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General Information
Symbol
Dmel\eve
Species
D. melanogaster
Name
even skipped
Annotation Symbol
CG2328
Feature Type
FlyBase ID
FBgn0000606
Gene Model Status
Stock Availability
Gene Snapshot
even skipped (eve) encodes a homeobox-containing transcriptional repressor that acts in concert with co-repressors such as those enoded by gro and Gug. It represses pair-rule and segment polarity genes, contributing to anterior/posterior axis specification and mesoderm and central nervous system development. [Date last reviewed: 2019-03-07]
Also Known As
Complementation group F, l(2)46Ce, E(eve)
Key Links
Genomic Location
Cytogenetic map
Sequence location
2R:9,979,319..9,980,795 [+]
Recombination map
2-61
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
GO Summary Ribbons
Protein Family (UniProt)
Belongs to the even-skipped homeobox family. (P06602)
Summaries
Gene Group (FlyBase)
HOX-LIKE HOMEOBOX TRANSCRIPTION FACTORS -
HOX-like (HOXL) homeobox transcription factors are sequence-specific DNA binding proteins that regulate transcription. They encompass transcription factors encoded by the Hox genes of the Antennapedia and the Bithorax gene complexes and genes closely related in sequence. HOXL transcription factors are major regulators of animal development. (Adapted from FBrf0232555).
Protein Function (UniProtKB)
May play a role in determining neuronal identity. May be directly involved in specifying identity of individual neurons. Pair-rule protein required for segmentation; involved in transforming the broad, spatial, aperiodic expression patterns of the gap genes into a system of precise periodic expression patterns of the pair-rule and segmentary polarity genes.
(UniProt, P06602)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
eve: even skipped
Homozygous lethal; embryos homozygous for a null allele or a deficiency fail to undergo segmentation and their ventral surfaces are covered by a lawn of short denticles pointed toward the midline; denticles in the anterior region show thoracic characteristics suggesting that segmental identities persist in the absence of segmentation. All derivatives of gnathal segments are missing, such as maxillary sense organs, cirri, mouth hooks, labial sense organs and the mandibular parts of the cephalopharyngeal skeleton; the labrum, antennal sense organs, and a rudimentary skeleton are the only remains of the larval head. Posteriorally, anal plates and some sensory organs persist as do remnants of spiracles, filzkorper, and tufts. Homozygotes and hemizygotes for hypomorphic alleles display pair-rule segmentation defects. Denticle bands and adjacent naked cuticle of the prothoracic, metathoracic and even-numbered abdominal segments removed; some naked cuticle of the adjacent segment removed as well (i.e., the odd numbered parasegments are removed). Combinations of alleles with Df(2R)eve raised at different temperatures can achieve an array of phenotypes between these extremes. Expression of eve is first detected at the eleventh nuclear division following fertilization; at this stage, eve protein is uniformly distributed among the nuclei, both at the periphery and deep within the egg; by the thirteenth nuclear division, the anterior one-third of the embryo is devoid of detectable protein; over the next 20 minutes, the antibody staining in the posterior two-thirds of the embryo becomes concentrated in seven transverse stripes four or five cells wide separated by stripes three to four cells wide with lower levels of staining. By the time of germ-band elongation, the seven stripes have become narrowed and sharply defined and seven new weakly expressing stripes, one to two cells wide, appear between the major stripes; during germ-band elongation all stripes gradually disappear. As eve stripes become more sharply defined so too do ftz stripes, no longer overlapping eve stripes, but forming a complementary pattern. At the same time, a group of expressing cells appears at the posterior end of the germ band; these cells form a ring around the anal plate during germ-band shortening. Also during germ-band shortening, a specific subset of sixteen neurons in each hemisegment of the CNS expresses eve product as does a row of cell clusters on either side of the dorsal midline; lateral to these clusters are curious rings of weakly staining cells; the dorsal cells do not appear to be neuronal (Frasch, Hoey, Rushlow, Doyle, and Levine, 1987, EMBO J. 6: 749-59; Frasch and Levine, 1987, Genes Dev. 1: 981-95). In homozygous eve1 embryos switched to restrictive temperature during neurogenesis, four specifically studied eve-expressing neurons in each hemisegment are found to persist; two of them develop normally, but two send axonal processes to abnormal destinations [Doe, Smouse, and Goodman, 1988, Nature (London) 333: 376-78]. Frasch and Levine observe that segmentation-gene-mutations generally have reciprocal effects on the expression of eve and ftz, leading them to postulate that their promoters respond reciprocally to the same positional cues. eve concluded to be an early pair-rule gene, since its expression is modified by gap-gene mutations, but not by most other pair-rule gene mutations nor by segment-polarity gene mutations. Three pair-rule genes do influence eve expression: in either eve or h genotypes, eve expression is reduced and in run embryos eve is overexpressed (Frasch and Levine, 1987). In eve embryos, en stripes do not appear (Macdonald, Ingham, and Struhl, 1986, Cell 47: 721-34). Ubx protein is detected at high level in odd-numbered parasegments from 7 through 13 rather than in every parasegment from 6 through 12 (Martinez-Arias, and White, 1988, Development 102: 325-38). ftz stripes are disrupted in regularity of position, size, and timing (Carroll and Scott, 1986, Cell 45: 113-26).
Summary (Interactive Fly)
transcription factor - homeodomain - pair rule gene establishing epidermal cell fate - aCC motoneuron identity is specified by a genetic cascade involving and - and are required for cardiac-specific differentiation of a numb-dependent lineage decision
Gene Model and Products
Number of Transcripts
1
Number of Unique Polypeptides
1

Please see the GBrowse view of Dmel\eve or the JBrowse view of Dmel\eve 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 5.46
Sequence Ontology: Class of Gene
Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0088390
1406
376
Additional Transcript Data and Comments
Reported size (kB)
1.4 (northern blot, sequence analysis)
Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0087478
40.0
376
9.73
Polypeptides with Identical Sequences

There is only one protein coding transcript and one polypeptide associated with this gene

Additional Polypeptide Data and Comments
Reported size (kDa)
376 (aa); 40 (kD predicted)
Comments
External Data
Crossreferences
PDB - An information portal to biological macromolecular structures
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\eve using the Feature Mapper tool.

