[75C1-75C1];[75D4-75D4];
A set of isogenic deficiency stocks created by FLP-induced recombination between FRT-carrying transgenic insertions; molecularly defined deletion endpoints correspond to initial location of the progenitor insertions. Initial core set of 209 isogenic deletions provides ~60% euchromatic genome coverage.
75C1;75D4
Df(3L)X25/Df(3L)ED225 results in lethality.
Df(3L)XR38/Df(3L)ED225 animals have a defect in the programmed cell death of vCrz neurons: 15.3 +/- 0.5 neurons are present at 7 hours after puparium formation (these neurons are no longer present in wild-type animals at this stage).
Df(3L)grim-A6C/Df(3L)ED225 animals have a defect in the programmed cell death of vCrz neurons: 16 +/- 0 neurons are present at 7 hours after puparium formation (APF) (these neurons are no longer present in wild-type animals at this stage) and 16 +/- 0 neurons are present at 16 hours APF. 8.8 +/- 1.5 surviving EW3-sib cells are seen in these animals (these cells die during embryogenesis in wild type).
Inferred to overlap with: Df(3L)MM2.
Ventral neuroblast-clusters of Df(3L)MM2/Df(3L)ED225 mutant larvae display supernumerary cells compared with wild-type. Df(3L)MM2/Df(3L)ED225 is semi-lethal. The flies that emerge live for only one or two days.
Df(3L)ED225 mutant embryos show a significantly decreased number of cells in all ventral nerve cord segments (T1 to T3 and A1 to A9 to A9-10), associated with increased proportion of apoptotic cells (casp3-positive cells), and show a significant increase in the mitotic index of neuroblasts, but not of neuroblast daughter cells, only in T3 segment, as compared to controls.
Df(3L)ED225/Df(3L)ED225 mutant embryos display increased proliferation of thoracic neuroblast daughter cells cells at stage 14, and abdominal neuroblasts at stages 14 and 15, but no significant difference in proliferation of thoracic neuroblasts at stages 12, 14 or 15, thoracic neuroblast daughter cells at stage 12 or 15, abdominal neuroblasts at stage 12, or abdominal neuroblast daughter cells at stage 12, 14 or 15, as compared with controls. These mutants show no significant change in number of EL neurons, as compared with controls.
Heterozygous animals have a defect in the programmed cell death of vCrz neurons: 9.6 +/- 1.9 neurons are present at 7 hours after puparium formation (these neurons are no longer present in wild-type animals at this stage).
In contrast to controls, no chromosomal breaks in the 75C1-2 region are found in chromosomes bearing the deficiency.
This deficiency removes the 75C1, 75C1′ (a new small band between 75C1 and 75C2) and 75C2 bands, replacing them with a fine unknown band “X” visible between the bands 75B9-10 and 75C4; the band “X” most probably comprises the material of the 75B11-13 fine bands and the distal part of the 75C1 band.
Confirmed by 3-step PCR confirmation as shown in http://www.drosdel.org.uk/del_confirm.php Confirmed by lack of complementation to a known lethal mutation predicted to fall between the progenitor insertions.
Limits computationally determined from location of progenitor P insertion on genome sequence between P{PZ}W05014 and P{lacW}l(3)j14E7j14E7