Breaks in 3' D regulatory sequences.
larval hindgut & embryo & cell (with Df(3L)fz-GS1a)
In stage 16 D3/Df(3L)fz-GS1a mutant embryos, the cells of the large intestine are short and rounded in contrast to the thin columnar cells of wild-type.
Behaves as a null allele when assayed in the embryo.
80% of hemizygous embryos have severe defects throughout the nerve cord, showing thinning of longitudinal connectives and fusion of commissures. The remaining midline glia cells are more frequently located anterior to the anterior commissure than in wild-type embryos. The cell bodies of the midline glia lie along the ventral surface of the commissures and do not migrate and ensheath the commissures.
In(3L)D3/Df(3L)D-5rv6 embryos exhibit variable segmentation defects. Severe phenotype involves deletions removing half of the segments, intermediate phenotype involves weaker partial deletions and segment fusions, weak phenotype causes naked cuticle in segments A2 and A8. Embryos also exhibit variable defects in head development.
D3/Df(3L)fz-GS1a has larval hindgut & embryo & cell phenotype, suppressible | partially by dppUAS.cSa/Scer\GAL4en-e16E
When dppScer\UAS.cSa is expressed under the control of Scer\GAL4en-e16E in D3/Df(3L)fz-GS1a embryos, significant, though variable rescue of the D3/Df(3L)fz-GS1a hindgut phenotype is seen.
Shows tissue specific loss of D expression in the embryo.
There is some uncertainty in the designation of D1, D3 and "D9" as dominant D alleles. The wing phenotype of D3 (a protein null) is similar, if not identical, to D1 when assayed in outcrossed individuals; it is thus possible that the phenotype of D1 itself is not due to changes at the D locus.
Associated with a recessive lethal phenotype that maps to 70D1-2.