External Data
Crossreferences
Linkouts
Gene Ontology (23 terms)
Molecular Function (4 terms)
Terms Based on Experimental Evidence (4 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (0 terms)
Biological Process (18 terms)
Terms Based on Experimental Evidence (10 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (9 terms)
CV Term
Evidence
References
non-traceable author statement
traceable author statement
traceable author statement
non-traceable author statement
traceable author statement
traceable author statement
Cellular Component (1 term)
Terms Based on Experimental Evidence (1 term)
CV Term
Evidence
References
inferred from direct assay
Terms Based on Predictions or Assertions (0 terms)
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
northern blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Expression was examined at four phases of embryonic stage 5. The striped pattern becomes visible in phase 1 (0-5'), all stripes except stripe 7 are expressed during phase 2 (5-17'), and their spacing and expression levels become largely uniform by phase 3 (17-30'). The stripes initially appear less clearly separated and more graded.
Ectopic eve expression is incapable of activating eve expression outside of its normal domain and causes a premature loss of transcripts within its normal domains of expression.
eve transcripts are first detected in stage 3 embryos, and displays a low level of expression throughout the embryo. The expression pattern is refined over the next four hours of development. eve expression exhibits a pair-rule pattern, and is expressed in a graded fashion, both along the anterior-posterior axis and the dorsal-ventral axis, with the highest levels of transcript being present in the dorsal-posterior regions. eve is expressed in odd-numbered parasegments in seven stripes, but later in development is expressed coincidently with en, in the posterior section of each parasegment. In the later stages of embryonic development, following germ band retraction, eve transcripts are detected in the neurogenic region in the ganglion mother cells of each segment.
Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
distribution deduced from reporter
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
inferred from author statements
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
eve colocalises with the cholinergic markers Scer\GAL4ChAT.7.4 and, in a strain also expressing Scer\GAL4EL.eveRC, cha in nearly all EL neurons. It also colocalizes with GABA, in a strain coexpressing Scer\GAL4EL.eveRC, in ~25% of EL neurons in larval abdominal segment 1, ~50% in segment 2, and 70-75% in segments 3 and 4.
eve stripes 2, 3, and 4 show sexually dimorphic expression.
eve protein is expressed in the DA1 muscle and two pericardial cells per hemisegment in embyros.
eve is expressed in two pericardial cell nuclei and in 10-11 nuclei of the dorsal acute muscle 1 in each segment.
eve is expressed in two Eve pericadial cells (EPC) and one DA1 muscle per hemisegment in stage 13 embryos.
eve is expressed in a segmentally repeated subset of heart precursor cells starting shortly after tin expression is observed in these cells.
eve protein is expressed in the first progeny of NBs 1-1, 4-2, and 5-2.
The position of run protein stripes was compared to that of other segmentation genes. The eve protein stripes lie anterior to the run protein stripes but overlap them partially. Two rows of eve expression are anterior to a two-row region of overlap with run followed by two rows of run expression and then two rows of non-expression before the next eve stripe.
eve protein is expressed in a complementary pattern to ftz protein. eve and ftz expression domains overlap at earlier stages of development, and then after stripe sharpening appear to be mutually exclusive, perhaps due to the regulation of ftz by eve.
In the early embryo,eve protein is expressed at low levels in a broad band from ~20% to ~70% egglength, as embryogenesis continues, the eve expression pattern is resolvedinto seven stripes of expression in every odd-numbered parasegemt. Thisparir-rule pattern is first visable at the end of the cleavage stage, andpersists through gastrulation and germ band elongation, where the stripes areresolved to span approximately three cells each. At the beginning of germ bandelongation, seven additional stripes of approximately two cells each can bedetected in the even-numbered parasegments. At this time, the anterior boarderof the eve stripes becomes well defined and sharp. Prior to germ bandretraction the segmentally repeated pattern disappears, and eve expressionpersists only in the posterior-most region of the germ band. As germ bandretaction begins, eve protein is detected in the neurogenic region of theembyo, and is observed in clusters of approximately four to six cells on eitherside of the ventral furrow in a segmentally repeated fashion. Prior to thecompletion of germ band retraction, lateral clusters of eve expressing cellsappear. Ultimately eve expression is detected in a subset of neurons in eachsegment, and this expression persists through embryonic and larval development.
In the early embryo,eve protein is expressed at low levels in a broad band from ~20% to ~70% egglength, as embryogenesis continues, the eve expression pattern is resolvedinto seven stripes of expression in every odd-numbered parasegemt. Thisparir-rule pattern is first visable at the end of the cleavage stage, andpersists through gastrulation and germ band elongation, where the stripes areresolved to span approximately three cells each. At the beginning of germ bandelongation, seven additional stripes of approximately two cells each can bedetected in the even-numbered parasegments. At this time, the anterior boarderof the eve stripes becomes well defined and sharp. Prior to germ bandretraction the segmentally repeated pattern disappears, and eve expressionpersists only in the posterior-most region of the germ band. As germ bandretaction begins, eve protein is detected in the neurogenic region of theembryo, and is observed in clusters of approximately four to six cells oneither side of the ventral furrow in a segmentally repeated fashion. Prior tothe completion of germ band retraction, lateral clusters of eve expressingcells appear. Ultimately eve expression is detected in a subset of neurons ineach segment, and this expression persists through embryonic and larvaldevelopment.
Marker for
Subcellular Localization
CV Term
Evidence
References
inferred from direct assay
Expression Deduced from Reporters
Reporter: P{ChAT-GAL4.7.4}
Stage
Tissue/Position (including subcellular localization)
Reference
ellipsoid body

Comment: strong expression

adult mushroom body

Comment: strong expression

eye

Comment: strong expression

Reporter: P{CQ2-GAL4}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{EL-GAL4-eveRC}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve.st3-GAL4.S}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve'-tau/lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-GAL4.eme}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-GAL4.RKK}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-GAL4.RN2}
Stage
Tissue/Position (including subcellular localization)
Reference
RP2 motor neuron

