Ovarian follicle cell clones of Atg1Δ3D
exhibit impaired autophagy induction.
Chimeric ovaries composed from an Atg1Δ3D
hemizygous germline and wild-type follicle cells are defective in autophagy, as starvation does not induced lysotracker staining in the mutant germline cells, but in the enveloping wild-type follicle cells. Atg1Δ3D
germline chimeras develop functional ovaries, and their egg-laying behavior and hatching rates are indistinguishable from sibling control chimeras, albeit the offspring develop with a delay of 2 days. When the Atg1Δ3D
germline chimeras are crossed with Atg1Δ3D
heterozygous males, the resulting Atg1Δ3D
homozygous mutant animals die in late larval stages, similar to Atg1Δ3D
homozygous mutants derived from heterozygous mothers. There are no defects in egg chamber development or egg morphology.
Heat-shock induced mitotic recombination results in Atg1Δ3D
homozygous mutant follicle cell clones in 69% of the egg chambers with most of them being mosaic. Flies containing Atg1Δ3D
mutant follicle cell clones lay very few eggs that resemble those generated by irradiation, lacking dorsal appendages and embryonic cuticle, and only 5% of the eggs hatched. Approximately 89% of the eggs laid by females containing Atg1Δ3D
mutant follicle cell clones exhibit dorsal appendage defects; consequently, only 11% of the chimeric eggs hatched. Defective dorsal appendage formation is only observed in 15% of the eggs containing control clones, and 58% of the control eggs hatched. Given that 15% of the control eggs show egg defects, the frequency of the egg phenotype that is solely due to the Atg1Δ3D
deletion (74%) is in accordance with the frequency of follicle cell clones observed in Atg1Δ3D
chimeras (69%), suggesting that almost every egg chamber containing Atg1Δ3D
mutant follicle cell clones results in defective eggs.