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General Information
Symbol
Dmel\en
Species
D. melanogaster
Name
engrailed
Annotation Symbol
CG9015
Feature Type
FlyBase ID
FBgn0000577
Gene Model Status
Stock Availability
Gene Snapshot
engrailed (en) encodes a homeodomain-containing transcription factor that is essential for posterior compartment identity and for compartment boundary formation and maintenance. It positively regulates the hh gene and negatively regulates the Hedgehog targets encoded by ci, ptc and dpp. [Date last reviewed: 2019-03-07]
Also Known As

Eng, spermatheca, en1, spt

Key Links
Genomic Location
Cytogenetic map
Sequence location
2R:11,524,006..11,528,210 [-]
Recombination map

2-64

RefSeq locus
NT_033778 REGION:11524006..11528210
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
GO Summary Ribbons
Gene Ontology (GO) Annotations (31 terms)
Molecular Function (4 terms)
Terms Based on Experimental Evidence (4 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000678674
(assigned by GO_Central )
Biological Process (25 terms)
Terms Based on Experimental Evidence (14 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:dome; FB:FBgn0043903
Terms Based on Predictions or Assertions (11 terms)
CV Term
Evidence
References
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000678675
(assigned by GO_Central )
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000678674
(assigned by GO_Central )
traceable author statement
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:PTN000678674
(assigned by GO_Central )
inferred from biological aspect of ancestor with PANTHER:PTN000678674
(assigned by GO_Central )
Protein Family (UniProt)
Belongs to the engrailed homeobox family. (P02836)
Summaries
Gene Group (FlyBase)
NK-LIKE HOMEOBOX TRANSCRIPTION FACTORS -
NK-like (NKL) homeobox transcription factors are sequence-specific DNA binding proteins that regulate transcription. NKL transcription factors are homeobox genes closely related to Hox-like genes, a number of which are found in the NK cluster. Many of the NKL members contain an Engrailed Homology 1 (EH1) motif. (Adapted from FBrf0232555 and PMID:22094586).
Protein Function (UniProtKB)
This protein specifies the body segmentation pattern. It is required for the development of the central nervous system. Transcriptional regulator that represses activated promoters. Wg signaling operates by inactivating the SGG repression of EN autoactivation.
(UniProt, P02836)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
en: engrailed (T.Kornberg)
thumb
en: engrailed
From Eker, 1929, Hereditas 12: 217-22.
Four classes of alleles, all recessive. (1) en1. Viable hemizygous and homozygous; fertile. Longitudinal cleft extends from rear border of scutellum forward, may be reduced to median nick or posterior flattening of scutellum. Wings larger, broader, and thin textured with spatulate end; venation and distribution of sensilla abnormal in posterior wing compartment. Variable duplication of anterior triple row bristles on posterior margin; alula reduced, with costal-like bristles. In males, extra sex comb often present (Brasted, 1941, Genetics 26: 347-73), smaller than normal, and in mirror-image position in posterior compartment. Duplications of transverse rows in female prothoracic leg, extra bristles in mesothoracic and metathoracic tarsi (Garcia-Bellido, and Santamaria, 1972, Genetics 72: 87-104; Lawrence, Struhl, and Morata, 1979, J. Embryol. Exp. Morph. 51: 195-208). Action of en1 is autonomous except for scutellar cleft (Tokunaga, 1961, Genetics 46: 157-76; Stern and Tokunaga, 1968, Proc. Nat. Acad. Sci. USA 60: 1252-59; Garcia-Bellido, and Santamaria, 1972, Genetics 72: 87-104). Clones of en cells of posterior compartment origin fail to respect anterior-posterior compartment border in wing disc as do mwh clones in wing discs of en1 homozygotes (Morata and Lawrence, 1975, Nature 255: 614-17; Morata and Lawrence, 1976, Dev. Biol. 50: 321-37). en abnormalities are associated with posterior compartment structures only, except for scutellar cleft. Restriction of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase (Cunninghamn, Smith, Makowski, and Kuhn, 1983, Mol. Gen. Genet. 191: 238-43) and of a protein recognized by monoclonal antibody PS2 (Brower, 1984, Nature 310: 496-98; 1987, EMBO J. 5: 2649-56) to posterior compartment of wing disc altered by en1. Interaction with ci, cg, sx (House, 1953, Genetics 38: 200-15; House, 1953, Genetics 38: 309-27; House, 1961, Genetics 46: 871; Mukherjee, 1965, Genetics 51: 285-304; Datta and Mukherjee, 1971, Genetics 68: 269-86) and fu (Fausto-Sterling and Smith-Schiess, 1982, EMBO J. 1: 827-33) partially increase phenotype. No suppression by su(Hw). (2) Lethal alleles with normal cytology. Embryonic lethal. Anterior margin of each segment defective. Pair rule defects in naked cuticle of T1, T3, A2, A4, A6, A8 result in pair-wise fusion of adjacent segments. Autonomous effects in adult cuticular clones observed in posterior compartment of proboscis, thorax, abdomen, and genitalia. enlethal clones are without effect in anterior compartments and in eye-antennal region (Kornberg, 1981, Proc. Nat. Acad. Sci. USA 78: 1095-99; Kornberg, 1981, Dev. Biol. 86: 363-72; Lawrence and Struhl, 1982, EMBO J. 1: 827-33). The en1/enlethal heterozygote characterized by wing abnormalities only; disruption of anterior crossvein, gap in vein IV, and occasional socketted bristles on posterior margin. In some combinations complementation is complete or nearly so (Condie and Brower, 1989, Dev. Biol. 135: 31-42). No maternal effect (Lawrence, Johnston and Struhl, 1983, Cell 35: 27-34). (3) Deficiencies and lethal alleles with inversion or translocation breakpoints. Embryonic lethal. Embryonic segment defects slight and variable. Alleles of this class in heterozygous combination witn en1 produce adults more extreme than en1. For example, in en1/en2, legs are truncated, the tarsi reduced to densely bristled stumps; wings are greatly enlarged and spatulate with greater disruption of veins IV and V; higher penetrance of socketed bristles along the posterior margin. Extreme scutellar cleft. At 29, duplication of anterior compartment bristles in mirror-image symmetry in posterior compartment of second antennal segment (Morata, Kornberg, and Lawrence, 1983, Dev. Biol. 99: 27-33). (4) Non-lethal alleles with breakpoints. Hemizygous viable, embryos normal. Heterozygous with other allele classes, variable gaps in wing veins IV and V. Variable reductions or deletions in male and female genitalia (Epper and Sanchez, 1983, Dev. Biol. 100: 387-98). Scutellum may also be affected.
spt: spermatheca
At 28, female has two spermathecae but ducts partly fused; at 25, only one enlarged spermatheca on one duct; at 18, a duct with three branches, each bearing a spermatheca. Temperature-sensitive period in third larval instar. Female fertility not greatly affected. RK3.
Summary (Interactive Fly)

transcription factor - homeodomain - engrailed class - segment polarity gene - involved in compartment identity and boundary formation - positively regulates the and negatively regulates the Hedgehog targets and

Gene Model and Products
Number of Transcripts
2
Number of Unique Polypeptides
1

Please see the JBrowse view of Dmel\en 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

Gene model reviewed during 5.49

Sequence Ontology: Class of Gene
Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0088096
2465
552
FBtr0088095
2792
552
Additional Transcript Data and Comments
Reported size (kB)

3.6, 2.7, 1.4 (northern blot)

Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0087198
59.4
552
7.07
FBpp0087197
59.4
552
7.07
Polypeptides with Identical Sequences

The group(s) of polypeptides indicated below share identical sequence to each other.