Comment: reference states 13 hours of developmental time

aCC neuron

Comment: reference states 13 hours of developmental time

dendrite of motor neuron

Comment: reference states 21 hours of developmental time

Reporter: P{eve-GAL4.RRa}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-GAL4.RRC}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-GAL4.RRK}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-lacZ1.7}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-lacZ5.2}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-lacZ5.9}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-lacZ6.3}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-lacZ8.0}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{eve-lacZ.C}
Stage
Tissue/Position (including subcellular localization)
Reference
organism | striped

Comment: eve stripes 3 and 7

Reporter: P{evestripe2-lacZ}
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{MSE-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\eve 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
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, and Transgenic Constructs
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
abdominal 3 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 3 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 3 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 3 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 3 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 3 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 3 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 3 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 3 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 3 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 4 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 4 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 4 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 4 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 4 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 4 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 4 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 4 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 4 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 4 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 5 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 5 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 5 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 5 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 5 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 5 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 5 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 5 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal 5 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155
abdominal 5 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng
abdominal anterior fascicle & abdominal segment 3
abdominal anterior fascicle & abdominal segment 4
abdominal anterior fascicle & abdominal segment 5
abdominal posterior fascicle & abdominal segment 3, with Scer\GAL4elav-C155
abdominal posterior fascicle & abdominal segment 3, with Scer\GAL4ftz.ng
abdominal posterior fascicle & abdominal segment 4, with Scer\GAL4elav-C155
abdominal posterior fascicle & abdominal segment 4, with Scer\GAL4ftz.ng
abdominal posterior fascicle & abdominal segment 5, with Scer\GAL4elav-C155
abdominal posterior fascicle & abdominal segment 5, with Scer\GAL4ftz.ng
abdominal segment 3 & somatic muscle
abdominal segment 4 & somatic muscle
abdominal segment 5 & somatic muscle
epidermis & larval midgut & embryo
larval brain & neuroblast (with eve1)
larval brain & neuroblast (with eve5)
Orthologs
Human Orthologs (via DIOPT v7.1)
Homo sapiens (Human) (2)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
8 of 15
Yes
Yes
8 of 15
Yes
Yes
Model Organism Orthologs (via DIOPT v7.1)
Mus musculus (laboratory mouse) (3)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
9 of 15
Yes
Yes
 
7 of 15
No
Yes
1 of 15
No
No
Rattus norvegicus (Norway rat) (3)
4 of 13
Yes
Yes
4 of 13
Yes
Yes
Xenopus tropicalis (Western clawed frog) (2)
3 of 12
Yes
Yes
3 of 12
Yes
Yes
Danio rerio (Zebrafish) (3)
7 of 15
Yes
Yes
5 of 15
No
Yes
5 of 15
No
Yes
Caenorhabditis elegans (Nematode, roundworm) (3)
8 of 15
Yes
Yes
 
1 of 15
No
No
1 of 15
No
No
Arabidopsis thaliana (thale-cress) (0)
No records found.
Saccharomyces cerevisiae (Brewer's yeast) (0)
No records found.
Schizosaccharomyces pombe (Fission yeast) (0)
No records found.
Orthologs in Drosophila Species (via OrthoDB v9.1) ( EOG09190EWC )
Organism
Common Name
Gene
AAA Syntenic Ortholog
Multiple Dmel Genes in this Orthologous Group
Drosophila melanogaster
fruit fly
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
Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG091509BT )
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
Mayetiola destructor
Hessian fly
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) ( EOG090W08IT )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Bombyx mori
Silkmoth
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
Cimex lectularius
Bed bug
Acyrthosiphon pisum
Pea aphid
Acyrthosiphon pisum
Pea aphid
Zootermopsis nevadensis
Nevada dampwood termite
Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( EOG090X0C5Q )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strigamia maritima
European centipede
Strigamia maritima
European centipede
Strigamia maritima
European centipede
Ixodes scapularis
Black-legged tick
Tetranychus urticae
Two-spotted spider mite
Daphnia pulex
Water flea
Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( EOG091G0JVN )
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 v7.1)
Drosophila melanogaster (Fruit fly) (8)
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 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 ( 0 )
    Allele
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Disease Associations of Human Orthologs (via DIOPT v7.1 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.
    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
    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
    Gene Group - Pathway Membership (FlyBase)
    External Data
    Linkouts
    SignaLink - A signaling pathway resource with multi-layered regulatory networks.
    Genomic Location and Detailed Mapping Data
    Chromosome (arm)
    2R
    Recombination map
    2-61
    Cytogenetic map
    Sequence location
    2R:9,979,319..9,980,795 [+]
    FlyBase Computed Cytological Location
    Cytogenetic map
    Evidence for location
    46C10-46C10
    Limits computationally determined from genome sequence between P{lacW}Adamk13906&P{EP}Pka-R2EP2162 and P{PZ}14-3-3ζ07103
    Experimentally Determined Cytological Location
    Cytogenetic map
    Notes
    References
    46C3-46C11
    (determined by in situ hybridisation)
    46C-46C
    (determined by in situ hybridisation)
    Complementation data from unspecified deficiency chromosomes.
    Experimentally Determined Recombination Data
    Left of (cM)
    Right of (cM)
    Notes
    Stocks and Reagents
    Stocks (21)
    Genomic Clones (13)
     

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

    cDNA Clones (3)
     

