bk1 << NetA << rut << bk4
This deletion removes a single ribosomal protein-coding gene (though other genes are also removed).
Embryos hemizygous for Df(1)NP5 have thinner or occasionally absent axon commissures in the ventral nerve cord, with the posterior commissure more severely affected, and also exhibit occasional breaks in the longitudinal connectives; midline crossing of EW, EG and SP1 neurons is disrupted.
The cap cell of the LCh1 organ migrates ventrally instead of dorsally in Df(1)NP5 embryos.
Df(1)NP5 mutant embryos do not show dendritogenesis defects in the aCC motoneurons (the number of dendritic tips is normal) compared to controls.
Df(1)NP5 mutants exhibit fragmented commissures and gaps in longitudinal connectives.
90% of Df(1)NP5/Y embryos show defects in axon guidance in the Bolwig's nerve.
Df(1)NP5 embryos show defects in the commissures of the central nervous system; 2% of anterior commissures are absent, 4% of anterior commissures are thin, 8% of posterior commissures are absent and 15% of posterior commissures are thin. 10% of segments fail to separate the anterior and posterior commissures correctly.
Flies heterozygous for the deletion do not show a Minute bristle phenotype.
Df(1)NP5 embryos exhibit salivary gland guidance defects. In wild-type embryos the salivary glands lie parallel to the CNS midline, while 23% of Df(1)NP5 embryos have glands that curve away laterally and 9% have glands that curve medially towards the midline. This phenotype occurs as the glands migrate along the visceral mesoderm, as the invagination of the salivary glands is normal. Gut constriction is not affected in these mutants. The commissures of the ventral nerve cord are abnormally thin or completely absent in Df(1)NP5 embryos.
Embryos heterozygous for Df(1)NP5, removing one copy of NetA and NetB exhibit normal commissures, however the longitudinal tracts, when visualized with BP102 antibody, are thinner between segments and thicker within segments. When fascicles are visualized with Fas2, embryos homozygous or heterozygous for Df(1)NP5 reveal irregularities and interruptions in the longitudinal Fas2 bundles. The heterozygote Df(1)NP5 phenotype is not enhanced in embryos also heterozygous for sliunspecified, robo1unspecified, or scbunspecified. In contrast, the frequency of midline guidance errors is increased in sliunspecified/+ or robo1unspecified/+, but not scbunspecified embryos also heterozygous for Df(1)NP5.
No abnormalities are seen in SNa and SNc projections. Lateral migration of peripheral and exit glia appears normal.
In mutant embryos, the there are defects in the posterior commissure and there are breaks in the longitudinal connectives.
Homozygous lethal, lethality is rescued by Dp(1;f)LJ9 and Dp(1;f)LJ4. Hemizygous embryos display a range of phenotypes in the CNS, most notably a thinning or absence of the commissures in the ventral nerve cord. This defect can be rescued by restoring midline expression of either NetA or NetB gene.
Homozygous lethal. Lethality can be rescued by Dp(1;f)LJ9. Embryo exhibits CNS phenotype: commissures are much thinner and sometimes completely absent, occasional breaks in the longitudinal tracts. Commissural phenotype is rescued by expression of P{slit-NetA} or P{slit-NetB}. There are no segmentation defects, no gross changes in the fate or pattern of midline cells or CNS neurons, no increase in cell death. Embryos exhibit occasional errors in the projection pattern of the motor nerves, including lack if innervation of muscles 6 and 7. Projection of sensory axons into the CNS is almost completely normal.
The recombinant chromosome is deficient for 12E9-12E11;12F2-5 and has the inversion breakpoints 12F2-12F5;17C2. Another inversion, roughly In(1)2;10, is also present.