The range of stages during which lethality of alc^Δ12.125 homozygotes, alc^Ad2/alc^Δ12.125 or alc^Δ12.125/Df(2R)Np5 occurs is similar, ranging from first instar larvae to pupal stages.

In alc^Δ12.125/+ adults, negative geotaxis and phototaxis are weakly impaired at 1 day after eclosion and more strongly impaired by 7 days after eclosion. A similar, but more severe phenotype is seen in adults with alc^Δ12.125 homozygous eyes and antennae (inducing homozygous somatic clones in the eye and antenna with Scer\GAL4^ey.PH; Scer\FLP1^Scer\UAS.cDa and killing non-mutant cells in the eye with W^GMR.PG): phototaxis and negative goetaxis are seriously impaired at one day after eclosion and by day 7 both behaviors are absent. These behavioral phenotypes are co-incident with progressive neuro-degeneration in the antenna, retina and optic lobes, characterized by the death of neurons and the formation of vacuoles. They are also co-incident with abnormalities in electro-retinogram (ERG) profiles: on and off transients and the amplitude of depolarization for the stimulus duration are all reduced. Strikingly, progressive neurodegeneration in these animals appears to be activity dependent: degeneration of the retina is dramatically reduced when animals are raised in the dark.

Retinal development in alc^Δ12.125 homozygous clones during pupal stages appears to be normal - photoreceptors are specified and patterned correctly and apical-basal polarity of cells in the developing retina is normal. Normal development in these clones is unaffected by starvation of larvae prior to pupation. However, when these clones are made in the follicle epithelia of starved adults, they do cause defects in apical-basal of the epithelium.