Sine oculis is present at the birth of the eye primordium, and has a direct role in this process. In mutants there is an increase in cell death in the region of the primordium. Movement of the primordium into the head is arrested at an early stage. Clones of so and of eya mutant cells overproliferate and fail to differentiate into neurons.
Mutant clones retain their epithelial organization and lead to abnormal folding of the disc.
The previously reported cell death phenotype is a secondary result of cell overgrowth. Development of eye tissue in the posterior and lateral regions but not the anterior region of so and eya mutant discs is rescued by ectopic expression of the respective genes. Ectopic expression of so has little or no effect on antennal, wing, or leg disc development, while ectopic eya expression often causes mild growth alterations resulting in extra folds in the epithelium and, rarely, formation of small ectopic ommatidial arrays in the antennal disc. Coexpression of so and eya leads to a dramatic increase in the development of ectopic eye tissue in antennal discs. These ommatidial arrays lead to adult eye structures.