552 aa isoforms: en-PA, en-PB
Additional Polypeptide Data and Comments
Reported size (kDa)
Comments

en protein is used as a marker for the embryonic dorsal large intestine.

Polyclonal antibody is to the entire en protein.

en expression in the epidermis, but not the central nervous system, is disrupted in embryos which over express bcd. This disruption results in either the loss or fusion of en stripes.

Two monoclonal antibodies were generated against en (and also recognize inv), designated 4D9 and 4F11. 4D9 is directed to an engrailed specific region of the homeodomain, and recognizes en protien in several different species, but does not cross react with other homeodomain proteins.

External Data
Post Translational Modification

Phosphorylated. Phosphorylation may directly or allosterically modify its function.

(UniProt, P02836)
Linkouts
Sequences Consistent with the Gene Model
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\en 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
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
large intestine primordium | restricted

Comment: along outer curve of large intestine

dorsal ectoderm anlage

Comment: anlage in statu nascendi

mesectoderm anlage

Comment: anlage in statu nascendi

mesoderm anlage

Comment: anlage in statu nascendi

trunk mesoderm anlage

Comment: anlage in statu nascendi

ventral ectoderm anlage

Comment: anlage in statu nascendi

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

Comment: reference states 3-12 hr AEL

Additional Descriptive Data

en is expressed in posterior midline glia but not in anterior midline glia in stage 12 embryos. After its early pair rule and segment polarity expression patterns in early embryos, en expression becomes more expansive. At stage 10, en expression along with run expression divides the midline into four regions, anterior (runt[+], en[-]), middle (runt[-], en[-]), posterior (runt[-], en[+]), and extreme posterior (runt[-], en[-]). At stage 10, en is expressed in 2 midline cells. A second, late phase of en expression was activated in the extreme posterior runt[-] en[-] cells that, in combination with the early en[+] cells, generated a single posterior en[+] region containing around eight cells. By the end of stage 11, en is expressed in all posterior midline glia. These en[+] cells give rise to the posterior midline glia, MP4-6, and the median neuroblast.

Expression pattern inferred from unspecified enhancer trap line.

Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
larval dorsal multidendritic neuron | subset

Comment: expressed in one dorsal multidendritic neuron per segment

in situ
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

en protein is co-expressed with gsb-n protein in neuroblasts NB6-1, NB6-2, NB6-4, NB7-1, and later NB7-3.

en protein is expressed at similar levels in wing and haltere discs.

The en protein is localized to the nucleus, but becomes diffuse during mitosis.

en protein is expressed in 14 stripes beginning at embryonic stage 8. After stage 11, expression does not overlap with that of ci. en protein expression in the wing disc also does not overlap with that of ci

en protein is expressed in a two cell wide row of cells anterior to the segment boundaries of each segment. Expression in the posterior row of cells decreases as a groove forms at the segment boundary.

The en protein is expressed in a specified subset of neuroblasts in embryonic stages 8-11. (see also FBrf 42042)

Delayed changes in en expression were observed in response to ectopic eve expression in evehs.PS embryos. Four different expression patterns were observed depending on the timing of ectopic eve protein induction.

In wghs.P embryos, the en protein stripes broaden posteriorly, spanning maximally about one-third of the segment. This is a similar expression pattern to that found in nkd mutant embryos.

en expression was observed sequentially in 5 "centers" anterior to the mandibular segment starting at embryonic stage 8. These are the "en antennal stripe", the "en head spot", the "en intercalary spot", the "en expression in the anterior dorsal hemispheres" and the "en expression in the clypeolabrum". Later two of the spots split, generating the "en antennal spot" and the "en secondary head spot". The migration of these en-expressing cells was followed throughout embryonic development.

en expression is diminished in wg and arm mutants. An allelic series was described for each with with increasingly severe segment polarity phenotypes and earlier and more severe loss of en expression. The segmental stripes decay with a similar asymmetric pattern in wg and arm mutants.

en protein is expressed in stripes in the posterior region of each segment in the developing embryo, the detection of en expression in the even numbered stripes slighted preceeds the detection of odd numbered stripes.

en protein is expressed in stripes in the posterior region of each segment in the developing embryo. Detection of en expression in the even-numbered stripes slightly preceeds detection in odd-numbered stripes.

The en protein is expressed in the posterior half of each segment.