    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 sequences
    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
        Other 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: eve l(2)46Ce
          Source for merge of: eve l(2)46Cg
          Source for merge of: eve l(2)46CFh l(2)46CFj l(2)46CFp
          Additional comments
          Other Comments
          DNA-protein interactions: genome-wide binding profile assayed for eve protein in 0-12 hr embryos; see mE1_TFBS_eve collection report.
          eve functions in an eve --> grn --> zfh1 regulatory cascade within the aCC motoneuron, along with suppressing exex expression. By contrast, there is only partial cross-regulation between eve, grn, zfh1 and exex in the RP2 motoneuron.
          eve acting as a repressor, regulates axonal projections.
          eve represses exex in a gro-dependent fashion. Cross-repressive interactions between exex and eve delimit exex expression to ventral and lateral motor neurons and eve expression to dorsal motor neurons.
          Cross-repressive interactions between the "identity genes" lbe, lbl, Dr and eve are essential for the specification of cardiac and muscular fates in the developing embryo.
          Parasegment widths are defined early in the embryo by the relative levels of ftz and eve proteins at stripe junctions.
          ftz and eve are expressed in the pole cells of nos- embryos.
          The 7.7kb 3' regulatory region of eve contains both composite and discrete neuronal and early blastoderm enhancers, and multi-stripe positioning by gap gene repressor gradients.
          eve and tup constitute a bimodal switch regulating axonal growth and directing motor axons to ventral (tup) or dorsal (eve) regions of the muscle field during embryogenesis.
          eve is needed for the correct differentiation of the eve-expressing subset of pericardial cells, possibly as a direct target of zfh1.
          In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
          The mechanism of transcriptional repression by eve protein involves a direct interaction with the Tbp protein.
          In vitro DNA-binding studies reveal pros reduces eve regulatory region binding to DNA to very low levels.
          prd regulates late even skipped expression through a composite binding site for the paired domain and the homeodomain. Mutagenesis of either binding site leads to significant reduction in the activity of the late element, indicating that both domains are required for regulation.
          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 ad lacks a pair rule phase to its expression.
          hop may activate Stat92E to regulate transcription of target genes such as eve.
          An injection of a monoclonal antibody against the eve homeodomain, in conjunction with chromophore-assisted laser inactivation (CALI), precisely phenocopies the eve mutant phenotype.
          The stripe 3+7 enhancer is about 500bp in length and maps about 3.3kb upstream of the transcription start site. The enhancer is regulated by one or more ubiquitously distributed activators.
          eve protein has broad DNA recognition properties in vitro that are likely to be important determinants of its distribution on DNA in vivo.
          Two binding sites for Stat92E protein have been identified in the eve stripe 3 enhancer region.
          In vitro transcription experiments suggest that eve protein represses transcription by inhibiting binding of TFIID to the promoter.
          The gt transcriptional repressor defines the anterior border of stripe 2 of eve. A single gt binding site maps 50bp from the nearest activator site in the eve stripe 2 enhancer.
          The full length and 0.9kb fragment of scs and a 430bp fragment from gypsy carrying 12 su(Hw) binding sites (gypsy\su(Hw)BR430) can block the interaction of defined eve stripe enhancers when positioned between the enhancer and target promoter.
          cas, eve, unpg and ac are expressed in specific neuroblast sublineages. Expression studies using pbl and stg mutants suggest that neuroblasts have an intrinsic gene regulatory hierarchy controlling unpg and ac expression but that cell cycle- or cytokinesis-dependent mechanisms are required for cas and eve CNS expression.
          Early and late eve expression have distinct roles in regulating downstream genes. Early 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.
          Crystallographic of the eve homeodomain complexed to an AT-rich oligonucleotide at 2.0 A resolution reveals a novel arrangement of two homeodomains bound to one 10bp DNA sequence in tandem fashion.
          The physical association of exd protein with Ubx protein and other HOM proteins is studied using a yeast two-hybrid system.
          The development of eve cells (cells from parasegments 4-12 that give rise to the pericardial cells of the heart) depends on at least wg and hh. Mosaic analysis demonstrates wg produced in the mesoderm alone is sufficient to generate eve cells. Also action of wg+ in the wild type ectoderm can restore the eve cells in the underlying wg- mesoderm. These two classes of mosaic clones demonstrate that wg protein in either germ layer is sufficient for the development of eve cells in the mesoderm and the patterning the mesoderm. Uniform expression of wg in the mesoderm only is sufficient to rescue the repeated clusters of eve expressing cells.
          Dpic\eve has been cloned and sequenced and compared with D.melanogaster eve.
          eve stripe 2 and 3 enhancers have been used to misexpress segmentation and homeotic genes.
          eve efficiently blocks, or "squelches", Tbp-enhanced transcription in cotransfected Schneider L2 cells. Squelching does not require eve DNA-binding sites on the reporter plasmids used, but is dependent on the presence of the eve repression domain.
          Cell cycle progression and progression through S phase is required for eve expression in the CNS, cytokinesis is not required. Pc group genes are required for the repression of eve expression in the CNS.
          Within the hierarchy of genes expressed in GMC4-2a nub and pdm2 lie downstream of pros and ftz and upstream of eve.
          sna can repress a heterologous enhancer.
