Heterozygous female flies that are homozygous for Shawn¹/Shawn¹ only in their eyes have defective electroretinogram (ERG) responses to light that do not show on or off transients and have a smaller depolarization amplitude compared to controls. Photoreceptor cell bodies in flies with Shawn¹/Shawn¹ mutant retinas display many swollen mitochondria that often lack most of their cristae, vacuolization, and autophagic-like profiles; in addition, mutants harbor numerous terminals with very few organelles such as synaptic vesicles. Similar to controls, ommatidia show on average 7 rhabdomeres. Shawn¹/Shawn¹ third instar larvae show evidence of disrupted mitochondrial function.

Shawn¹/Shawn² third instar larvae maintain synaptic transmission (EJPs) at normal levels during prolonged high-frequency stimulation (recordings from the neuromuscular junction); Shawn¹/Shawn² mutants show significant increases in EJC amplitude at different external Ca[2+] concentrations (0.3, 0.4, 0.5mM) compared to controls ( Shawn¹/Shawn^Δ6.3 mutants also show significant increases at 0.4mM Ca[2+]). Spontaneous mEJCs from Shawn¹/Shawn² mutants are not significantly different to controls and quantal content (EJC/mEJC) is thus increased in mutants; mutants also show elevated paired pulse facilitation. Shawn¹/Shawn² third instar larval NMJs have presynaptic terminals similar to controls, with normal numbers and morphology of synaptic vesicles and active zones and no obvious defects in mitochondrial morphology. Shawn¹/Shawn² third instar larval body wall musculature shows severe degeneration, including swollen mitochondria, electron-dense inclusions and autophagic profiles.