48A;48B5
48A;48B
48A1;48B5-48B7
shn << bk1 << E(Pc) << obk << bk2
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.
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 embryos are very abnormal compared to wild-type.
ciD expression is derepressed in the posterior compartments of embryos and imaginal discs.
homozygous lethal
Kornberg.
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.
200kb deletion.
Limits of break 1 from polytene analysis (FBrf0089694) Limits of break 2 from polytene analysis (FBrf0037248)