pros17 mutants that are also heterozygous for pros17 show a much more severe lens phenotype than either individual mutant, with many ommatidia having reduced, defective, or missing lenses. These mutants also display a reduced number of cone cells per ommatidia.
Overexpression of prosL.Scer\UAS under the control of Scer\GAL4sev.EP in homozygous svspa-pol mutant eyes results in a significant increase in R7 photoreceptor numbers, with three to four often present in individual ommatidia. In addition, no cone cells are detected and adult lenses fail to form.
svspa-pol ttk1 double mutant eyes show a much stronger rough eye phenotype than either single mutant: the surface of the eye is nearly flat with irregularly spaced bristles. Only a few malformed ommatidia, many of which have open holes at their apices, are visible. Photoreceptors in the remaining ommatidia have strongly deformed rhabdomeres. svspa-pol ttk1 pupal eye discs have no cone cells.
The increased cell death seen in svspa-pol eye discs is blocked by BacA\p35GMR.PH, although the adult eye is not rescued in these flies, and it lacks cone cells but has excess secondary pigment cells.
The svspa-pol eye phenotype is enhanced by Poxnhs.sev, with the eye lacking all lenses and most bristles. The number of cone cells present in mid-pupal eye discs is reduced compared to svspa-pol single mutants and those that are seen are smaller than normal and seem to be undergoing apoptosis. Flies carrying two copies of Poxnsv.PJ in a svspa-pol/+ background have a weak rough eye phenotype, which is stronger in a homozygous svspa-pol background.
Hadorn, Jan. 1951.