ATP6AP2^Δ1 homozygotes bearing ATP6AP2^L98S or ATP6AP2^ΔKKxx display severe mortality during the pupal stage; the surviving adults display poor mobility, decreased or absent climbing capabilities, blistered wings, and reduced head size, and die 3 to 4 days after eclosion, as compared to controls. ATP6AP2^Δ1 homozygotes bearing ATP6AP2^+t2.6 or ATP6AP2^AxxA are viable.

ATP6AP2^Δ1 homozygous third instar larvae bearing ATP6AP2^L98S display a severe increases in the number of both optic lobe neuroblasts and of both optic lobe and central brain neurons (during mid-to-late third instar), and display a severe increase in the size of fat body lipid droplets, as compared to controls. In a ATP6AP2^Δ1-homozygous background, ATP6AP2^L98S clones exhibit significant increases in the size of lipid droplets and in the number of autophagosomes/lysosomes (identified as Lysotracker-positive or Atg8a-positive puncta) in the third instar larval fat body, as compared to neighboring ATP6AP2^T:Hsap\MYC clones.

Homozygous clones result in planar cell polarity phenotypes which are generally stronger in the pupal than in the adult stages. In the pupal wing, a significant delay in prehair formation and an occasional multiple wing hair phenotype are seen. In the adult, hair and bristle polarity defects are seen in the adult wing and notum respectively.