cac^F eye somatic clone cells in 3-day-old flies display synaptic transmission defects as evidenced by the loss of 'on' and 'off' transients in their electroretinogram traces, however, their depolarization amplitude is not significantly different from wild-type rescue flies (i.e. combined with Dp(1;3)DC131 for genomic rescue). In 30-day-old flies the depolarization amplitude as well as the transients are significantly reduced compared to controls.

3-day-old cac^F mutant flies rescued with cac^GR-R1673P display 'on' and 'off' transients that are actually larger compared to wild-type rescue flies but no restoration of transients is observed in cac^F mutants rescued with cac^GR-R1664Q. The depolarization amplitude is comparable among all the various genotypes. The loss of transients as well as the decreased depolarization amplitude observed in cac^F mutant retinal cells at 30 days old flies is only improved in mutant flies of the same age rescued with cac^GR-R1664Q but not cac^GR-R1673P.

30-day old cac^F mosaic flies show a slight change in retinal morphology in the mutant clones but the photoreceptors retain all seven rhabdomeres and normal overall structure compared to cac^F mutants rescued with Dp(1;3)DC131. cac^F flies rescued with cac^GR-R1664Q do not exhibit any obvious photoreceptor defects at this age, whereas flies rescued with cac^GR-R1673P display photoreceptor degeneration (disrupted rhabdomeres, cytoplasm filled with autophagic vesicles).

At the ultrastructural level, in cac^F mutant photoreceptor cells display expanded terminals, accumulation of autophagic vacuoles and signs of synaptic degeneration at the level of lamina where they make connection with laminar neurons. These defects are partially rescued in cac^F;cac^GR-R1664Q flies, but the neurodegeneration is further exacerbated in cac^F;cac^GR-R1673P flies.

cac^F heterozygotes do not display any significant aberrations in their electroretinogram traces not even when combined with either cac^GR-R1673P or cac^GR-R1664Q genomic fragments.

Flies carrying cac^F mutant photoreceptor clones exhibit defects in synaptic transmission. Mosaic photoreceptors at day 3 show aberrantly expanded terminals that are more densely filled with synaptic vesicles when compared to controls. As the flies age the terminals expand further, and the cartridge structure in the lamina is lost. The number of capitate projections and active zones decrease dramatically, whereas the number of mitochondria per terminal is increased. There is an significant accumulation of autophagic vacuoles (AVs), in particular fusion-primed intermediate AVs, in aged photoreceptor terminals.