photoreceptor cell & axon (with Df(3L)W4)
photoreceptor cell R1 & axon
photoreceptor cell R2 & axon
photoreceptor cell R3 & axon
photoreceptor cell R4 & axon
photoreceptor cell R5 & axon
photoreceptor cell R6 & axon
Follicle border cell clusters either fully clonal or mosaic for not1/not1 show severely delayed migration; these border cell clusters are frequent split in stage 9/10 egg chambers; border cell clusters frequently contain increased numbers of border cells and polar cells, although extra polar cells occur in clusters with wild-type polar cells; border cells undergo early tumbling and show a redistribution of the number and size of protrusions from a front bias in controls to the sides; outer border cells show mislocalization of the polarity determinants aPKC and crb.
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
not1/Df(3L)W4 has some die during P-stage phenotype, enhanceable by Prosbeta6[+]/Prosβ61
not1 has abnormal cell migration | oogenesis | somatic clone phenotype, non-enhanceable by SCARGD11380/Scer\GAL4αTub84B.PL
not1 has abnormal cell migration | somatic clone | oogenesis phenotype, suppressible | partially by SCARGD11380/Scer\GAL4αTub84B.PL
not1 has abnormal cell migration | somatic clone | oogenesis phenotype, non-suppressible | partially by SCARGD11380/Scer\GAL4αTub84B.PL
not1 has border follicle cell | somatic clone phenotype, non-enhanceable by SCARGD11380/Scer\GAL4αTub84B.PL
not1 has border follicle cell | somatic clone phenotype, suppressible | partially by cpbUAS.cWa/Scer\GAL80αTub84B.PL
not1 has border follicle cell | somatic clone phenotype, non-suppressible by SCARGD11380/Scer\GAL4αTub84B.PL
The prepupal lethality and photoreceptor axon targeting phenotype of not1/Df(3L)W4 animals is enhanced by one copy of Pros261; 78.5% of animals show prepupal lethality and 69.4% show a strong "nonstop" phenotype (more than 50% of photoreceptor cell axon bundles pass the lamina and hyperinnervate the medulla).
not1 is rescued by notTag:MYC