          A potent repressor domain within the eve protein has been identified; localised between amino acids 212 and 245 and rich in Pro and hydrophobic amino acids.
          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.
          In vivo crosslinking has been used to directly measure DNA binding of the homeodomain protein eve. eve protein binds at uniformly high levels throughout the length of their genetically identified target genes and at a lower, but significant level to genes eve is not expected to regulate. Studies suggest that ftz and eve has similar DNA binding specificities in vivo.
          The eve product represses wg expression and transforms cells that would normally secrete naked cuticle into denticle secreting cells.
          Ectopic ttk causes complete or near complete repression of ftz and significant repression of eve, odd, h and runt.
          Expression of eve has been used as a marker for a subset of neuroblasts in study of requirement for wg gene product for neuroblast specification and formation in the CNS.
          Complementation group identified in an EMS and DEB screen to isolate deficiencies that uncover Jra.
          Expression of prd depends on activation by gap gene hb, Kr, kni and gt products. Primary pair rule gene products act primarily in subsequent modulation rather than activation of prd stripes. Factors activating prd expression in the pair rule mode interact with those activating it along the dorso-ventral axis.
          The eve gene product is a direct repressor that can repress activated transcription but does not function by binding to the TATA box of promoters. Deletion analysis reveals that both the proline and alanine rich regions of the eve gene product are required for maximal repression.
          wg expression is aberrantly activated and regulated in pair rule mutant embryos.
          The role of eve in the regulation of run mRNA expression in the early embryo has been investigated.
          Activation of en at the anterior margins of the parasegments requires repression of run and odd by eve.
          Elements redundantly involved in enhancer activity in the autoregulatory domain of ftz are conserved in the AE homologs of D.virilis and D.hydei and in the developmentally regulated genes eve and Ubx.
          The eve stripe 3 enhancer lies 1.7kb upstream of the stripe 2 enhancer. The two enhancers must be separated by a minimum distance for proper stripe expression, though the order of enhancers can be reversed without affecting the normal expression pattern.
          eve can repress transcription at a distance. Tissue culture cell, in vitro transcription and DNaseI footprinting assays suggest that repression involves cooperative binding between eve molecules bound at distant sites in a manner similar to that used by some prokaryotic repressors.
          Expression analysed in CNS study of neuroblasts and ganglion mother cells.
          In vitro studies showed that Ubx and eve protein exert active and opposite effects on in vitro transcription when bound to a common site upstream of a target (Adh) core promoter: Ubx acts as an activator and eve acts as a repressor, and both affect the extent of preinitiation complex formation. A subsequent step renders mature complexes transiently refractory to activation and repression.
          Heat shock inducible eve transgene has been used to test the effects of eve expression on transcription of ftz, odd, run, prd, wg (proposed to be direct targets of eve), and eve, h and en (proposed to be indirect targets of eve). Delayed effects on eve and en appear to be mediated by odd and run. Ectopically expressed eve acts in a concentration-dependent manner on its different target genes.
          eve protein expression during embryogenesis has been studied in D.melanogaster and grasshopper.
          The 69kD ttk protein isoform binds multiple sites in the promoter and genetically defined autoregulatory element of eve.
          Maternally supplied ttk protein helps to establish the timing of the onset of zygotic expression of eve and ftz thereby preventing premature activation.
          Comparison of CpG distribution in the coding region of 121 genes from six species supports the mCpG mutational hotspot explanation of CpG suppression in methylated species at position II-III and III-I.
          Mutant analysis shows that wild type eve function is required to set up expression of ac in row D of the embryonic proneural cluster.
          Promoter fusions and expression pattern analysis show that a 480bp region is necessary and sufficient to direct eve stripe 2 expression. The gene products of bcd, hb, Kr and gt all bind within this 480bp region.
          Apical localization of pair-rule transcripts restricts lateral protein diffusion allowing pair-rule proteins to define sharp boundaries and precise spatial domains.
          The cis and trans activating factors responsible for autoregulation are characterised using a combination of DNA binding and P-element transformation assays. Ecol\lacZ reporter gene studies demonstrate that eve autoregulation is mediated, at least in part, by a 100bp minimal autoregulatory sequence (MAS) located about 5kb upstream from the eve transcription start site. Results provide evidence that the eve protein acts combinatorially with other transcription factors to enhance its own expression.
          Mutations in zygotic pair rule gene eve interact with RpII140wimp.
          DNA binding assays and transient co-transfection assays in cultured cells suggest that repression of eve stripe 2 expression involves competition or short-range quenching mechanism. The binding of gt and Kr interferes with the binding of bcd and hb activators at overlapping or neighbouring sites within the eve stripe 2 promoter element.
          Ecol\lacZ reporter gene constructs carrying an eve promoter fragment were used to analyse the bcd, hb, Kr and gt binding sites present in the eve promoter. bcd, hb, Kr and gt are responsible for the expression of stripe 2. Mutations in the bcd or hb protein binding sites cause reduced expression of stripe 2 but do not alter the spatial limits. Mutations in Kr or gt protein binding sites do change the spatial limits of stripe 2.
          eve does not affect transcription from the mus209 promoter of mus209-Ecol\CAT reporter constructs.
