Open Close
General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
enIIB86, enB86, enIIB
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes

Approximate location of a 54bp deletion/1 base insertion that begins in the codon for amino acid 75. A 104 residue polypeptide is produced. The exact position of the deletion was not reported (FBrf0086432).

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Point mutation.

53bp deletion around codon 75 causing a frameshift. A GC is reversed in codon 70. The altered coding sequence encodes a 104 residue polypeptide.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Flies expressing en45.T:Ivir\HA1 in a homozygous en54 mutant background are fertile with no phenotypic defects aside from minor defects in the wing veins in the posterior compartment in some flies.

30% of Df(2R)enΔ530/en54 wings exhibit split veins in the posterior compartment.

Homozygous en54 mutant embryos display a highly disturbed ventral nerve cord architecture. The commissures are fused, or posterior commissures are thinner than normal or absent, suggesting that axons are either misrouted or missing. Longitudinal tracts are globally less affected than commissures in these mutants.

Hindgut boundary cell rows and rings form normally in mutant embryos.

Occasional adult escapers are seen for enAdv-1/en54. enAdv-1/en54 escapers have en-type wing phenotypes, including transformation of posterior wing margin to an anterior fate, in addition to the additional vein phenotype seen in In(2R)Adv/+ flies.

The development of 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) is not affected in mutant embryos.

Embryos develop merged denticle belts.

5% of en1/en54 flies have a gap in the fourth wing vein at 25oC.

Homozygous embryos do not show duplications of the RP2 neuron.

Mutants exhibit pairwise fusion of the abdominal segments, failure of head involution and extensive cell death causing a shortened cuticle.

Pair-rule defects in the naked cuticle of T1, T3, A2, A4, A6 and A8 result in the pair-wise fusion of adjacent segments. Spacing of apodemes is almost completely irregular and pattern of the somatic muscles is also extremely disturbed. Cells derived from the anterior segment border present signals essential for muscle guidance.

Strong allele.

Larvae show no proventricular defects.

No reduction in rate of germ band extension, in wg, ptc, en triple mutants.

Defects in posterior compartments of each segment.

en54/en1 flies have wild-type shape wings and a wild-type scutellum. Vein III appears thickened and tends to have a posteriorwards bulge about halfway along its length. The anterior crossvein (ACV) is often reduced or absent. Small plexae of vein tissue tend to occur close to the ACV and the posterior crossvein. Vein IV is frequently interrupted and often carries campaniform sensilla. Bristles are occasionally seen in the posterior row, but they never have the characteristics of the middle triple row.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions

Loss of the anterior crossvein is seen in dppd6 en54 double heterozygous flies.

Approximately 60.5% of fra1/en54 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.

Approximately 33% of fra1/en54 double mutants are adult lethal.

25% of ph-d505/+; en54/+ double heterozygotes have a gap in the fourth wing vein at 25oC. 0% and 5% of ph-p410/+; en54/+ double heterozygotes have a gap in the fourth wing vein at 25oC and 29oC respectively. The penetrance of the phenotype at 29oC is increased to 25% if the flies are also expressing hhhs.PI and decreased to 0% if the flies are also heterozygous for hhts2. 100% of ph-p410/Y; en54/+ double heterozygotes have a gap in the fourth wing vein at 25oC. ph-p410/Y; en54/+ is lethal at 29oC. 0% of ph-plac/+; en54/+ double heterozygotes and 100% of ph-plac/Y; en54/+ double heterozygotes have a gap in the fourth wing vein at 25oC. 100% of ph-d2 ph-p2/Y ; en54/+ flies have a gap in the fourth wing vein at 29oC. 0% of ph-d401/Y; en54/+ double heterozygotes do not have a gap in the fourth wing vein at 25 or 29oC.

Xenogenetic Interactions

Agam\eninv-12A rescues many aspects of the embryonic phenotype. Agam\enen-12A-5R and Agam\enen-10B-5 rescue causes slight defects in the posterior compartments of the wings, both sexes are fertile.

Complementation and Rescue Data

Expression of en45.T:Ivir\HA1 rescues the lethality seen in en54 mutant homozygotes.

Images (0)
Stocks (2)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (29)