Marker for
Subcellular Localization
CV Term
Evidence
References
Expression Deduced from Reporters
Reporter: P{en2.4-GAL4}e16E
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enB}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enC}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enD}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enE}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enF}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enG}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{enI}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{en-lacZ(ryXba)}
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{en-w.181lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lwB}enAuI
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\en 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) 4-6
  • 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 ( 129 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 41 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of en
Transgenic constructs containing regulatory region of en
Deletions and Duplications ( 27 )
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
abdominal tergite & macrochaeta
abdominal tergite & trichome
abdominal tergite | anterior & trichome
embryonic/larval pericardial cell & embryonic myoblast, with Scer\GAL4how-24B, Scer\GAL4twi.PG
fat body/gonad primordium & parasegment 4, with Scer\GAL4twi.PGa
fat body/gonad primordium & parasegment 5, with Scer\GAL4twi.PGa
fat body/gonad primordium & parasegment 6, with Scer\GAL4twi.PGa
fat body/gonad primordium & parasegment 6, with Scer\GAL4zen.Kr.PF
fat body/gonad primordium & parasegment 7, with Scer\GAL4twi.PGa
fat body/gonad primordium & parasegment 7, with Scer\GAL4zen.Kr.PF
fat body/gonad primordium & parasegment 8, with Scer\GAL4twi.PGa
fat body/gonad primordium & parasegment 8, with Scer\GAL4zen.Kr.PF
fat body/gonad primordium & parasegment 9, with Scer\GAL4twi.PGa
motor neuron & growth cone & embryo, with Scer\GAL4elav-C155
UMI interneuron & axon, with Scer\GAL4sim.PS
VUM neuron & axon, with Scer\GAL4sim.PS
wing (with en28)
wing & macrochaeta
Orthologs
Human Orthologs (via DIOPT v8.0)
Homo sapiens (Human) (7)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
10 of 15
Yes
Yes
1  
9 of 15
No
Yes
2 of 15
No
Yes
1 of 15
No
No
1 of 15
No
No
1  
1 of 15
No
No
1 of 15
No
Yes
Model Organism Orthologs (via DIOPT v8.0)
Mus musculus (laboratory mouse) (5)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
10 of 15
Yes
Yes
0  
9 of 15
No
Yes
0  
2 of 15
No
Yes
1 of 15
No
Yes
1 of 15
No
Yes
Rattus norvegicus (Norway rat) (3)
8 of 13
Yes
Yes
1 of 13
No
Yes
1 of 13
No
Yes
Xenopus tropicalis (Western clawed frog) (2)
8 of 12
Yes
Yes
3 of 12
No
Yes
Danio rerio (Zebrafish) (4)
11 of 15
Yes
Yes
10 of 15
No
Yes
10 of 15
No
Yes
9 of 15
No
Yes
Caenorhabditis elegans (Nematode, roundworm) (3)
7 of 15
Yes
Yes
1 of 15
No
Yes
1 of 15
No
Yes
Arabidopsis thaliana (thale-cress) (1)
1 of 9
Yes
Yes
Saccharomyces cerevisiae (Brewer's yeast) (1)
1 of 15
Yes
Yes
Schizosaccharomyces pombe (Fission yeast) (1)
1 of 12
Yes
Yes
Ortholog(s) in Drosophila Species (via OrthoDB v9.1) ( EOG09190CJ9 )
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 pseudoobscura pseudoobscura
Drosophila persimilis
Drosophila willistoni
Drosophila virilis
Drosophila mojavensis
Drosophila grimshawi
Drosophila grimshawi
Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG09150BG9 )
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
Mayetiola destructor
Hessian fly
Aedes aegypti
Yellow fever mosquito
Anopheles darlingi
American malaria mosquito
Anopheles gambiae
Malaria mosquito
Culex quinquefasciatus
Southern house mosquito
Culex quinquefasciatus
Southern house mosquito
Orthologs in non-Dipteran Insects (via OrthoDB v9.1) ( EOG090W092G )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Bombyx mori
Silkmoth
Bombyx mori
Silkmoth
Apis florea
Little honeybee
Apis florea
Little honeybee
Apis mellifera
Western honey bee
Apis mellifera
Western honey bee
Bombus impatiens
Common eastern bumble bee
Bombus impatiens
Common eastern bumble bee
Bombus terrestris
Buff-tailed bumblebee
Bombus terrestris
Buff-tailed bumblebee
Linepithema humile
Argentine ant
Linepithema humile
Argentine ant
Linepithema humile
Argentine ant
Megachile rotundata
Alfalfa leafcutting bee
Megachile rotundata
Alfalfa leafcutting bee
Nasonia vitripennis
Parasitic wasp
Nasonia vitripennis
Parasitic wasp
Nasonia vitripennis
Parasitic wasp
Dendroctonus ponderosae
Mountain pine beetle
Dendroctonus ponderosae
Mountain pine beetle
Tribolium castaneum
Red flour beetle
Pediculus humanus
Human body louse
Pediculus humanus
Human body louse
Rhodnius prolixus
Kissing bug
Rhodnius prolixus
Kissing bug
Cimex lectularius
Bed bug
Cimex lectularius
Bed bug
Acyrthosiphon pisum
Pea aphid
Acyrthosiphon pisum
Pea aphid
Zootermopsis nevadensis
Nevada dampwood termite
Zootermopsis nevadensis
Nevada dampwood termite
Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( EOG090X04G4 )
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
Tetranychus urticae
Two-spotted spider mite
Tetranychus urticae
Two-spotted spider mite
Tetranychus urticae
Two-spotted spider mite
Daphnia pulex
Water flea
Daphnia pulex
Water flea
Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( EOG091G0XBB )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strongylocentrotus purpuratus
Purple sea urchin
Ciona intestinalis
Vase tunicate
Gallus gallus
Domestic chicken
Gallus gallus
Domestic chicken
Paralogs
Paralogs (via DIOPT v8.0)
Drosophila melanogaster (Fruit fly) (1)
5 of 10
Human Disease Associations
FlyBase Human Disease Model Reports
    Disease Model Summary Ribbon
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Allele
    Disease
    Evidence
    References
    Potential Models Based on Orthology ( 0 )
    Human Ortholog
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 2 )
    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.
    Homo sapiens (Human)
    Gene name
    Score
    OMIM
    OMIM Phenotype
    DO term
    Complementation?
    Transgene?
    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
    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
    enhanceable
    Starting gene(s)
    Interaction type
    Interacting gene(s)
    Reference
    suppressible
    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
    KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
    Genomic Location and Detailed Mapping Data
    Chromosome (arm)
    2R
    Recombination map

    2-64

    Cytogenetic map
    Sequence location
    2R:11,524,006..11,528,210 [-]
    FlyBase Computed Cytological Location
    Cytogenetic map
    Evidence for location
    47F17-48A1
    Limits computationally determined from genome sequence between P{lacW}Tapδk17005&P{lacW}k05103 and P{lacW}l(2)k13403k13403&P{lacW}Egmk14708
    Experimentally Determined Cytological Location
    Cytogenetic map
    Notes
    References
    48A-48A
    (determined by in situ hybridisation)
    Experimentally Determined Recombination Data
    Notes
    Stocks and Reagents
    Stocks (37)
    Genomic Clones (15)
     

    Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete

    cDNA Clones (99)
     

    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
    Additional comments

    The highly divergent mosquito engrailed protein Agam\en is able to substitute for en protein during all stages of development. Agam\en expression by enhancer-trapping is precise enough to restore viability to en mutants.

    enspt fails to complement en1.

    Other Comments

    DNA-protein interactions: genome-wide binding profile assayed for en protein in 0-12 hr embryos; see mE1_TFBS_en collection report.

    Ectopic expression of en prior to neuronal specification can misroute axons, whereas en has no major effect when ectopically expressed in neurons only. Therefore, the action of en on axonal pathfinding occurs at early stages, before neuronal cell fate is established.

    A 139bp minimal pairing sensitive element (PSE) from en regulatory DNA has been defined. This element mediates Pairing Sensitive Silencing (PSS). The PSE includes 8 protein binding sites at least 5 of which are important for pairing sensitive silencing. One of these is for pho protein, and another has the GAGAG sequence known to be bound by Trl and psq proteins.

    fz and fz2 are required during embryogenesis to maintain epidermal en and wg expression.

    hh is required for activation of en during regeneration of fragmented imaginal discs.

    wg mutant embryos have residual mirror-symmetric pattern due to an en-dependent signal specifying anterior denticle fates. The en-dependent signal acts unidirectionally and wg activity imposes the asymmetry.

    Three EMS induced en alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.

    When en is removed from Posterior cells, they transform into the Anterior cells of the same parasegment, rather than Anterior cells of the same segment.

    In the developing abdomen the state of en, whether off or on, determines whether a cell is of Anterior or Posterior type. en acts in the Anterior compartment, where it is induced by hh gene product, in a narrow band of cells, which has crossed the Anterior/Posterior compartment boundary. en causes these cells to form a special type of cuticle.

    Cell affinities in the adult abdomen depend on en : cells of the P compartment have affinities that are distinct from A cells.

    Transport or stability of wg gene product is reduced within en expressing cells.

    pho encodes a sequence-specific DNA binding protein that interacts with PRE in the en gene.

    In solution the en homeodomain binds to a DNA molecule containing a single TAAT sequence in an analogous manner to that observed in the X-ray co-crystal structure. en also binds to a more complex site, having overlapping TAAT sequences, in more than one orientation.

    eg is necessary for the maintenance of en and zfh2 expression in the serotonin neurons.

    Interactions between en and polyhomeotic are required to maintain the anterior-posterior boundary and posterior cell fate in the wing.

    Segment polarity gene expression is necessary for the survival of specific rows of epidermal cells.

    en promotes the development of the dorsolateral fat body, midgut visceral mesoderm and somatic gonads while it suppresses development of somatic muscles, heart and ventral fat body. There is a balance between fat body and somatic gonadal precursor (SGP) development with tin, wg and en driving cells in the primary clusters towards SGP development and srp driving them towards fat body development.

