The retina of animals containing homozygous eyes is indistinguishable from that of controls at mid-pupal development (44 hours after puparium formation). However, by eclosion, the retina is disrupted; although apparently normal rhabdomeres are still visible, photoreceptor cells bodies are variable in size and the array of ommatidia is disordered. Five days after eclosion, the phenotype is more severe; many cell bodies are swollen, and many have lost their rhabdomeres.

At eclosion, some photoreceptor cell terminals in the lamina lack mitochondrial profiles, while other contain small, abnormal mitochondria in animals containing homozygous retinas. The mean ratio of the volume of mitochondrial profiles per photoreceptor cell terminal volume is 0.121 +/- 0.018 in the mutant animals, compared with 0.224 +/- 0.015 in controls. The mitochondria in the mutant terminals are often abnormal in morphology, having irregular invaginations. Multi-lamellar bodies, which are characteristic of neural degeneration, are seen. Five days after eclosion, the mutant photoreceptor cell terminals in the lamina are severely degenerated.

The synaptic terminal degeneration and damage to the retina seen in flies with homozygous retinas is not suppressed if the flies are reared in the dark.

SdhA¹¹¹⁰ has eye photoreceptor cell | somatic clone phenotype, non-suppressible by Miro^Sd32