Imprecise excision of the progenitor insertion, resulting in a deletion that removes 246bp flanking the annotated Atg13 transcription start site.
Atg13Δ74/Atg13Δ81 mutant mosaic germline cells are defective in autophagy (as monitored by the lack of lysotracker staining). However, the chimeras are fully fertile with normal egg-laying behavior and hatching rates. There are no defects in egg chamber development or egg morphology. These germline mosaics do not show disruption of nurse cell apoptosis.
Homozygous clones in the larval fat body fail to induce autophagy in response to starvation.
Atg13Δ74/Atg13Δ74 is a non-enhancer of increased cell number | pupal stage phenotype of Df(2R)BSC696/hrmΔ1
Atg13Δ74/Atg13Δ74 is a non-suppressor of increased cell number | pupal stage phenotype of Df(2R)BSC696/hrmΔ1
Atg13Δ74, Scer\GAL4fkh.PH, hrmΔ1/hrm[+] has increased cell number | pupal stage phenotype
Atg13Δ74/Atg13Δ74 is a non-enhancer of salivary gland | pupal stage phenotype of Df(2R)BSC696/hrmΔ1
Atg13Δ74/Atg13Δ74 is a non-suppressor of salivary gland | pupal stage phenotype of Df(2R)BSC696/hrmΔ1
Atg13Δ74, Scer\GAL4fkh.PH, hrmΔ1/hrm[+] has salivary gland | pupal stage phenotype
Autophagy is no longer induced by expression of Atg1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4Cg.PA in clones of cells that are also homozygous for Atg13Δ74.