49D3-49D4;50A2
49D3-49D4;50A2-50A3
49D;50A
49C1-49C2;49E2-49E3
49D3-49D4;50A2-50A5
49D3-49D4;49F15-50A3
Nacα << bk1 << bic << sie << bk2 << drk
Lethal in combination with Df(2R)vg62.
No effect on In(1)wm4h position-effect variegation.
Heterozygous females produce embryos with defects in segmentation and head structure, and also a variable and occasionally very high proportion of undeveloped eggs. Bicaudal embryos are not seen.
Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.
Shows no maternal enhancement of dpphr4.
Homozygous lethal. Heterozygotes show occasional nicking of the wings.
Midgut development of mutant embryos is wild type.
Homozygous embryos are very abnormal compared to wild-type. Differentiation of Malpighian tubule material is variable.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Dominant enhancer of nodDTW.
Does not exhibit dominant flightlessness.
Enhances BicD in heterozygotes (Mohler and Wieschaus, 1986) homozygous lethal
Bridges, 11 April 1928.
The Df(2R)vg-B 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(2R)vg-B 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.
Uncovers the distal, but not the proximal, breakpoint of the In(2R)Arp1 inversion.
Limits of break 1 from polytene analysis (FBrf0036848) Left limit of break 2 from polytene analysis (FBrf0036848) Right limit of break 2 from polytene analysis (citation unavailable)