    Multiple domains contribute to en protein repression activity. The eh1 region interacts with the gro repressor.

    CrebA, en double mutant phenotype confirms that CrebA is not involved in segment polarity.

    Either en or inv is required to uncouple the ptc-gsb regulatory circuit in row 5 neuroblasts during neurogenesis.

    Genes known to be expressed in compartment-specific manner in discs are expressed in analogous patterns in each primordia.

    Adjacent and conserved ftz and cofactor binding sites within the en intron enhancer are necessary and sufficient for transcriptional activation. The cofactor sites can be specifically bound by ftz-f1, and the ftz homeodomain and ftz-f1 bind cooperatively in vitro.

    Cross-regulatory relationships among hh, wg and en, as well as their initial mode of activation, in the anterior head are significantly different from those in the trunk.

    pros does not modulate en regulatory region binding to DNA.

    The expression of wg and en in the adult antenna is controlled by age-dependent mechanisms.

    βTub60D is directly repressed by en protein. The first intron of the βTub60D locus contains several en protein binding sites.

    Pc, Psc and polyhomeotic proteins are associated with identical regulatory elements of en in tissue culture cells and differentially distributed on regulatory sequences of inv.

    en is one of a class of genes with TATA-less promoters that have the conserved DPE sequence.

    Amino acids in the N-terminal arm of the homeodomain, as well as at position 54 of the homeodomain, control the DNA binding specificity of the homeodomain.

    Cells in anterior compartments lacking ci express hh and adopt a posterior fate without expressing en.

    ara-caup are expressed at patches on the wing, located one at each side of the DV compartment border. The posterior border of the patches is defined by repression by en.

    Despite the absence of a syncytium in C.floridanum embryos monoclonal antibodies to en, Ubx and abd-A demonstrate their cognate proteins are expressed in a conserved pattern in the post-gastrulation stages of development. The expression of the eve cognate protein is not completely conserved and lacks a pair rule phase to its expression.

    The varied phenotypes of en alleles can be explained by the differential effects these mutants have on the combination of en and inv activities.

    en and inv share a regulatory region and encode redundant functions.

    Interfaces between posterior (en on) and anterior (en off) cells are required for pattern formation. wg could play the role of the morphogen, at least within part of the segmental pattern.

    Four segment polarity genes, hh, wg, gsb and en all function in concert to determine the formation and specifications of three hh-dependent eg-neuroblasts (6-4, 7-3 and 2-4).

    Elevated en expression does not disrupt eye morphogenesis.

    en is not required for hh activation or maintenance in the eye disc. Elevated en levels repress dpp, ptc and ci expression.

    en is post-translationally modified by casein kinase II (CK-II). The targets for CK-II phosphorylation in vitro are serine residues 394, 397, 401 and 402, and phosphorylation by CK-II stimulates DNA binding.

    Maintenance but not initiation of en gene expression in the embryo requires trx, which is also required to maintain stable long-term expression of the homeotic genes throughout development. trx is required for normal en expression in the wing imaginal disc. trx-dependent loss of en expression in the dorsal fat body is correlated with female sterility.

    Early ph-p gene expression is under the control of bcd and en as activators and of osk as an inhibitor.

    Early eve expression is required for the activation of both even and odd numbered en stripes and late eve stripes strengthen the expression of odd numbered en stripes.

    en has a dual role in wing development: a general role in patterning the appendage, achieved through the activation of secreted proteins like hh and dpp, and a more specific one, determining posterior identity, in which the inv gene may be implicated.

    The organisation of the tail region of the embryo is documented from studies of cuticular markers enabling a more direct comparison between homologous structures on the embryo and larval cuticle.

    en+ is a dose-dependent modifier of the ci locus. Lack of pairing at the ci locus can facilitate the en--dependent expression of the ci phenotypes.

    en is involved in regulation of serotonin cell development.

    odd and nkd are required to restrict en expression. odd represses expression of ftz, an activator of en. nkd prevents activation of en by ftz without affecting ftz expression.

    The transition from inter-dependent wg and en expression to wg autoregulation may involve several segment polarity genes.

    en is a candidate oc target gene in ocelli formation.

    Msr-110 is a direct target for regulation by en. Normal expression of Msr-110 is dependent upon en function.

    Clonal analysis supports the view that dpp is a direct target of repression by en, and that en defines the posterior extent of the dpp stripe in the wing imaginal disc. The en-hh-ptc regulatory loop that is responsible for segmental expression of wg in the embryo is reused in imaginal disks to create a stripe of dpp expression along the A/P compartment boundary.

    ph-d and ph-p activation in germ band elongated embryos could be mediated by en binding to en-binding sites upstream of each of the ph-d and ph-p transcription units.

    inv can perform a subset of functions attributed to en including the ability to confer posterior compartment identity, but does not appear to organize the anterior-posterior compartment boundary.

    The establishment of the anterior-posterior organiser and control of compartment identity are genetically distinguishable and inv may perform a discrete subset of functions previously ascribed to en.

    en both directs the posterior compartment pathway and creates the compartment border in wing development.

    Maintenance of restricted wg transcription during late gastrulation requires en-independent wg autoregulatory activity.

    en governs growth and patterning in both anterior and posterior wing compartments by controlling the expression of the hh and dpp products as well as the response of the cells to them. en activity programs wing cells to express hh whereas the absence of en activity programs them to respond to hh by expressing dpp. Consequently, posterior cells secrete hh product and induce a stripe of neighboring anterior cells across the compartment boundary to secrete dpp.

    gro and hh regulate en expression in the anterior compartment of the wing.

    opa activity is essential for the appropriate level and timing of en and wg expression in all parasegments, but does not determine their restricted spatial domains of expression.

    Clones lacking en function can respect a boundary of lineage restriction. hh mediates the interaction between anterior dpp-expressing cells and posterior en-expressing cells.

    en is required for patterning of the posterior wing margin, specifically to inhibit the formation of stout and socketed bristles (characteristic of the anterior wing margin) posterior to wing vein 3. en participates, presumably indirectly, in cell-cell interactions.

    Three pairing sensitive (PS) sites map to a 1.6kb fragment of en. PS sites of en can suppress expression of a linked marker gene (w) carried in P-elements, dependent on the presence of two copies of the P-element in proximity in the genome.

    en pairing sensitive (PS) sites apparently normally act to promote interactions between distantly located en regulatory sites and the en promoter.

    wg product made in the mesoderm can sustain en expression in the ectoderm.

    en-mediated repression of Ubx is necessary for the parasegment 6 identity.

    wg acts through dsh and arm to affect the expression of en and cuticle differentiation.

    Comparisons of early development to that in other insects have revealed conservation of some aspects of development, as well as differences that may explain variations in early patterning events.

    The exd protein modulates the DNA binding activity of en to a different site. In direction of increasing cytology: inv+ en-

    Maintenance of en expression does not always require wg activity.

