The neuroepithelium of aosΔ7 L3 larvae is overgrown compared to wild type. In the subsequent stage, ectopic and precocious neuroblasts are scattered throughout this enlarged neuroepithelium.
Virtually all eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.
argosΔ7/+ flies have normal eyes at 20[o]C.
argosΔ7/argos257, argosΔ7/argosW11 and argosΔ7/argosp1 flies have blisters in the eye.
Eggs derived from females with mosaic argosΔ7 egg chambers have the normal number of two dorsal appendages.
Only 5% of eggs derived from argosΔ7/argosW11 females have defects in dorsal appendage morphology, which include a reduced distance between the two appendages and appendages that are shorter than normal.
argosΔ7/Df(3L)Exel6129 flies have eyes with a roughened appearance and prominent blistering along the posterior margin.
argosΔ7 clones in the eye disc induce the formation of extra photoreceptor cells; 46.2% of ommatidia within these clones have 8 photoreceptor cells, 40.7% of ommatidia have 9, 11.1% have 10 and 1% have 11.
Stage 15 argosΔ7 embryos have ~36 genital disc precursor cells, while wild type embryos have only 22 at this stage.
Stage 16 argosΔ7 homozygous embryos have more oenocytes per cluster than wild-type. Unlike rhoScer\UAS.cdCa; Scer\GAL4en-e16E the oenocyte clusters in these embryos do not show a multi-modal distribution of cell numbers with peaks corresponding to multiples of 3. Analysis of larval oenocyte precursor delamination shows that it occurs continuously rather than in widely spaced cycles with 3 delaminating cells per cycle as seen in wild-type. In the resulting oenocyte clusters terminal differentiation of some oenocytes is blocked or delayed.
63% of ommatidia in argosΔ7/argosA254Δ15 animals exhibit extra R cells. Of those that ommatidia that remain about 47% exhibit misrotations, about 10% exhibit achirality, and about 4% exhibit the wrong chirality. About 43% of ommatidia in argosΔ7/argos5F4 animals exhibit extra R cells. Of those that ommatidia that remain about 45% exhibit misrotations, about 5% exhibit achirality, and none exhibit the wrong chirality. About 11% of ommatidia in argosΔ7/argosrlt animals exhibit extra R cells. Of those that ommatidia that remain about 52% exhibit misrotations, about 1% exhibit achirality, and about 1% exhibit the wrong chirality. Of the misrotated ommatidia just less than half are underrotated.
In argos5F4/argosΔ7 transheterozygotes 45% of adult ommatidia have extra photoreceptors. Many of the ommatidia with a normal complement of photoreceptor cells have polarity defects up to 59% of ommatidia are misrotated, while only 5% appear achiral and usually less than 1% have the wrong chirality. It appears that a transformation of mystery cells to photoreceptor R3/R4 is the cause of the extra photoreceptor cells. When the eye discs of these mutants are examined about 60% of immature clusters exhibit extra photoreceptor precursor cells. In row 7-8 the number of extra cells decreases to about 25%. In the adult only about 15% of clusters have ectopic R3/R4 cells.
argosΔ7/argos05845 escaper adults have extensive blistering along the posterior edge of the eye.
Extra EPCs (eve-positive heart associated or pericardial cells) and DA1 and DO2 founders (and subsequently muscles) are seen in mutant embryos. Additional founders of the P2 and p15 lineages of the developing embryonic mesoderm are seen.
Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity.
Ommatidial spacing is not affected in argosΔ7 somatic clones in the eye, even in very large clones.
The number of chordotonal organs in the lateral cluster is increased from 5 to 6 in mutant embryos. In stage 11 embryos, the oenocyte precursor whorl is enlarged and contains many extra cells and by stage 16 oenocyte clusters containing 15-27 cells are seen.
Homozygous clones in the eye disc that include several ommatidia show no defects in R8 precursor specification. Positioning of R8 precursors is unaffected by mutant cells in posterior columns. In larger clones that are more than 10 ommatidia wide the pattern of R8 specification is disrupted.
Heterozygotes show a quantitative effect on wing shape in intervein regions C and D compared to wild type.
Mutant embryos show a 'cyclops' phenotype in which the optic lobes are enlarged and show dorsal fusion.
Homozygous embryos have missing or malformed H-piece structures.
At stage 16 optic lobes are enlarged and fused. Frontal and hypocerebral ganglion are enlarged and the recurrens nerve is thickened.
Germline clones fail to rescue the female sterile phenotype of Fs(3)Apc.
Germline clones reveal no requirement for argos in the oocyte in patterning the egg, or in the viability or patterning of the embryo. Follicle cell clones cause a fused dorsal appendage phenotype. Larvae hatch from the eggs, with dorsal-ventral pattern unperturbed. argosΔ7/argosW11 hypomorphic females lay a significant proportion of eggs with fused dorsal appendages.
Abnormal CNS axon pattern phenotype. An increase in number of midline glia and lateral chordotonal organs is also observed.
argosΔ5/argosΔ7 embryos exhibit expansion of the denticle belts. Wing, leg, haltere and eye/antenna argosΔ5/argosΔ7 mutant discs can be in vivo cultured.
The number of midline glia cells is increased to an average of 5.3 +/- 0.2 cells per segment in homozygous embryos.
Additional small denticles are often found located anteriorly to the abdominal denticle belts in homozygous embryos, in the most extreme cases forming a complete additional row anterior to row 1. Extra small denticles are also found in row 6, resulting in a slightly higher density of denticles compared to wild-type.
Transheterozygotes with Df(3L)st-g18 die before hatching. Transheterozygotes with Df(3L)st-k7 or Df(3L)st-f13 have rare escapers, adult survivors develop a characteristic eye phenotype, bulging of the posterior part of the eye that spreads into the anterior part.
Homozygous clones in the eye cause extra outer photoreceptors, severity of the phenotype depends on the size of the clone. Homozygotes display severe disruption and broadening of the embryonic head skeleton, broadening of the ventral epidermis as shown by increased distance between the Keilin's organs.