          The effects of an altered nucleocytoplasmic ratio on transcripts that normally undergo changes in transcript pattern in cell cycle 14 is studied. The development of the seven-striped transcript pattern of the segmentation gene eve is independent of the nuclear density and cell cycle program.
          prd RNA expression has been studied in eve- embryos.
          The product of the eve gene probably interacts with a subset of the 'pair-rule' repressor elements located in the ftz promoter.
          eve amorphic mutants eliminate all segmental periodicity.
          Ubx, Kr and eve expression are altered in fs(1)h mutant embryos.
          Transcription of eve has been studied in vitro.
          In vitro DNA footprinting analysis shows that eve and zen can bind to sites in the mus209 5' flanking region.
          eve can repress transcription from the Ubx promoter.
          Injection of protein synthesis inhibitors into early embryos induces expression of eve mRNA in virtually all regions of the embryo.
          Analysis of eve gene expression reveals that distinct regulatory programs are required to first establish and then refine the periodic pattern of eve expression.
          A transient expression assay has been employed to investigate the potential of homeobox genes to function as transcriptional activators.
          Ecol\lacZ reporter gene constructs have been used to identify cis control elements within the eve promoter that might mediate interactions with trans-acting factors encoded by gap and pair-rule genes.
          The development of the eve and ftz stripes in h-, run-, eve- and en- embryos demonstrates that individual cells are allocated to parasegments with respect to the anterior margins of the eve and ftz stripes.
          Mutations in eve do not affect the spatial expression pattern of gt.
          The on/off periodicity of the pair-rule gene eve involves the interaction of the hb and Kr proteins with defined eve promoter elements.
          Genetic analysis demonstrates that eve is required for efficient homeotic gene expression in the visceral mesoderm.
          The DNA binding activities of the en, eve, prd and zen proteins have been compared.
          eve protein expression has been analysed in various mutants that disrupt segmentation.
          Homozygous lethal; embryos homozygous for a null allele or a deficiency fail to undergo segmentation and their ventral surfaces are covered by a lawn of short denticles pointed toward the midline; denticles in the anterior region show thoracic characteristics suggesting that segmental identities persist in the absence of segmentation. All derivatives of gnathal segments are missing, such as maxillary sense organs, cirri, mouth hooks, labial sense organs and the mandibular parts of the cephalopharyngeal skeleton; the labrum, antennal sense organs and a rudimentary skeleton are the only remains of the larval head. Posteriorally, anal plates and some sensory organs persist as do remnants of spiracles, filzkorper and tufts. Homozygotes and hemizygotes for hypomorphic alleles display pair-rule segmentation defects. Denticle bands and adjacent naked cuticle of the prothoracic, metathoracic and even-numbered abdominal segments removed; some naked cuticle of the adjacent segment removed as well (i.e., the odd numbered parasegments are removed). Combinations of alleles with Df(2R)eve raised at different temperatures can achieve an array of phenotypes between these extremes. Expression of eve is first detected at the eleventh nuclear division following fertilization; at this stage, eve protein is uniformly distributed among the nuclei, both at the periphery and deep within the egg; by the thirteenth nuclear division, the anterior one-third of the embryo is devoid of detectable protein; over the next 20 minutes, the antibody staining in the posterior two-thirds of the embryo becomes concentrated in seven transverse stripes four or five cells wide separated by stripes three to four cells wide with lower levels of staining. By the time of germ-band elongation, the seven stripes have become narrowed and sharply defined and seven new weakly expressing stripes, one to two cells wide, appear between the major stripes; during germ-band elongation all stripes gradually disappear. As eve stripes become more sharply defined so too do ftz stripes, no longer overlapping eve stripes, but forming a complementary pattern. At the same time, a group of expressing cells appears at the posterior end of the germ band; these cells form a ring around the anal plate during germ-band shortening. Also during germ-band shortening, a specific subset of sixteen neurons in each hemisegment of the CNS expresses eve product as does a row of cell clusters on either side of the dorsal midline; lateral to these clusters are curious rings of weakly staining cells; the dorsal cells do not appear to be neuronal (Frasch, Hoey, Rushlow, Doyle and Levine, 1987; Frasch and Levine, 1987). In homozygous eve1 embryos switched to restrictive temperature during neurogenesis, four specifically studied eve-expressing neurons in each hemisegment are found to persist; two of them develop normally, but two send axonal processes to abnormal destinations (Doe, Smouse and Goodman, 1988). Frasch and Levine observe that segmentation-gene-mutations generally have reciprocal effects on the expression of eve and ftz, leading them to postulate that their promoters respond reciprocally to the same positional cues. eve concluded to be an early pair-rule gene, since its expression is modified by gap-gene mutations, but not by most other pair-rule gene mutations nor by segment-polarity gene mutations. Three pair-rule genes do influence eve expression: in either eve or h genotypes, eve expression is reduced and in run embryos eve is overexpressed (Frasch and Levine, 1987). In eve embryos, en stripes do not appear (Macdonald, Ingham, and Struhl, 1986). Ubx protein is detected at high level in odd-numbered parasegments from 7 through 13 rather than in every parasegment from 6 through 12 (Martinez-Arias and White, 1988). ftz stripes are disrupted in regularity of position, size and timing (Carroll and Scott, 1986).
          Origin and Etymology