    Wild type activity of five segment polarity genes, wg, ptc, en, nkd and hh, can account for most of the ventral pattern elements in the embryo. wg is required for naked cuticle. wg generates the diversity of cell types within the segment but each specific cell identity depends on the activity of ptc, en, nkd and hh.

    wg functions as an extracellular signal maintaining en expression.

    en is a specific repressor of activated transcription, and may act via a different mechanism than eve, perhaps by interfering with interactions between transcriptional activators and the general transcription machinery. A minimum repression domain of 55 residues, rich in alanine, can function when fused to a heterologous DNA binding domain. Unlike the repression domains of eve and Kr, the en repression domain is moderately charged.

    A temporal asymmetry in the regulatory interactions between wg, en and gsb explains the difference in phenotypes between the mutants.

    The positioning of en stripes in the embryo is largely determined by the actions of negative regulators: run is required to limit the domains of en-expression in odd-numbered parasegments, while odd is required to limit the domains of en-expression in even-numbered parasegments. Activation of en at the anterior margins of the parasegments requires repression of run and odd by eve.

    The BRE region of Ubx includes binding sites for hb, ftz, tll, en and twi. The binding of their products and the interplay between them is responsible for generating the expression pattern directed by the BRE.

    Overexpression of wg protein does not prevent parasegmental, restricted en expression, therefore wg is not acting as a local instructive signal or a morphogen.

    Choice of cell fate made by en expressing cells in embryonic parasegments is mediated by wg, in a function distinct from its early role in maintaining en expression. en expressing cells respond differently to wg at different stages of development:early wg stabilizes the subdivision of the body axis by maintaining en expression, whereas later input generates cell-type diversity.

    Experiments designed to identify cis-acting regulatory elements of en revealed a tendency for fragments of en DNA to target insertions to genes that are expressed in stripes.

    en alleles fall into four classes, all recessive. Class 1: en1 (See en1 allele record for full description). Viable hemizygous and homozygous; fertile. Longitudinal cleft extends from rear border of scutellum forward, may be reduced to median nick or posterior flattening of scutellum. Wings larger, broader and thin textured with spatulate end; venation and distribution of sensilla abnormal in posterior wing compartment. Variable duplication of anterior triple row bristles on posterior margin; alula reduced, with costal-like bristles. Clones of en1 cells of posterior compartment origin fail to respect anterior-posterior compartment border in wing disc as do mwh1 clones in wing discs of en1 homozygotes. en1 abnormalities are associated with posterior compartment structures only, except for scutellar cleft. Not suppressed by su(Hw)1. Class 2: Lethal alleles with normal cytology. Embryonic lethal. Anterior margin of each segment defective. Pair rule defects in naked cuticle of T1, T3, A2, A4, A6, A8 result in pair-wise fusion of adjacent segments. Autonomous effects in adult cuticular clones observed in posterior compartment of proboscis, thorax, abdomen and genitalia. The en1/"enlethal" heterozygote characterized by wing abnormalities only; disruption of anterior crossvein, gap in vein IV and occasional socketted bristles on posterior margin. Class 3: Deficiencies and lethal alleles with inversion or translocation breakpoints. Embryonic lethal. Embryonic segment defects slight and variable. Alleles of this class in heterozygous combination witn en1 produce adults more extreme than en1. For example, in en1/en2, legs are truncated, the tarsi reduced to densely bristled stumps; wings are greatly enlarged and spatulate with greater disruption of veins IV and V; higher penetrance of socketed bristles along the posterior margin. Extreme scutellar cleft. Class 4: Non-lethal alleles with breakpoints. Hemizygous viable, embryos normal. Heterozygous with other allele classes, variable gaps in wing veins IV and V. Variable reductions or deletions in male and female genitalia. Scutellum may also be affected.

    en is activated by ftz and repressed by odd, and low levels of eve cause ftz-dependent activation of en through repression of odd.

    Embryos mutant for two or more Pc-group genes (Pc, Scm, Pcl, Psc, Asx, E(Pc), E(z), ph-d, pho and esc) show strong ectopic en expression, but only weak derepression occurs if embryo is mutant at only one of the Pc group genes. This effect is independent of the function of en itself, and wg. Expression of en in esc mutant embryos is almost normal, suggesting that esc may function in a pathway different from the other genes in the group.

    Ectopic uniform wg expression results in expansion of the en expression domain in a posterior direction: original parasegment borders remain unchanged.

    The 88kD ttk protein isoform binds a site upstream of the en promoter.

    wg signalling operates by inactivating the sgg repression of en autoregulation.

    Expression pattern of hh coincides with that of en in the epidermis. Though initially independent of en, hh expression later becomes en-dependent. In the absence of ptc function, wg expression, which is normally en-dependent, no longer requires en.

    Clonal analysis shows that no clones straddle the anterior edge of en stripes in the embryo. However, posterior cells of each stripe lose en expression, producing mixed clones.

    wg and en function in patterning the larval epidermis.

    In embryos homozygous for sm, en expression fades towards the end of the extended germband phase suggesting that sm is important in maintaining en after its initial activation.

    en expression pattern in the embryonic head strengthens the hypothesis that the clypeolabrum evolved from the fusion of paired labral appendages.

    en expression becomes independent of wg extracellular influence and relies on positive autoregulation. Autoregulation is transient so does not supply a mechanism for determination of the en-cell fate.

    en cannot completely rescue the ptc phenotype when in double mutant combinations.

    In transfection assays en is an active transcriptional repressor. Active repression is distinct from the effects of passive homeodomain-containing proteins which repress when competing with activators for binding sites and activate when competing with en. Active repression activity maps outside the en homeodomain and this activity can be transferred to a heterologous DNA binding domain.

    When a fragment of en DNA extending from -2.4kb to +0.8kb is included in the CaSpeR vector the eye colour of transformants often behaves anomalously, half of the homozygotes have a lighter eye colour than the heterozygotes and a quarter have the same eye colour as the heterozygotes. This occurred at many different insertion sites whether the upstream en fragment is directly adjacent to w+mC or when it is 1kb away. The suppression of eye colour is dependent on the proximity of the two copies of the transposon, either in cis or trans. The protein that mediates this phenomenon is probably not a homeodomain-containing protein as deletion of the homeodomain binding sites results in suppression of w expression.

    Mutations in zygotic polarity gene en do not interact with RpII140wimp.

    Appropriate en activity is required for proper restriction of the dpp expression domain as well as being required for maintenance of the posterior compartment fate.

    en represses ciD expression in the posterior compartments of embryos and imaginal discs.

    en mutants exhibit variable pair rule fusions and segment polarity reversals.

    ptc is negatively regulated by en in the early extended germ band.

    en intron 1 works as a stripe specific enhancer.

    The crystal structure of a complex containing the en homeodomain and a duplex DNA site has been determined.

    A modification and reduction in en and Dfd protein distribution is seen in mutant cad embryos.

    sim gene product is required for the normal expression of en.

    en protein represses transcriptional activation by ftz protein by competition for binding to homeodomain binding sites in vitro.

    The en1/"enlethal" heterozygote characterized by wing abnormalities only; in some combinations complementation is complete or nearly so.

    A transient expression assay has been employed to investigate the potential of homeobox genes to function as transcriptional activators.

    A monoclonal antibody (MAb4D9) reacts specifically to en proteins in a variety of species. An ancestral function of en may have been in neurogenesis and its other functions in arthropods may represent a more recent addition.

    The expression of en protein in Drosophila, grasshopper and crayfish has been compared.

    Genetic analysis demonstrates that en is dispensable for efficient homeotic gene expression in the visceral mesoderm.

