spin^Δ2b/spin^E14.1 transheterozygotes show small amounts of adult escapers, depending on culture conditions. Adult escapers exhibit progressive locomotor defects, such as difficulty in righting after a fall. These defects worsen during the days after emergence and result in death within 5-12 days. The escapers appear morphologically normal except for a subtle, completely penetrant extra wing vein phenotype.

Germline clones of spin^E14.1 give rise to malformed oocytes. The eggs are between one and two thirds of wild-type length. The dorsal appendages are abnormally formed and their distance is somewhat widened.

spin^E14.1 clones in the retina result in a large number of abnormal membranous inclusions in the cell bodies of the photoreceptors. One population of inclusions contains multilayered membranes often together with partially degraded organelles which are likely to be secondary lysosomes. A second population consists of organelles with a single limiting membrane surrounding many small regularly shaped internal vesicles, which typically represent late endosomes. In the lamina, spin^E14.1 mutant cartridges also accumulate large membranous inclusions mainly in the glial cell bodies but these correspond only to secondary lysosomes and not to late endosomes. The inclusions are present in presynaptic photoreceptor projections and postsynaptic monopolar cells. spin^E14.1 clones do not affect laminar architecture, rhabdomere morphology, number of photoreceptor terminals per cartridge, or number of glial invaginations per photoreceptor terminal.

The larval NMJ of spin^E14.1/spin^Δ2b mutants contain abnormal ultrastructural membrane compartments in the cytoplasm of bnch mutant boutons that are not present in wild-type controls. The excitatory junctional potentials (EJPs) produced by abdominal muscles in 1mM ca²⁺ from spin^E14.1/spin^Δ2b mutants are not significantly different from those produced by wild-type, indicating that exocytosis is not affected in mutants. When motor neurons from the mutants are repetitively stimulated at 10Hz, the amplitude of the EJP measured from spin^E14.1/spin^Δ2b mutants declines to 55-60% of the original response after 10 minutes, while no such decline is observed for wild-type animals. Additionally, spin^E14.1/spin^Δ2b mutant boutons show a significant decrease in the uptake of FM1-43 dye compared with controls. These results indicate that the mutants have a defect in synaptic vesicle endocytosis.

Electroretinogram recordings from 1-day-old flies with mosaic spin^E14.1 eyes are not significantly different to wild type. However, electroretinogram recordings from 40-day-old flies with mosaic eyes reveal reduced depolarization in response to light and smaller or absent on/off transients compared to 40-day-old wild-type flies.