          Discoverer
          Etymology
          Identification
          External Crossreferences and Linkouts ( 47 )
          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 Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
          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
          Flygut - An atlas of the Drosophila adult midgut
          GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
          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.
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          BioGRID - A database of protein and genetic interactions.
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          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
          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 (37)
          Reported As
          Symbol Synonym
          Eve
          (Anreiter and Sokolowski, 2018, Webber et al., 2018, Amourda and Saunders, 2017, Mbodj et al., 2016, Yasugi and Nishimura, 2016, Baëza et al., 2015, Fiedler et al., 2015, West et al., 2015, Lacin et al., 2014, Ocorr et al., 2014, Slattery et al., 2014, Zhang et al., 2014, Chang et al., 2013, Fuse et al., 2013, Ishitani and Ishitani, 2013, Kim et al., 2013, Kohwi et al., 2013, Muha and Müller, 2013, Rudolf et al., 2013, Tixier et al., 2013, Boukhatmi et al., 2012, Crombach et al., 2012, Fujioka et al., 2012, Jaeger et al., 2012, Manning et al., 2012, Oyallon et al., 2012, Reim et al., 2012, Sun et al., 2012, Yoshiura et al., 2012, Benchabane et al., 2011, Bravo-Ambrosio and Kaprielian, 2011, Carrasco-Rando et al., 2011, Grigorian et al., 2011, Hafer et al., 2011, Haralalka et al., 2011, Kohwi et al., 2011, Mariappa et al., 2011, Papatsenko and Levine, 2011, Stagg et al., 2011, Xin et al., 2011, Yang and Su, 2011, Bulchand et al., 2010, Csiszar et al., 2010, Kitajima et al., 2010, Mace et al., 2010, Monastirioti et al., 2010, Morton de Lachapelle and Bergmann, 2010, Ruiz et al., 2010, Stacey et al., 2010, Tran et al., 2010, Umulis et al., 2010, Bhuin and Roy, 2009, Guruharsha et al., 2009, Huh et al., 2009, Mann et al., 2009, Meyer et al., 2009, Das et al., 2008, Dougherty et al., 2008, Haecker et al., 2008, Jain and Gavis, 2008, Lacin et al., 2008, Loer et al., 2008, Noyes et al., 2008, Speicher et al., 2008, Tsuji et al., 2008, Vichas and Zallen, 2008, Wong et al., 2008, Beckett and Baylies, 2007, Johnson et al., 2007, Junion et al., 2007, Kim et al., 2007, Lacin et al., 2007, Massarwa et al., 2007, Monier et al., 2007, Rogulja-Ortmann et al., 2007, Schafer et al., 2007, Toledano-Katchalski et al., 2007, Walthall et al., 2007, Wei et al., 2007, Zhao et al., 2007, Albrecht et al., 2006, Alexander et al., 2006, Beckett and Baylies, 2006, Betschinger et al., 2006, Carmena et al., 2006, Han et al., 2006, Liu et al., 2006, Liu et al., 2006, Sellin et al., 2006, Slack et al., 2006, Veitia, 2006, Zaffran et al., 2006, Menon et al., 2005, Merianda et al., 2005, Cheesman et al., 2004, Mellerick and Liu, 2004, Rawson et al., 2003, Song and Taylor, 2003, Yu et al., 2002)
          eve
          (Bozek et al., 2019, Ditzler et al., 2019, Graham et al., 2019, Bischof et al., 2018, Boisclair Lachance et al., 2018, Constance et al., 2018, Haines and Eisen, 2018, Lim et al., 2018, Mortensen et al., 2018, Rickert et al., 2018, Wang et al., 2018, Waters et al., 2018, Wharton et al., 2018, Andrioli et al., 2017, Barr and Reinitz, 2017, Barr et al., 2017, Erceg et al., 2017, Hang and Gergen, 2017, Hu et al., 2017.6.13, Mir et al., 2017, Nie et al., 2017, Pollak et al., 2017, Samee et al., 2017, Transgenic RNAi Project members, 2017-, Werner et al., 2017, Bürglin and Affolter, 2016, Crocker et al., 2016, Kwon et al., 2016, Ma et al., 2016, Peng et al., 2016, Prata et al., 2016, Urbach et al., 2016, Vincent et al., 2016, Dahlberg et al., 2015, de Taffin et al., 2015, Duque and Sinha, 2015, Kok et al., 2015, Rebeiz et al., 2015, Tikhonov et al., 2015, Bothma et al., 2014, Boyle et al., 2014, Cheung et al., 2014, Ciglar et al., 2014, Gambetta and Müller, 2014, Guilgur et al., 2014, Haye et al., 2014, Jiang and Singh, 2014, Mannervik, 2014, Martinez et al., 2014, Melnikova et al., 2014, Palsson et al., 2014, Paré et al., 2014, Samee and Sinha, 2014, Spahn et al., 2014, Wolfram et al., 2014, Zarin et al., 2014, Zarin et al., 2014, Alfieri et al., 2013, Chen et al., 2013, Combs and Eisen, 2013, Fujioka et al., 2013, Hombría and Sotillos, 2013, Jennings, 2013, Kim et al., 2013, Li and Gilmour, 2013, Liu and Ma, 2013, Manu et al., 2013, Mirzoyan and Pandur, 2013, Paris et al., 2013, Samee and Sinha, 2013, Saunders et al., 2013, Sung et al., 2013, Surkova et al., 2013, Webber et al., 2013, Webber et al., 2013, Xiong and Zhou, 2013, Zeidler and Bausek, 2013, Amrute-Nayak and Bullock, 2012, Andrioli et al., 2012, Aswani et al., 2012, Busser et al., 2012, Crombach et al., 2012, Garcia et al., 2012, Gordon and Ruvinsky, 2012, Gutiérrez et al., 2012, He et al., 2012, Kim et al., 2012, Kvon et al., 2012, Manning et al., 2012, Nikulova et al., 2012, Nowak et al., 2012, Perry et al., 2012, Touma et al., 2012, Van Bortle et al., 2012, Zarin et al., 2012, Bhat et al., 2011, Dobi et al., 2011, Dunipace et al., 2011, Erokhin et al., 2011, Fowlkes et al., 2011, Goto et al., 2011, Harrison et al., 2011, Helman et al., 2011, Kaplan et al., 2011, Kim et al., 2011, Kuzin et al., 2011, Li and Arnosti, 2011, Li et al., 2011, Liu and Ma, 2011, Ludwig et al., 2011, Maeda and Karch, 2011, Mikhaylova and Nurminsky, 2011, Miles et al., 2011, Nègre et al., 2011, Schroeder et al., 2011, Struffi et al., 2011, Tsurumi et al., 2011, Vorwald-Denholtz and De Robertis, 2011, Walrad et al., 2011, Zhang and Arnosti, 2011, Zhang et al., 2011, Zhu and Bhat, 2011, Zhu and Bhat, 2011, Aswani et al., 2010, Bataillé et al., 2010, Borok et al., 2010, Braid et al., 2010, Bulchand et al., 2010, Itasaki and Hoppler, 2010, Jia and Huan, 2010, Lin et al., 2010, Lusk and Eisen, 2010, Meyer et al., 2010, Neely et al., 2010, Prazak et al., 2010, Ribeiro et al., 2010, Simões et al., 2010, Spirov and Holloway, 2010, The modENCODE Consortium, 2010, The modENCODE Consortium, 2010, Tulin and Stathopoulos, 2010, Wang et al., 2010, Zhang et al., 2010, Babaoglan et al., 2009, Bertet et al., 2009, Buechling et al., 2009, Butler et al., 2009, Fang