Atg101^6h homozygotes develop slower as larvae take longer to reach either pupal stage or adulthood.

Atg101^6h homozygous adults exhibit significantly shorter and wider midguts: posterior midgut epithelium is thicker, the lumen is wider and the visceral muscles are disorganized. The posterior midgut contains fewer apparently polyploid cells with large nuclei and more apparently diploid cells with small nuclei: (esg-positive) intestinal stem cells and enteroblasts are significantly increased in number and ofter clustered, despite of no change in the overall mitotic index of the gut; enterocytes are decreased in number are larger and show larger nuclei; enteroendocrine cell numbers are unchanged.

Atg101^6h homozygous adults also show wing posture defects and enlarged abdomens, as well as progressively decreased locomotion in negative geotaxis assays, which correlates with signs of neurodegeneration (i.e. accumulation of ubiquitin and Ref(2)p punctate structures in the adult brain).

Atg101^6h prevents both starvation and developmental autophagy, as both starved third instar larvae and wandering late third insta larvae fail to show the expected accumulation of larger autolysosomes (i.e. red-only GFP-RFP-Atg8a dots) in the fat body, and delay midgut histolysis, as the gastric caeca persists at 4h after puparium formation.

Atg101^6h homozygous larvae do not show changes in the number of neuromuscular junction boutons.