FlyBase curator comment: this entry represents a transgenic construct where the particular construct used cannot be determined.
Adult females expressing Atg1TRiP.cUa under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 produce embryos that fail to form autophagosomes at cellularization (which itself appears normal). These embryos also display a much reduced hatching rate.
Atg1RNAi.UAS.cUa, Scer\GAL4VP16.mat.αTub67C has majority die during embryonic stage | maternal effect phenotype, suppressible | maternal effect | partially by mTorRNAi.UAS.cUa, Scer\GAL4VP16.mat.αTub67C
Atg1RNAi.UAS.cUa, Scer\GAL4Tub.PU is a suppressor of abnormal oxidative stress response | adult stage phenotype of Scer\GAL4Tub.PU, Zer1HMS01025
Atg1RNAi.UAS.cUa, Scer\GAL4VP16.mat.αTub67C is a suppressor | maternal effect | partially of majority die during embryonic stage | maternal effect phenotype of Scer\GAL4VP16.mat.αTub67C, mTorRNAi.UAS.cUa
Atg1RNAi.UAS.cUa/Scer\GAL4Cg.PU is a suppressor of autophagosome | somatic clone | third instar larval stage phenotype of wcyA
Expression of Atg1TRiP.cUa driven by Scer\GAL4cg.PU suppresses increases in autophagosomes seen in wcyA/wcyA fat body third instar larval clones.
The low hatching rate of embryos from mothers expressing either TorTRiP.cUa or Atg1TRiP.cUa under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 is nearly completely restored when the two transgenes are expressed simultaneously.