Atg7d77 heterozygous larvae exhibit a mild decrease in the number of RP2 motor neurons, compared to controls.
Atg7d14/Atg7d77 transheterozygous adults exhibit significant decreases in gut diameter and area, but not in gut length, as compared to controls.
Atg7d14/Atg7d77 transheterozygotes are short lived compared to controls.
Mushroom body gamma neurons in Atg7d14/Atg7d77 animals show a very mild pruning defect.
Embryos derived from Atg7d14/Atg7d77 females develop with normal kinetics at least until the end of cellularisation and the beginning of gastrulation. The mutant eggs show a significant delay in the clearance of the paternal mitochondrial derivatives compared to wild type. Early fertilised eggs have multivesicular clusters which are largely devoid of microvesicles.
Compared with wild-type, Atg7d14/Atg7d77 flies show reduce memory scores at a young age (3 days of age), which further declines relative to controls at later time points (20 days of age). Wild-type flies show a decline in both anesthesia-sensitive and olfactory short-term memory, both of which can be ameliorated by spermidine-feeding. Notably, the olfactory short term memory-protective effects of spermidine-administration are eliminated in the mutants.
Atg7d77/Atg7d14 mutants display basal autophagy defects in larval fat body cells.
Flies lacking Atg7d77/Atg7d14 are viable, but unable to induce autophagy.
Eggs derived from Atg7d77 homozygous mutants show a slight reduction in hatching rates compared with heterozygous controls, with 18% of the eggs displaying eggshell defects, suggesting that Atg7 mutations have only minor effects on egg development.
While all seven rhabdomeres are detected in the ommatidia of young (<2 day old) Atg7d77 flies, after 20 days of light/dark cycling, few rhabdomeres are found.
Nutrient-deprived Atg7d77/Atg7d14 mutant flies display reduced levels of autophagy (punctate Lysotracker staining) in region two of the germarium and in stage eight degenerating egg chambers compared to controls.
Fewer apoptotic (TUNEL positive) cells are seen in region two cysts in nutrient-deprived Atg7d77/Atg7d14 mutant flies than are seen in wild type. Degenerating stage eight egg chambers in starved Atg7d77/Atg7d14 mutants show low or no TUNEL-positive staining compared with controls, although nuclear DNA condensation is still observed in these egg chambers.
Atg7d14/Atg7d77 fat body cells show a strong reduction of autophagosomes and autolysosomes following 3 hours of starvation compared to control cells.
Midgut cells of Atg7d14/Atg7d77 larvae show a strong reduction of autophagosomes and autolysosomes compared to control larvae, at the wandering stage, just prior to pupariation. No major defects are seen in elimination of the larval midgut or in adult midgut epithelium formation in Atg7d14/Atg7d77 animals during metamorphosis. However, DNA fragmentation indicative of cell death is greatly reduced in the mutant midgut at the time of pupariation (DNA fragmentation is readily detected at this stage in control midguts) and there is an approximately 4 hour increase in the average time required to complete metamorphosis in the mutant animals.
Under conditions of complete starvation or a sugar-only diet, Atg7d14/Atg7d77 mutants show an accelerated lethality compared to control flies. The mutant flies also show a reduced life span compared to controls under normal environmental conditions.
Atg7d14/Atg7d77 mutants are hypersensitive to treatment with paraquat compared to controls.
Atg7d14/Atg7d77 flies show a significant age-dependent decline in climbing performance. The brains of mutant adults contain ubiquitin-positive inclusion bodies in the neurons, with these structures being seen in 3 day old adults, and increasing in number with age. The brains of 30 day old mutant flies contain dead neurons in addition to the inclusion bodies, show moderate vacuolization and most brain cells show extensive DNA fragmentation (assayed using TUNEL labeling).