    Scr and en are derepressed in the absence of Pc and the bithorax complex function.

    Striped en expression during post-blastoderm development is controlled by a cis-regulatory programme distinct from that controlling the establishment of expression at the cellular blastoderm stage.

    en protein isolated from cultured cells and embryos is post-translationally modified.

    Heat shock induced en gene expression causes pattern defects similar to those in embryos lacking en gene product. The sensitivity to heat shock is only during the cellular blastoderm and early gastrulation periods when the en protein localises into segmentally reiterated stripes and represents only a small portion of the normal period of en gene expression.

    en is expressed in the posterior (but not the anterior) compartments of the embryo and larva.

    en mutant genital discs show reductions or deletions.

    "enlethal" alleles show no maternal effect.

    At 29oC, duplication of anterior compartment bristles in mirror-image symmetry in the posterior compartment of second antennal segment occurs.

    "enlethal" clones are without effect in anterior compartments and in eye-antennal region.

    Origin and Etymology
    Discoverer
    Etymology

    The gene is named "engrailed", a heraldic term from the middle-age french "engraile", literally "dented by hail", after the mutant phenotype of a notch in the scutellum.

    Identification
    External Crossreferences and Linkouts ( 70 )
    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
    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
    PDB - An information portal to biological macromolecular structures
    SignaLink - A signaling pathway resource with multi-layered regulatory networks.
    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.
    KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
    MIST (genetic) - An integrated Molecular Interaction Database
    MIST (protein-protein) - An integrated Molecular Interaction Database
    Synonyms and Secondary IDs (25)
    Reported As
    Symbol Synonym
    Apa
    En
    (Bajpai and Sinha, 2020, Zhang and Cai, 2020, Fan et al., 2019, Zandvakili et al., 2019, Crossman et al., 2018, Davis and Rebay, 2018, Kastl et al., 2018, Rickert et al., 2018, Garcia-Garcia et al., 2017, Luo et al., 2017, Smelkinson et al., 2017, Beira and Paro, 2016, Lee et al., 2016, Mbodj et al., 2016, Glassford et al., 2015, Li et al., 2015, McKay et al., 2015, Boekhoff-Falk and Eberl, 2014, Boube et al., 2014, Lacin et al., 2014, Lacin et al., 2014, Li et al., 2014, Slattery et al., 2014, Bejsovec, 2013, Chang et al., 2013, Da Ros et al., 2013, Ibrahim et al., 2013, Li et al., 2013, Morozov and Ioshikhes, 2013, Palm et al., 2013, Pengelly et al., 2013, Sambrani et al., 2013, Bartoletti et al., 2012, Cheng et al., 2012, Formaz-Preston et al., 2012, Fujioka et al., 2012, Jaeger et al., 2012, Kunttas-Tatli et al., 2012, Legent et al., 2012, Perry et al., 2012, Rojas-Ríos et al., 2012, Swarup and Verheyen, 2012, Wu et al., 2012, Xia et al., 2012, Callejo et al., 2011, Kohwi et al., 2011, Olson et al., 2011, Rodriguez, 2011, Wang et al., 2011, Wojcinski et al., 2011, Zhang et al., 2011, Zhou and Kalderon, 2011, Bhatia et al., 2010, Kremer et al., 2010, Pines et al., 2010, Thomsen et al., 2010, Tran et al., 2010, Yagi et al., 2010, Zheng et al., 2010, Ayers et al., 2009, Gambetta et al., 2009, Guo and Wang, 2009, Kategaya et al., 2009, McKay et al., 2009, Mosimann et al., 2009, Seibert et al., 2009, Smith-Bolton et al., 2009, Stöbe et al., 2009, Vied and Kalderon, 2009, Estella and Mann, 2008, Lebreton et al., 2008, López-Onieva et al., 2008, McCully et al., 2008, Mitchell et al., 2008, Noyes et al., 2008, Peterson-Nedry et al., 2008, Takacs et al., 2008, Tran and Doe, 2008, Vincent et al., 2008, Wheeler et al., 2008, Chandraratna et al., 2007, Chao et al., 2007, Colomb et al., 2007, Kim et al., 2007, Makhijani et al., 2007, Molnar et al., 2007, Noro and Mann, 2007, Overton et al., 2007, Sasamura et al., 2007, Smelkinson et al., 2007, Callejo et al., 2006, de Navas et al., 2006, Ference and Barolo, 2006, Gallet et al., 2006, Goodman et al., 2006, Jennings et al., 2006, Meyer et al., 2006, Ogden et al., 2006, Rives et al., 2006, Strigini et al., 2006, Waldrop et al., 2006, Wehn and Campbell, 2006, Zhou et al., 2006, Dawber et al., 2005, Horabin, 2005, Karcavich and Doe, 2005, Wei et al., 2005, Brodu et al., 2004, Mellerick and Liu, 2004, Song and Taylor, 2003, Han et al., 2000, Mayor et al., 2000)
    Engrailed/Invected
    Es
    V
    en
    (Estacio-Gómez et al., 2020, Srinivasan and Mishra, 2020, Bageritz et al., 2019, Bailetti et al., 2019, Bredesen and Rehmsmeier, 2019, Bridi et al., 2019, Camara et al., 2019, Chen, 2019, Chen and Zou, 2019, Clark et al., 2019, De et al., 2019, Graham et al., 2019, Li et al., 2019, Shokri et al., 2019, Ahaley, 2018, Valsecchi et al., 2018, Wiese et al., 2018, Zhu et al., 2018, Bonneaud et al., 2017, Dutta and Li, 2017, Eagen et al., 2017, Erceg et al., 2017, Karaiskos et al., 2017, Liu et al., 2017, Luo et al., 2017, Recasens-Alvarez et al., 2017, Requena et al., 2017, Transgenic RNAi Project members, 2017-, van Tienen et al., 2017, Bürglin and Affolter, 2016, De et al., 2016, Field et al., 2016, Kwon et al., 2016, Lorberbaum et al., 2016, Ma et al., 2016, Massey and Wittkopp, 2016, Morata and Herrera, 2016, Ray et al., 2016, Shlyueva et al., 2016, Urbach et al., 2016, Willsey et al., 2016, Zheng et al., 2016, Bonchuk et al., 2015, Chen et al., 2015, Im et al., 2015, Kallsen et al., 2015, Kok et al., 2015, Kunttas-Tatli et al., 2015, Lin et al., 2015, Nasedkin et al., 2015, Rudolf et al., 2015, Schertel et al., 2015, Cheng et al., 2014, Eliazer et