Heterozygous ttk1e11 females lay normal eggs.
The nuclei in homozygous follicle cell clones are more densely packed as compared to the surrounding wild-type tissue.
Cells derived from mosaic clones of ttk1e11 do not participate in dorsal appendage morphogenesis. Mutant cells clump together, block surrounding cells, and occasionally split the dorsal appendage.
Cells derived from mosaic clones of ttk1e11 at S10B show dramatic apical constriction of normally cuboidal cells. Basal surfaces of mutant cells are slightly shrunken and rounder than control cells, but far larger than their apical surfaces. Mutant nuclei are more closely packed at later stages of oogenesis, but this effect is not pronounced at early stages.
Cells derived from mosaic clones of ttk1e11 are taller than control cells.
ttk1e11 mutant eye clones display severe degeneration of the corneal lens, with ommatidia and sensory bristles failing to properly develop.
In 87% of ttk1e11 mutant third instar eye disc clones, 2-3 presumptive R7 photoreceptor cells are observed seven rows posterior to the morphogenetic furrow, compared to just one R7 cell in control tissue. A reduced number of cone cells are observed in mutant clones.
ttk1e11 mutant embryos display defects in tracheal patterning.
Follicle cells in ttk1e11 clones show a decrease in the size of cell nuclei and quantification of the number of cells in these clones compared to the number in their sister clones shows that on average they are twice as large, which implies that ttk1e11 mutant cells have undergone an extra round of mitotic division.
In mosaic egg chambers in which border cells retain ttk[+] function, border cell migration is completed normally. However, homozygous border cells show a severe migration defect and remain at the anterior tip of the stage 10 egg chamber. Homozygous centripetal cells appear to be delayed in their inward migration.
ttk1e11 mutant stage 15 embryos show defects in the separation of tritocerebral and mandibular commissures.
Only 40% of eggs laid by ttk1/ttk1e11 mothers are wild-type,, the rest exhibit a dorsal appendage phenotype, 3% having only the nub of an appendage.
The second mitotic wave is normal in ttk1e11 clones in the eye disc.
Glia undergo ectopic rounds of replication in mutant embryos. Stage 12 embryos have 17.8 +/- 2.23 glia associated with the longitudinal connectives (compared to 9.9 +/- 0.76 in wild-type embryos).
Homozygous clones in the adult eye cause degeneration of the corneal lens and a failure of photoreceptor development. Rhabdomeres of photoreceptors are not observed in clones, but residual cellular structures in the mutant ommatidia are still recognizable. Genetically mosaic ommatidia are not seen near the boundary of the clone. Ectopic neurons are not seen between or below the developing ommatidia in homozygous clones in third instar larvae. Larval eye development seems close to normal in the absence of ttk, although the ommatidial clusters in clones were somewhat disorganised. Cone cell development appears normal. In homozygous clones in the developing pupal eye, some cone cells failed to develop. Photoreceptors appear normal even up to midpupal stage.
The number of lch5 neurons is approximately doubled in homozygous embryos.
Neurons and sheath cells of es and ch organs are duplicated at the expense of support cells. There is no modification of md neurons, they are present in the normal number and pattern.
ttkbose1/ttk1e11 flies have extra R7 photoreceptor cells in some ommatidia.
Embryonic development arrests before dorsal closure. Transformation of ommatidial cells into nonommatidial cell types in mosaic flies.