60E1-60E2;60E6
60E1-60E2;60E5-60E6
E(wa) << bk1 << Dll << bk2 << RpL19
Deletion removing entire Dll transcription unit.
entire putative transcription unit deleted. Deleted for the region from approximately coordinate 90 kb through 180 kb and beyond on the molecular map of Cohen et al. Deletion removes the entire Dll coding region <up>Cohen, Bronner, Kuttner, Jurgens and Jackle, 1989, Nature (London), 338: 432-34</up>.
Df(3R)sbd45 dominantly enhances the transformation of arista to leg phenotype seen in Df(2R)Dll-MP heterozygotes. Df(2L)al dominantly enhances the transformation of arista to leg phenotype seen in Df(2R)Dll-MP heterozygotes. Df(2R)M60E dominantly enhances the transformation of arista to leg phenotype seen in Df(2R)Dll-MP heterozygotes.
Df(2R)Dll-MP mutant embryos have fewer neurons and fewer support cells in the dorsal organ (DO) and terminal organ than wild type animals. No cell death is seen (TUNEL staining) and the remaining neurons exhibit aberrant morphologies. The DO dendrites are loosely associated rather than tightly bundled and the axons of the remaining DO neurons form a single fascicle projected towards the subesophageal ganglion. No fascicles target the larval antennal lobe (LAL). Df(2R)Dll-MP mutants also exhibit loss of a primary axon bundle that emanates from the mushroom bodies and projects along the dorsal and ventral tracts of the supraesophageal commissure.
In Df(2R)Dll-MP mutant embryos the brain commissures are defective and the microtubule-associated Futsch protein is consistently mislocalised. One of the three supraesophageal commissures seen in wild type is missing in Df(2R)Dll-MP mutants. Both of the primary axon tracts that make up the subesophageal commissure are also missing.
Heterozygotes show a partial transformation of the arista to leg.
No effect on the eye pigment phenotype of wT81.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Recessive lethal. Heterozygote shows partial transformation of aristae to tarsal segments. Dominant phenotype suppressed in either Pcl10 or Df(2R)en28 heterozygotes. Df(2R)Dll/+ shows almost complete suppression of the extra-sex combs phenotypes of Pc4/+, PcT7/+, Pcl10/+, Pcl11/+, AntpScx/+, Msc/+, and MscT3/+.
Moscoso del Prado.
The Df(2R)Dll-MP chromosome acts as a dominant weak 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 assumed to be a false positive result (the suppressor may not be within the bounds of the deficient region) because the 2L TAS array on the chromosome is missing (as assayed by in situ hybridization) and it has previously been shown (FBrf0137248, FBrf0158986) that partial or complete deficiency of the 2L TAS array on the homologue suppresses silencing of brown-red variants of P{3'WP-2,wvar}2Lt.
Ref: Cohen et al., 1989, Nature 338: 432--434
Cytologically normal.
Limits of break 1 from polytene analysis (FBrf0056560) Left limit of break 2 from polytene analysis (citation unavailable) Right limit of break 2 from polytene analysis (FBrf0056560)