Df(3R)E(spl)δ-6 removes promoter sequence from HLHm7, but leaves the coding sequence intact.
Scer\FLP1-mediated recombination between the two progenitor insertions has resulted in a 41kb deletion.
Stage 9/10 Df(3L)Brd-C1/Df(3R)E(spl)δ-6 transheterozygous embryos display loss of apical-basal cell polarity and of epithelial integrity; both of these defects are rescued by sdtΔ3-GFP but not by sdtGFP3.
Df(3R)BSC751/Df(3R)E(spl)δ-6, Df(3R)ED6232/Df(3R)E(spl)δ-6, or Df(3R)E(spl)δ-6/Df(3R)Exel6204 mutant embryos display a significant increase in the number of Ap neurons, as compared with controls.
Df(3R)E(spl)δ-6/Df(3R)grob32.2, in combination with gro+t10.4, mutant embryos display a significant increase in the number of Ap neurons, as compared with controls.
39% of embryos homozygous for the Df(3L)Brd-C1 and Df(3R)E(spl)δ-6 deletions and carrying one copy of Dp(3;2)E(spl)δ-8 fail to hatch and only 2% reach pupal stages.
Df(3R)E(spl)δ-6 Dp(3;2)E(spl)δ-8Δα46 double mutant flies do not show defects in bristle development.
Df(3R)E(spl)δ-6/Dp(3;2)E(spl)δ-8 embryos are able to hatch.
Dp(3;2)E(spl)δ-8Δα46 rescues the neurogenic phenotype associated with Df(3R)E(spl)δ-6.
Animals homozygous for the Df(3L)Brd-C1 and Df(3R)E(spl)δ-6 deletions and carrying one copy of Dp(3;2)E(spl)δ-8Δα46 are 100% embryonic lethal.
Flies homozygous for Df(3R)E(spl)δ-6 and carrying one copy of Dp(3;2)E(spl)δ-8Δα46 are viable and fertile with no detectable mutant morphological phenotype.
Df(3R)E(spl)δ-6/Df(3R)E(spl)δ-6 mutant embryos display a significant increase in the number of Ap neurons, as compared with controls.
Homozygous intestinal stem cell (ISC) clones show an overproliferation of small ISC-like cells. The density and specification of large polyploid enterocytes is unaffected.
Mutant embryos have a strong neurogenic phenotype.