Homozygous clones in the wing fail to form hairs or have very small hairs. Subtle defects in polarity are also seen in these wings.
9.7% of not1/Df(3L)W4 animals show prepupal lethality and 19.4% have a strong "nonstop" phenotype (more than 50% of photoreceptor cell axon bundles pass the lamina and hyperinnervate the medulla). In mosaics in which about 60-80% of cells in the eye are homozygous (and the optic lobe is wild type), the axons of photoreceptor cells R1-R6 terminate in the lamina (as in wild type). Minor defects in ommatidial polarity and cell number are seen in these mosaic eyes; 88% of ommatidia have a normal number and array of photoreceptor cells, 12% of ommatidia lack between 1 to 4 photoreceptor cells and about 19% of the normal ommatidia are misoriented. Rhabdomere morphology indicates that mutant R1-R6 cells do not adopt an R7 cell fate. In mosaic animals with homozygous clones in the lamina precursors and lamina neurons the photoreceptor cell pattern appears normal. Normal rows of wild-type epithelial, marginal and medulla glial cells form beneath these clones. Mutant clones and wild-type control clones in the glial precursor cell (GPC) area are similar in size and frequency. In mosaic animals which have homozygous clones in the GPC area the number of mutant glial cells bordering the lamina plexus is markedly reduced compared to controls. Blocks of mutant cells are never seen adjacent to the lamina plexus.
In hemizygotes R1-R6 neurons project through the lamina and terminate in the medulla. A few appear to stop in the lamina. In the developing optic ganglia the regions of the outer proliferation centre (OPC) and lamina precursor cells (LPC) are closer together and the shape of the inner proliferation centre (IPC) is oval rather than round.
strong hyperinnervation of optic medulla anlagen