li et al., 2004, Voas and Rebay, 2004)
cut
(Arya et al., 2019, Jeong et al., 2019, Bischof et al., 2018, Du et al., 2018, Richardson and Portela, 2018, Tokusumi et al., 2017, Han et al., 2016, Huang et al., 2016, Auer et al., 2015, Jasper, 2015, Javeed et al., 2015, Lin et al., 2015, Lin et al., 2015, Lo et al., 2015, Andrés et al., 2014, Guo et al., 2014, Marr et al., 2014, Mouri et al., 2014, Singari et al., 2014, Smith and Shilatifard, 2014, Tsikala et al., 2014, Wong et al., 2014, Xie et al., 2014, Zhang et al., 2014, Aoyama et al., 2013, Beckett et al., 2013, Groth et al., 2013, Iyer et al., 2013, Iyer et al., 2013, Kyrchanova et al., 2013, Moshkin et al., 2013, Schaaf et al., 2013, Schertel et al., 2013, Weasner and Kumar, 2013, Yu et al., 2013, Anderson et al., 2012, Ayukawa et al., 2012, Domanitskaya and Schüpbach, 2012, Kallijärvi et al., 2012, Mavromatakis and Tomlinson, 2012, Mouri et al., 2012, Nagel et al., 2012, Olesnicky et al., 2012, Smibert et al., 2012, Xie et al., 2012, Yue et al., 2012, Esteve et al., 2011, Furman and Bukharina, 2011, Kuzin et al., 2011, Lin et al., 2011, Pi et al., 2011, Ramos et al., 2011, Slattery et al., 2011, Strand and Micchelli, 2011, Tapadia and Gautam, 2011, Uddin et al., 2011, Zhai et al., 2011, Becam et al., 2010, Buffin and Gho, 2010, Campbell et al., 2010, Duncan et al., 2010, Figeac et al., 2010, Herr et al., 2010, Levine et al., 2010, Müller et al., 2010, Song et al., 2010, Sosin et al., 2010, Suissa et al., 2010, Tong et al., 2010, Tran et al., 2010, Usha and Shashidhara, 2010, Wang et al., 2010, Zhai et al., 2010, Campbell et al., 2009, Hödl and Basler, 2009, Krejcí et al., 2009, Li et al., 2009, Long et al., 2009, Shi and Noll, 2009, Shimono et al., 2009, Tuxworth et al., 2009, Bray et al., 2008, Casso et al., 2008, Duong et al., 2008, Golovnin et al., 2008, Golovnin et al., 2008, Herranz et al., 2008, Misulovin et al., 2008, Pierre et al., 2008, Sun et al., 2008, Tien et al., 2008, Vaccari et al., 2008, Wang and Sun, 2008, Zartman et al., 2008, Ebacher et al., 2007, Emmons et al., 2007, Golovnin et al., 2007, Goodfellow et al., 2007, Hatton-Ellis et al., 2007, Hughes and Thomas, 2007, Komiyama and Luo, 2007, Kugler and Nagel, 2007, Manak et al., 2007, Matthews et al., 2007, Parrish et al., 2007, Polesello and Tapon, 2007, Schwartz and Pirrotta, 2007, Tchurikov et al., 2007, Vrailas-Mortimer et al., 2007, Capelson and Corces, 2006, Childress et al., 2006, Crews and Brenman, 2006, Gonzalez et al., 2006, Herranz et al., 2006, Kulkarni et al., 2006, Mosimann et al., 2006, Negre et al., 2006, Pereira et al., 2006, Sosin et al., 2006, Vrailas and Moses, 2006, Boekhoff-Falk, 2005, Bolinger and Boekhoff-Falk, 2005, Burnette et al., 2005, Dorsett et al., 2005, Haddrill et al., 2005, Mandal et al., 2005, Kamimura et al., 2004, Li and Baker, 2004, Li et al., 2004, Rollins et al., 2004, Sugimura et al., 2004, Xu et al., 2004, Dimitri et al., 2003, Micchelli et al., 2003, Dorsett et al., 2002, Gause et al., 2001, Ivanov and Tchurikov, 2001, Ghysen and Dambly-Chaudiere, 2000, Jackson and Berg, 2000, Yaich and Bodmer, 2000, Courey et al., 1998, Jarman and Ahmed, 1998, Awasaki and Kimura, 1997, Czerny et al., 1997, Tchurikov, 1997.2.18, Tchurikov, 1997.4.3, Begun et al., 1994, Bodmer et al., 1990)
kinked-femur
Secondary FlyBase IDs
  • FBgn0000383
  • FBgn0001303
  • FBgn0029953
  • FBgn0062500
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Project
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References (1,082)