al., 2014, Ghavi-Helm et al., 2014, Gummalla et al., 2014, Herrera and Morata, 2014, Herz et al., 2014, Jiang et al., 2014, Jussen and Urbach, 2014, Kunttas-Tatli et al., 2014, Kuzhandaivel et al., 2014, Maier et al., 2014, Palsson et al., 2014, Rhee et al., 2014, Shi et al., 2014, Wang et al., 2014, Zarin et al., 2014, Aleksic et al., 2013, Alfieri et al., 2013, Brown and Kassis, 2013, Deshpande et al., 2013, Ducuing et al., 2013, Giannios and Tsitilou, 2013, Ibrahim et al., 2013, Lawrence and Casal, 2013, Li and Gilmour, 2013, Lu et al., 2013, Martin et al., 2013, Nakamura et al., 2013, Palm et al., 2013, Pengelly et al., 2013, Saunders et al., 2013, Webber et al., 2013, Almeida and Demongeot, 2012, Bejsovec and Chao, 2012, Chen et al., 2012, Fan et al., 2012, Follmer et al., 2012, Foronda et al., 2012, Gault et al., 2012, Gutiérrez et al., 2012, Hamaguchi et al., 2012, Hödl and Basler, 2012, Kim et al., 2012, Kvon et al., 2012, Langlais et al., 2012, Lemons et al., 2012, Marchal et al., 2012, Rojas-Ríos et al., 2012, Yamakawa et al., 2012, Abruzzi et al., 2011, Fiedler et al., 2011, Hogan et al., 2011, Juarez et al., 2011, Kim et al., 2011, Kuzin et al., 2011, Layalle et al., 2011, Ludwig et al., 2011, Mariappa et al., 2011, Molnar et al., 2011, Muliyil et al., 2011, Nègre et al., 2011, Ntini and Wimmer, 2011, Pérez et al., 2011, Shi et al., 2011, Stagg et al., 2011, Terriente-Félix et al., 2011, Tsurumi et al., 2011, Walrad et al., 2011, Watson et al., 2011, Weyers et al., 2011, Zhang et al., 2011, Zhou and Kalderon, 2011, Benitez et al., 2010, Biehs et al., 2010, Braid et al., 2010, Cheng et al., 2010, Chou et al., 2010, Cunningham et al., 2010, Ding et al., 2010, Gettings et al., 2010, Hartmann et al., 2010, Herranz et al., 2010, Jia et al., 2010, Jones et al., 2010, Jung et al., 2010, Kannan et al., 2010, Kazemian et al., 2010, Klein et al., 2010, Menéndez et al., 2010, Monier et al., 2010, Morozova et al., 2010, Pereanu et al., 2010, Piłat and Antosiewicz, 2010, Rousset et al., 2010, Schwartz et al., 2010, Seibert and Urbach, 2010, Subramanian and Gadgil, 2010, Swaminathan and Pile, 2010, Walrad et al., 2010, Wang et al., 2010, Wang et al., 2010, Yassin et al., 2010, Bejarano and Milán, 2009, Bischoff et al., 2009, Chaves et al., 2009, Fang et al., 2009, Gambetta et al., 2009, Gambetta et al., 2009, Gaziova and Bhat, 2009, Grieder et al., 2009, Grimm et al., 2009, Guo and Wang, 2009, Hou et al., 2009, Julius et al., 2009, Kategaya et al., 2009, Kumar et al., 2009, Kumar et al., 2009, Kwon et al., 2009, Landsberg et al., 2009, Larsen et al., 2009, Mallavarapu et al., 2009, May and Schiek, 2009, Mosimann et al., 2009, Mulinari and Häcker, 2009, Schuettengruber et al., 2009, Seibert et al., 2009, Seugnet et al., 2009, Tchuraev and Galimzyanov, 2009, Venken et al., 2009, Venken et al., 2009, Wheeler et al., 2009, Zhai et al., 2009, Beckervordersandforth et al., 2008, Blagburn, 2008, Bosveld et al., 2008, Casas-Tinto et al., 2008, Casso et al., 2008, Chan et al., 2008, Chaves and Albert, 2008, Coiffier et al., 2008, Colomb et al., 2008, Durant and Kassis, 2008, Gallet et al., 2008, Garaulet et al., 2008, González et al., 2008, Haecker et al., 2008, Hendrix et al., 2008, Hittinger and Carroll, 2008, Kim et al., 2008, Larsen et al., 2008, Mulinari et al., 2008, Park et al., 2008, Sánchez et al., 2008, Sanders et al., 2008, Shen et al., 2008, Siera and Cline, 2008, Tarone et al., 2008, Aerts et al., 2007, Bejarano et al., 2007, Beltran et al., 2007, Chan et al., 2007, Claret et al., 2007, Crickmore and Mann, 2007, Dominguez-Gimenez et al., 2007, Gebelein and Mann, 2007, Joly et al., 2007, Lee et al., 2007, Liu et al., 2007, Maeda et al., 2007, Nekrasov et al., 2007, Ntini E and Wimmer, 2007, Ringrose and Paro, 2007, Ruel et al., 2007, Sandmann et al., 2007, Sgaier et al., 2007, Sprecher et al., 2007, Umemori et al., 2007, Urbach, 2007, Vanderzwan-Butler et al., 2007, Von Ohlen et al., 2007, Wang and Gergen, 2007, Wang et al., 2007, Bartolome and Charlesworth, 2006, Beckett and Baylies, 2006, Bolivar et al., 2006, Bossing and Brand, 2006, Bowler et al., 2006, Buescher et al., 2006, Cho et al., 2006, Comet et al., 2006, Croker et al., 2006, Gallet et al., 2006, Jaeger and Reinitz, 2006, Jamieson et al., 2006, Kent et al., 2006, Meier et al., 2006, Molnar and de Celis, 2006, Mosimann et al., 2006, Muro et al., 2006, Negre et al., 2006, Peel et al., 2006, Scholtz and Edgecombe, 2006, Schwartz et al., 2006, Sprecher and Hirth, 2006, Sprecher et al., 2006, Urbach et al., 2006, Wendler et al., 2006, Wheeler et al., 2006, Yao et al., 2006, Yasunaga et al., 2006, Younossi-Hartenstein et al., 2006, Bejarano et al., 2005, Chanas and Maschat, 2005, Copley, 2005, Deshpande and Schedl, 2005, Glise et al., 2005, Goldstein et al., 2005, Gorfinkiel et al., 2005, Liu et al., 2005, McEwen and Peifer, 2005, Peel et al., 2005, Torroja et al., 2005, Brodsky et al., 2004, Grad et al., 2004, Gurunathan et al., 2004, Vander Zwan et al., 2003, Klebes et al., 2002, Srivastava et al., 2002, True et al., 2001, Emerald and Shashidhara, 2000, Lee et al., 1999, Freeland and Kuhn, 1996, Lundell et al., 1996, Muller and Bienz, 1992, Peifer et al., 1991, Masucci et al., 1990, Martinez Arias et al., 1988)
    Name Synonyms
    Apigmented abdomen
    Engrailed
