FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\enE
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General Information
Symbol
Dmel\enE
Species
D. melanogaster
Name
FlyBase ID
FBal0049458
Feature type
allele
Associated gene
Dmel\en
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
Delta2-3 transposase
(Gustavson et al., 1996)
Progenitor genotype
enXho25
(Gustavson et al., 1996)
Caused by aberration
Df(2R)enE
Cytology
Description

The deletion extends from 9.6kb upstream of the en transcription start site to 31.7kb downstream, deleting about half of the inv transcription unit.

(Cheng et al., 2014)

Df(2R)enE breaks at approximate coordinate 0 and -50 in the inv-en region, removing most of the en and inv transcription units, including all of the insertion from enXho25.

(Gustavson et al., 1996)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      Expression Data
      Reporter Expression
      Additional Information
      Statement
      Reference
       
      Marker for
      Reflects expression of
      Reporter construct used in assay
      Human Disease Associations
      Disease Ontology (DO) Annotations
      Models Based on Experimental Evidence ( 0 )
      Disease
      Evidence
      References
      Modifiers Based on Experimental Evidence ( 0 )
      Disease
      Interaction
      References
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Large homozygous clones induced in late third larval instar gonads are often associated with a disorganised terminal filament. Large terminal filament clones in the pupal ovaries are also associated with a failure to properly organise the terminal filament stack. Smaller posterior terminal filament cell clones have no detectable effect on terminal filament stack organisation.

      (Bolivar et al., 2006)

      Stage 15 enE embryos have only ~13 genital disc precursor cells, instead of the wild-type number of 22.

      (Chen et al., 2005)

      Stigmatophores do not form in enE mutants.

      (Merabet et al., 2005)

      Con-positive longitudinal fascicles and commissures are grossly disturbed in Df(2R)enE embryos (carrying both enE and invE). The muscles are grossly abnormal.

      (Siegler and Jia, 1999)

      enE invE double mutant clones of posterior origin show a variety of phenotypes in the wing. Clones distant from the A/P compartment boundary induce outgrowths and duplications both in and adjacent to the clones. Posterior clones at the A/P boundary sometimes cross into or displace the A/P boundary, while others straddle the normal site of the A/P restriction. Outgrowths and ectopic or disrupted venation are sometimes seen at the site of the normal A/P boundary. In a few rare cases, clones appear to obey the A/P lineage restriction from the posterior side. Posterior clone cells that have crossed or displaced the A/P boundary do not associate normally with anterior cells.

      (Blair and Ralston, 1997)

      Fails to complement the adult phenotype of en1. Causes extreme embryonic segmentation defects: its denticle belts fused into an almost continuous lawn.

      (Gustavson et al., 1996)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      NOT Suppressor of
      Statement
      Reference

      enE is a non-suppressor of decreased cell number | embryonic stage phenotype of ptc9

      (Chen et al., 2005)
      Other
      Statement
      Reference

      enE, fra1 has abnormal neuroanatomy phenotype

      (Joly et al., 2007)

      enE, fra1 has lethal | adult stage phenotype

      (Joly et al., 2007)
      Phenotype Manifest In
      Other
      Statement
      Reference

      enE, fra1 has larval ventral nerve cord phenotype

      (Joly et al., 2007)

      enE, fra1 has larval anterior commissure phenotype

      (Joly et al., 2007)

      enE, fra1 has larval posterior commissure phenotype

      (Joly et al., 2007)

      enE, fra1 has lateral tract phenotype

      (Joly et al., 2007)

      enE, ptc9 has genital disc primordium phenotype

      (Chen et al., 2005)

      enE, invE has embryonic hindgut phenotype

      (Iwaki and Lengyel, 2002, Takashima and Murakami, 2001)

      enE, invE has neuroblast NB7-3 phenotype

      (Deshpande et al., 2001)

      enE, invE has wing disc | posterior | somatic clone phenotype

      (Dahmann and Basler, 2000)

      ci94, enE, invE has wing disc | posterior | somatic clone phenotype

      (Dahmann and Basler, 2000)

      enE, invE, smo3 has wing disc | posterior | somatic clone phenotype

      (Dahmann and Basler, 2000)

      enE, invE has larval somatic muscle cell phenotype

      (Martin-Bermudo and Brown, 2000)

      enE, invE has tendon cell phenotype

      (Martin-Bermudo and Brown, 2000)

      enE, wgl-17 has denticle phenotype

      (Alexandre et al., 1999)

      enE, invE has larval RP2 motor neuron phenotype

      (Bhat and Schedl, 1997)

      enE, invE, wghs.PN has larval RP2 motor neuron | ectopic phenotype

      (Bhat and Schedl, 1997)

