21D1-21D2;22B2-22B3
21D1-21D2;22B2-22B3
22A2-22A3;22B2-22B3
22D1-22D2;22B2-22B3
Gsc << bk1 << ds << l(2)04111 << bk2 << Su(dx)
The 2L:1704902..1852362 release 6 coordinates of the right breakpoint are estimates. The left extent corresponds to the left end of cpb, which published results say is deleted.The right extent corresponds to the estimated position of the left end of 22B4, because published cytologies indicate it is not deleted.
Lethal in combination with Df(2L)BSC16.
Macrophages fail to migrate along the ventral cord in homozygous embryos, with much of the ventral abdomen remaining free of macrophages at stage 13-15.
Wild-type clones made in the ovaries of a mutant female, are significantly larger than clones of heterozygous mutant cells. This size difference is greater in clones initiated at 48 hours after egg laying (AEL) than 2 hours AEL.
Df(2L)ast2 in combination with a pair of introgressions from D.simulans spanning 30F1-31E7 to 35D7-36A14 Dsim\Int(2L)S and 21A1 to 22D1--23A2 Dsim\Int(2L)D Dsim\Int(2L)D produces semi-sterile male flies. These flies are female sterile.
Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.
No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.
Eye phenotype is dominantly enhanced by astK6.
Shows no maternal enhancement of dpphr4.
Suppressor of the dosage dependent (two or more copies of P{sev-svp1} or P{sev-svp2}) transformation of cone cells into R7 photoreceptors and at a lower frequency R7 cells into outer photoreceptors.
Deficient embryos show a variably penetrant mutant midgut phenotype: no constrictions form.
Homozygous embryos have head defects, do not complete germband retraction and tracheae are disconnected.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
The Df(2L)ast2 chromosome may act as a dominant 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 the eye colour phenotype in the presence of Df(2L)ast2 overlaps the eye colour phenotype in a wild-type background so it cannot be unequivocally demonstrated that the deficiency chromosome uncovers a suppressor of telomeric silencing.
This stock was originally labelled "Df(2L)ast1" but is assumed to be "Df(2L)ast2" based on its complementation behaviour.
Df(2L)ast1 as reported is necessarily haplolethal due to deletion of dpp. The original isolation may have included a transposition of some or all of the deleted region. Many studies that have reported haploviabiity of Df(2L)ast1 have probably in fact used a mis-labelled stock of Df(2L)ast2.
The left Df(2L)ast2 breakpoint lies within CG2839 or ds or in the region between them, and lies in the range 2L:626409..640599 (R5) (Predicted cytology: 21E2).
The right Df(2L)ast2 breakpoint lies within Gr22a or CG31933 or in the region between them, and lies in the range 2L:1794258..1821591 (R5) (Predicted cytology: 22B2-22B3).
All limits from polytene analysis (FBrf0042627)