43C5;44B6-44C1
43C5;44B6-44C1
43C5-43D1;44B6-44C1
bk1 << dpld << sax << bk2
Df(2R)cn83c/Df(2R)CA53 embryos are usually wild-type, but sometimes have segmentation defects and denticles in the third thoracic segment that resemble abdominal denticles. Df(2R)CA53/Df(2R)cn83c ; Scm1/+ embryos lack terminal structures and are U-shaped. Denticle belts of the 3rd to 7th abdominal segments are transformed posteriorly.
Dominantly causes tergite defects in less than 50% of run3 heterozygotes.
Homozygous embryos have smaller heads than normal, and have abnormal tracheae and segmentation. The midgut is smaller than normal, does not constrict and the midgut primordia do not fuse in some embryos. The hindgut and Malpighian tubules are variable in length and crinkled.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Large ventral cord cells.
Recovered as apparent cn double recombinants from test crosses of dysgenic-type males that were heterozygous for a maternally derived dp b cn bw second chromosome and paternally derived autosomes extracted from natural populations and capable of promoting male recombination.
The Df(2R)cn83c 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)cn83c 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. In addition, any suppression 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 one or more nonsuppressing deficiencies.
All limits from polytene analysis (FBrf0074016)