      Df(2R)gsb, enE, invE has neuroblast NB5-3 phenotype

      (Bhat and Schedl, 1997)

      Df(2R)gsb, enE, invE has larval RP2 motor neuron | ectopic phenotype

      (Bhat and Schedl, 1997)

      Df(2R)gsb, enE, invE has neuroblast NB5-6 phenotype

      (Bhat and Schedl, 1997)

      enE, invE has neuroblast NB5-3 phenotype

      (Bhat and Schedl, 1997)

      enE, invE has larval RP2 motor neuron | ectopic phenotype

      (Bhat and Schedl, 1997)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Approximately 60% of fra1/enE double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Nearly all the segments are affected in these embryos.

      (Joly et al., 2007)

      Stage 15 enE ptc9 embryos have increased levels of genital disc precursor cells, similar to levels seen in ptc9 single mutants.

      (Chen et al., 2005)

      Df(2R)enE mutant embryos (carrying both invE and enE) completely lack hindgut boundary cell rows and rings.

      (Iwaki and Lengyel, 2002)

      Neuroblast NB 7-3 is missing in 100% of Df(2R)enE hemisegments (in which embryos are mutant for both en and inv).

      (Deshpande et al., 2001)

      Df(2R)enE embryos (which are mutant for both en and inv) show slight overgrowth of the hindgut, although its overall morphology is almost normal. The border cells of the hindgut (which normally form an anterior and posterior ring at the ends of the hindgut and bilateral strands that connect the two rings) do not differentiate in these embryos.

      (Takashima and Murakami, 2001)

      Df(2R)enE clones (mutant for both en and inv) of posterior origin in the wing disc sort, when in contact with anterior cells, into anterior territory. Df(2R)enE; ci94 double mutant clones of anterior origin in the wing disc straddle the anterior/posterior (A/P) boundary, similar to ci94 single mutant clones. Unlike Df(2R)enE single mutant posterior clones, however, Df(2R)enE; ci94 double mutant clones of posterior origin only partially sort into anterior territory and straddle the A/P boundary (similar to ci94 or Df(2R)enE; ci94 clones originating in the anterior compartment). Df(2R)enE; ci94 double mutant clones of both anterior and posterior origin define straight borders with neighbouring wild-type anterior and posterior cells. Df(2R)enE; ci94 double mutant clones show smooth borders with adjacent wild-type cells when situated entirely within the posterior compartment. Unlike Df(2R)enE single mutant clones, Df(2R)enE smo3 double mutant clones of posterior origin in the wing disc invariably occupy only posterior territory and define straight borders to anterior cells at the normal position of the anterior/posterior (A/P) boundary. Df(2R)enE smo3 double mutant clones of anterior origin also occupy posterior territory and define straight borders to anterior cells at the normal position of the A/P boundary.

      (Dahmann and Basler, 2000)

      The specification of the majority of tendon cells is eliminated in Df(2R)enE embryos. Some muscles in these embryos have abnormal free ends.

      (Martin-Bermudo and Brown, 2000)

      enE wgl-17 double mutant embryos have segmentally repeated denticle whorls.

      (Alexandre et al., 1999)

      enE invE embryos have duplicated RP2 neurons in several hemisegments. This is due to the transformation of the NB5-3 neuroblast to a NB4-2 fate. enE invE embryos expressing wghs.PN, or enE invE Df(2R)gsb triple mutants have triplicated RP2 neurons. The triplication in enE invE Df(2R)gsb embryos is due to transformation of the NB5-3 and NB5-6 neuroblasts to a NB4-2 fate. gsbhs.PBH prevents the duplication of RP2 neurons seen in enE invE embryos when expressed during stage 8. ptc9 enE invE triple mutants lack RP2 neurons.

      (Bhat and Schedl, 1997)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      enE is rescued by enUAS.cGa/Scer\GAL4salm-459.2

      (Merabet et al., 2005)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Partially complements: obk1. Fails to complement the wing venation defects of obk1 but complements the antennal duplication and eye bristle phenotype.

      (Dworkin et al., 2001)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      References (30)