12E3;13A1
12E1;13A5
12E6;13A5
12E1;12F1
12E3;13A5
12E2-12E3;13A1
12E6;13A2-13A5
12E2-12E3;12F5-13A1
12F2-12F3;12F5-13A1
12E2-12E3;12F-13A1
12E2-12E3;12F5-13A
ben << bk1 << sesF << bk2 << eag
Embryos hemizygous for Df(1)KA9 exhibit severe defects in the ventral nerve cord, with a near complete loss of midline crossing in some axon commissures; midline crossing of EW, EG and SP1 neurons is severely disrupted.
Flies heterozygous for the deletion do not show a Minute bristle phenotype.
The morphology of the proventriculus is normal in hemizygotes.
Shows no maternal enhancement of dpphr4.
Dominantly causes tergite defects in less than 50% of run3 heterozygotes.
Embryos exhibit variable defects in the formation of commissural pathways. Scer\GAL4rho.PL induced expression of P{UAS-NETA} or P{UAS-NETB} significantly rescued the CNS phenotype.
CNS defect in embryos: axon commissures are drastically thinner or missing amd the longitudinal tracts are highly disorganised and discontinuous. Commissural phenotype is only weakly rescued by expression of P{slit-NetA} or P{slit-NetB}.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Hemizygous embryos were examined with polarised light microscopy and antibody staining and found to have wild type muscle pattern and contraction.
incomplete condensation and splitting of ventral nerve cord in hemizygous embryos
Lefevre.
Left limit of break 1 from polytene analysis (FBrf0080375) Right limit of break 1 from polytene analysis (FBrf0048204) Left limit of break 2 from polytene analysis (FBrf0086390) Right limit of break 2 from polytene analysis (FBrf0048204)