    (Castellanos et al., 2020, Zhang and Cai, 2020, Vimal et al., 2018, Kong et al., 2017, Forés et al., 2015, Hsiao et al., 2014, Jussen and Urbach, 2014, Katz et al., 2014, Lacin et al., 2014, Mannervik, 2014, Matsuoka et al., 2014, Yamulla et al., 2014, Zhang et al., 2014, Azzam and Liu, 2013, Barton et al., 2013, Da Ros et al., 2013, Hermle et al., 2013, Ibrahim et al., 2013, König and Shcherbata, 2013, Li et al., 2013, Morishita et al., 2013, Xin et al., 2013, Cheng et al., 2012, Green and Extavour, 2012, Kunttas-Tatli et al., 2012, Petzoldt et al., 2012, Tursun, 2012, Djiane et al., 2011, Giang et al., 2011, Layalle et al., 2011, Molnar et al., 2011, Momota et al., 2011, Nègre et al., 2011, Wang et al., 2011, Morozova et al., 2010, Pines et al., 2010, Reddy et al., 2010, Rousset et al., 2010, Tamori et al., 2010, Thomsen et al., 2010, Gaziova and Bhat, 2009, Guo and Wang, 2009, Leal et al., 2009, Liu et al., 2009, Mirth et al., 2009, Rand et al., 2009, Vied and Kalderon, 2009, Berger et al., 2008, Bury et al., 2008, Colomb et al., 2008, Franch-Marro et al., 2008, Ishihara and Shibata, 2008, Mugat et al., 2008, Peterson-Nedry et al., 2008, Raj et al., 2008, Takacs et al., 2008, Tran and Doe, 2008, Bejarano et al., 2007, Emmons et al., 2007, Israeli et al., 2007, Kim et al., 2007, Molnar et al., 2007, Noro and Mann, 2007, Reig et al., 2007, Ruel et al., 2007, Sasamura et al., 2007, Sharma and Nirenberg, 2007, Smelkinson et al., 2007, Tountas and Fortini, 2007, Von Ohlen et al., 2007, Bajard et al., 2006, Bayraktar et al., 2006, Bergsland et al., 2006, Ference and Barolo, 2006, Fraser, 2006, Gallet et al., 2006, Goodman et al., 2006, Herranz and Milan, 2006, Kopytova et al., 2006, Mahr and Aberle, 2006, Meyer et al., 2006, Slack et al., 2006, Strigini et al., 2006, Ward et al., 2006, Yoder and Carroll, 2006, Dawber et al., 2005, Karcavich and Doe, 2005, Orgogozo and Grueber, 2005, Pallavi and Shashidhara, 2005, Religa et al., 2005, Wawersik et al., 2005, Cheesman et al., 2004, Mellerick and Liu, 2004, Hsouna et al., 2003, Mayor et al., 2003, McDonald et al., 2003, Michaud and Tanguay, 2003, Song and Taylor, 2003, Bahri et al., 2001, Han et al., 2000, Nanda and Brand, 2000)
    Erased
    engrailed
    (Waters et al., 2018, De et al., 2016, Urbach et al., 2016, Wieschaus and Nüsslein-Volhard, 2016, Bonchuk et al., 2015, Lin et al., 2015, Mou et al., 2015, Cantera et al., 2014, Gummalla et al., 2014, Herz et al., 2014, Kuzhandaivel et al., 2014, McElroy et al., 2014, Deshpande et al., 2013, Fujioka et al., 2013, Ibrahim et al., 2013, Marianes and Spradling, 2013, Palm et al., 2013, Pengelly et al., 2013, Bejsovec and Chao, 2012, Enjolras et al., 2012, Follmer et al., 2012, Gault et al., 2012, Rojas-Ríos et al., 2012, Yamakawa et al., 2012, Dahmann et al., 2011, Eliazer and Buszczak, 2011, Fay et al., 2011, Fiedler et al., 2011, Hogan et al., 2011, Juarez et al., 2011, Kuzin et al., 2011, Mariappa et al., 2011, McKnight et al., 2011, Ntini and Wimmer, 2011, Peradziryi et al., 2011, Tsurumi et al., 2011, Weyers et al., 2011, Bhatia et al., 2010, Biehs et al., 2010, Braid et al., 2010, Cheng et al., 2010, Cunningham et al., 2010, Ding et al., 2010, Gettings et al., 2010, Hartmann et al., 2010, Herranz et al., 2010, Jones et al., 2010, Jung et al., 2010, Koulgi et al., 2010, Kremer et al., 2010, Menéndez et al., 2010, Pereanu et al., 2010, Piłat and Antosiewicz, 2010, Rand et al., 2010, Robinett et al., 2010, Schwartz et al., 2010, Seibert and Urbach, 2010, Swaminathan and Pile, 2010, Tran et al., 2010, Wang et al., 2010, Bejarano and Milán, 2009, Bischoff et al., 2009, Chen and Rasmuson-Lestander, 2009, Eivers et al., 2009, Fang et al., 2009, Gambetta et al., 2009, Grieder et al., 2009, Hou et al., 2009, Ji et al., 2009, Kategaya et al., 2009, Kumar et al., 2009, Kumar et al., 2009, Kwon et al., 2009, Landsberg et al., 2009, Larsen et al., 2009, Mosimann et al., 2009, Mulinari and Häcker, 2009, Schaaf et al., 2009, Zhai et al., 2009, Anderson and Pick, 2008, Beckervordersandforth et al., 2008, Blagburn, 2008, Bosveld et al., 2008, Casas-Tinto et al., 2008, Casso et al., 2008, Coiffier et al., 2008, DeVido et al., 2008, Durant and Kassis, 2008, Estes et al., 2008, Gallet et al., 2008, Garaulet and Sánchez-Herrero, 2008, Garaulet et al., 2008, Haecker et al., 2008, Hsouna and VanBerkum, 2008, Kim et al., 2008, Lebreton et al., 2008, Liu et al., 2008, Mieszczanek et al., 2008, Millard and Martin, 2008, Mulinari et al., 2008, Mulinari et al., 2008, Oktaba et al., 2008, Park et al., 2008, Sánchez et al., 2008, Shen et al., 2008, Siera and Cline, 2008, Casso et al., 2007, Chandraratna et al., 2007, Claret et al., 2007, Crickmore and Mann, 2007, Crickmore and Mann, 2007, Dominguez-Gimenez et al., 2007, Eugster et al., 2007, Gebelein and Mann, 2007, Gorfinkiel and Arias, 2007, Joly et al., 2007, Kondo et al., 2007, Lee et al., 2007, Maeda et al., 2007, Mulinari et al., 2007, Nekrasov et al., 2007, Ringrose and Paro, 2007, Schwartz and Pirrotta, 2007, Sprecher et al., 2007, Umemori et al., 2007, Vanderzwan-Butler et al., 2007, Wang and Gergen, 2007, Wang et al., 2007, Zinzen and Papatsenko, 2007, Beckett and Baylies, 2006, Bolivar et al., 2006, Bowler et al., 2006, Cho et al., 2006, Jaeger and Reinitz, 2006, Jamieson et al., 2006, Muller and Kassis, 2006, Peel et al., 2006, Pereanu and Hartenstein, 2006, Salazar-Ciudad, 2006, Sprecher and Hirth, 2006, Staudt et al., 2006, Tolhuis et al., 2006, Tucker and Chiquet-Ehrismann, 2006, Wendler et al., 2006, Wheeler et al., 2006, Bejarano et al., 2005, Brown et al., 2005, Dekanty et al., 2005, Goldstein et al., 2005, Hendriksen et al., 2005, Torroja et al., 2005, Tron et al., 2004, Klebes et al., 2002, Wilkie et al., 2001, Lee et al., 1999, Lundell et al., 1996, Martinez Arias et al., 1988)
    sparse SGPs 2
    transcript group V
    vasodilator-stimulated phosphoprotein
    Secondary FlyBase IDs
    • FBgn0003492
    • FBgn0014157
    • FBgn0016969
    Datasets (1)
    Study focus (1)
    Experimental Role
    Project
    Project Type
    Title
    • bait_protein
    Genome-wide localization of transcription factors by ChIP-chip and ChIP-Seq.
    References (1,943)