Atg9^d51 homozygotes and Atg9^d51/Atg9^Gal4KO transheterozygotes are near lethal and the few escapers are sterile; Atg9^d51 heterozygotes are viable. Atg9^Gal4KO/Atg9^d51 transheterozygous adults are short lived and exhibit a decrease in climbing capacity, as compared to controls.

Atg9^Gal4KO/Atg9^d51 transheterozygotes exhibit severed gut defects compared to controls: the larval gastric caeca shows a significant increase in size; the adult midgut shows a significant decrease in length, its posterior region shows a significant increase in thickness; the visceral mesoderm layer which surrounding the adult midgut is severely disrupted. The midgut epithelium integrity also seems disrupted compared to controls, as shown by the abnormal permeability to a non-absorbable food dye and by the observation that the epithelium, although still a monolayer, is composed of severely enlarged cells and abnormal apical membrane protrusions that frequently expand into the lumen. These midguts exhibit no significant differences in the numbers of total intestinal cells, intestinal stem cells, enteroendocrine cells or mitotic (PH3-positive) cells, as compared to controls.

Adult midgut enterocytes within Atg9^d51 homozygous clones are significantly larger than control enterocytes.

Atg9^Gal4KO/Atg9^d51 transheterozygotes exhibit autophagy defects, as they show abnormal accumulation of ubiquitinated protein aggregates in the adult thoracic muscles and do not exhibit the expected developmental or starvation-induced autophagy (assessed by the lysosome and autophagosome marker, Lysotracker) in the adult and larval fat body, respectively.