et al., 2009, Fernandez-Gonzalez et al., 2009, Fujioka et al., 2009, Gaziova and Bhat, 2009, Goering et al., 2009, Grimm et al., 2009, Guerin and Kramer, 2009, Hazelett et al., 2009, Kadam et al., 2009, Klingseisen et al., 2009, Kozlov et al., 2009, Lacin et al., 2009, Leal et al., 2009, Lee et al., 2009, Leung and Eisen, 2009, Li and Chen, 2009, Lim and Kraut, 2009, Liu et al., 2009, Liu et al., 2009, Lucchetta et al., 2009, Lüer and Technau, 2009, MacArthur et al., 2009, Moses, 2009, Myasnikova et al., 2009, Nanda et al., 2009, Ochoa-Espinosa et al., 2009, Papatsenko et al., 2009, Payankaulam and Arnosti, 2009, Peterson et al., 2009, Pisarev et al., 2009, Satija et al., 2009, Schaaf et al., 2009, Sellin et al., 2009, Shevelyov et al., 2009, Tchuraev and Galimzyanov, 2009, van Impel et al., 2009, Venken et al., 2009, Venken et al., 2009, Weber et al., 2009, Andrioli et al., 2008, Bauer and Bailey, 2008, Berger et al., 2008, Bosveld et al., 2008, Carrasco-Rando and Ruiz-Gómez, 2008, Crocker and Erives, 2008, de Wit et al., 2008, Fowlkes et al., 2008, Fujimoto et al., 2008, Fujioka et al., 2008, Hanyu-Nakamura et al., 2008, Hare et al., 2008, Kim et al., 2008, Larsen et al., 2008, Liu et al., 2008, Lucchetta et al., 2008, Oktaba et al., 2008, Park et al., 2008, Satija et al., 2008, Schroeder and Gaul, 2008, Segal et al., 2008, Stone et al., 2008, Surkova et al., 2008, Surkova et al., 2008, Surkova et al., 2008, Tögel et al., 2008, Turatsinze et al., 2008, Yu and Small, 2008, Zhu et al., 2008, Aerts et al., 2007, Bergmann et al., 2007, Bhat, 2007, Chandraratna et al., 2007, Curtis et al., 2007, da Silva and Vincent, 2007, Estrada et al., 2007, Halfon and Arnosti, 2007, Levine et al., 2007, Lott et al., 2007, Morais da Silva and Vincent, 2007, Roy et al., 2007, Sandmann et al., 2007, Sprecher et al., 2007, Stern et al., 2007, Surkova et al., 2007, Thomas and van Meyel, 2007, Ullah et al., 2007, Xing et al., 2007, Bartolome and Charlesworth, 2006, Biemar et al., 2006, Blankenship et al., 2006, Choksi et al., 2006, Garces and Thor, 2006, Grosskortenhaus et al., 2006, Hallikas et al., 2006, Holloway et al., 2006, Janssens et al., 2006, Jennings et al., 2006, Keranen et al., 2006, Layden et al., 2006, Lemons and McGinnis, 2006, Luengo Hendriks et al., 2006, Philippakis et al., 2006, Pym et al., 2006, Sandmann et al., 2006, Tucker and Chiquet-Ehrismann, 2006, Wheeler et al., 2006, Goldstein et al., 2005, Grosskortenhaus et al., 2005, Hoskins et al., 2005, Leaman et al., 2005, Mizutani et al., 2005, Oberstein et al., 2005, Pearson et al., 2005, Peel et al., 2005, Stathopoulos and Levine, 2005, Struffi and Arnosti, 2005, Grad et al., 2004, Gurunathan et al., 2004, Kreiman, 2004, Clyde et al., 2003, McDonald et al., 2003, Morozova et al., 2003, Nibu et al., 2003, Spirov and Holloway, 2003, Zeremski et al., 2003, Ludlam et al., 2002, Gursky et al., 2001, Wilkie et al., 2001, Shimell et al., 2000, Hewitt et al., 1999, Lee et al., 1999, Martinez Arias et al., 1988)
          l(2)46CFg
          l(2)46CFh
          l(2)46CFj
          l(2)46CFp
          l(2)46Cg
          Name Synonyms
          Complementation group F
          EVEN-SKIPPED
          eve PRE/TRE element
          even-skipped
          (Prata et al., 2016, Wieschaus and Nüsslein-Volhard, 2016, Dahlberg et al., 2015, West et al., 2015, Cheung et al., 2014, Gambetta and Müller, 2014, Guilgur et al., 2014, Samee and Sinha, 2014, Jennings, 2013, Kim et al., 2013, Manu et al., 2013, Webber et al., 2013, Zeidler and Bausek, 2013, Andrioli et al., 2012, Crombach et al., 2012, Manning et al., 2012, Nechipurenko and Broihier, 2012, Nowak et al., 2012, Reim et al., 2012, Dobi et al., 2011, Helman et al., 2011, Liu and Ma, 2011, Miles et al., 2011, Navarro et al., 2011, Papatsenko and Levine, 2011, Schroeder et al., 2011, Singh et al., 2011, Vorwald-Denholtz and De Robertis, 2011, Zhang and Arnosti, 2011, Bataillé et al., 2010, Braid et al., 2010, Lusk and Eisen, 2010, Mace et al., 2010, Ribeiro et al., 2010, Spirov and Holloway, 2010, Swaminathan et al., 2010, Wang et al., 2010, Buechling et al., 2009, Butler et al., 2009, Leal et al., 2009, Lee et al., 2009, Lüer and Technau, 2009, MacArthur et al., 2009, Myasnikova et al., 2009, Ochoa-Espinosa et al., 2009, Papatsenko et al., 2009, Peterson et al., 2009, Pisarev et al., 2009, Satija et al., 2009, van Impel et al., 2009, Weber et al., 2009, Zamparo and Perkins, 2009, Bosveld et al., 2008, Crocker and Erives, 2008, DeFalco et al., 2008, Fujimoto et al., 2008, Hare et al., 2008, Hsouna and VanBerkum, 2008, Kim et al., 2008, Liu et al., 2008, Lott et al., 2008, Lucchetta et al., 2008, Oktaba et al., 2008, Park et al., 2008, Surkova et al., 2008, Tögel et al., 2008, Turatsinze et al., 2008, Wu and Xie, 2008, Yu and Small, 2008, Halfon and Arnosti, 2007, Lott et al., 2007, Morais da Silva and Vincent, 2007, Payankaulam and Arnosti, 2007, Schwartz and Pirrotta, 2007, Silva and Vincent, 2007, Stern et al., 2007, Ullah et al., 2007, Xing et al., 2007, Albrecht et al., 2006, Biemar et al., 2006, Bird et al., 2006, Garces and Thor, 2006, Holloway et al., 2006, Keranen et al., 2006, Muller and Kassis, 2006, Payankaulam et al., 2006, Philippakis et al., 2006, Riley, 2006, Tucker and Chiquet-Ehrismann, 2006, Veitia, 2006, Brown et al., 2005, Goldstein et al., 2005, Oberstein et al., 2005, Sanchez-Soriano and Prokop, 2005, Schmidt-Ott et al., 2005, Zhang et al., 2004, Levine and Tjian, 2003, Skeath and Thor, 2003, Zeremski et al., 2003, Andrioli and Small, 2002, Dworak and Sink, 2002, Holloway et al., 2002, Klingler and Bucher, 2002, Liu and Kaufman, 2002, Gursky et al., 2001, Wilkie et al., 2001, Shimell et al., 2000, Frasch, 1994.6.3, Stanojevic, 1994.5.2)
          lethal(2)46Ce
          Secondary FlyBase IDs
          • FBgn0014159
          • FBgn0014984
          • FBgn0015483
          • FBgn0017400
          • FBgn0019712
          • FBgn0019718
          • FBgn0019720
          • FBgn0019721
          • FBgn0019816
          • FBgn0023205
          Datasets (1)
          Study focus (1)
          Experimental Role
          Project
          Project Type
          Title
          • transgene_used
          Genome-wide localization of transcription factors by ChIP-chip and ChIP-Seq.
          References (1,502)