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General Information
D. melanogaster
Deficiency (2R) engrailed
FlyBase ID
Feature type
Also Known As
enSFX31, enX31, Df(2R)enSFX31, Df(2R)enX31, enX31, Df(2R)en31, Df(2R)enSF31
Sequence coordinates
2R:11,445,082..11,445,082 (Df(2R)en-SFX31:bk1)
2R:11,648,602..11,648,602 (Df(2R)en-SFX31:bk2)
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

shn << bk1 << E(Pc) << obk << bk2

Genetic mapping information

Deletion of the entire en region.

Deletion extending from position -95 to +105, the mutation en1 is arbitrarily designated as position 0.

extends from coordinate -95 to +115 (Kuner et al., 1985)

Comments on Cytology

200kb deletion.

Limits of break 1 from polytene analysis (FBrf0089694) Limits of break 2 from polytene analysis (FBrf0037248)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Genes NOT Deleted / Disrupted
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
Molecular Data
Affected Genes Inferred by Location
Phenotypic Data
In combination with other aberrations

Loss of the anterior crossvein is seen in 41% of Df(2R)Pu-D17 Df(2R)en-SFX31 double heterozygous flies.

91% of Df(2R)enΔ530/Df(2R)en-SFX31 wings exhibit split veins in the posterior compartment.

Inferred to overlap with: Df(2R)enDelta530.

Df(2L)NL Df(2R)en-SFX31 double mutant embryos lack antennal sense organs.

Suppresses position effect variegation (PEV) at the w locus caused by In(1)wm4, PEV at the B locus caused by Dp(1;Y)BSCV and PEV at the Sb locus caused by T(2;3)SbV.

NOT in combination with other aberrations

No wing phenotypes are seen in dppd6 heterozygotes.

Df(2R)en-SFX31 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.

The gnathal lobes are reduced in mutant embryos.

Agam\enen-12A-5R fails to rescue the mutant phenotype. Agam\enen-10B-5 rescue causes slight defects in the posterior compartments of the wings, both sexes are fertile.

Homozygous lethal. When in combination with ci1, ci36 or ci57 the ci phenotype is enhanced. en mutants can be ranked by strength regarding their ability to induce a ci phenotype: en1 <= Df(2R)en30 <= en4 <= enEnci <= Df(2R)en-SFX31 <= en59.

Homozygous embryos are very abnormal compared to wild-type.

ciD expression is derepressed in the posterior compartments of embryos and imaginal discs.

homozygous lethal

Stocks (2)
Notes on Origin


Balancer / Genotype Variants of the Aberration
Separable Components
Other Comments

The Df(2R)en-SFX31 chromosome acts as a dominant moderate suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{wvar}KR3-2", a stable "brown-red" variant of the P{3'WP-2,wvar}2Lt insertion), but this is a false positive result (the suppressor is not within the bounds of the deficient region) because the region of the deficiency is covered by a combination of nonsuppressing deficiencies and deficiencies with suppressors that map to the 2L tip.

Heterozygotes with enXho23 and enSac27 display wing vein abnormalities but heterozygotes with enXho25 fail to survive.

Synonyms and Secondary IDs (18)
References (56)