Late pupae expressing
TorTED.Scer\UAS under the control of
Scer\GAL4ninaE.PU and reared in constant light conditions do not present any obvious defects in rhabdomere structure or in endomembranes in photoreceptors, as compared to controls.
Scer\GAL4bs.PM-mediated expression of
TorTED.Scer\UAS results in decreased terminal cell branching and induction of long, branched autocellular, seamed tubes extend well beyond the terminal cell nucleus.
TorTED.Scer\UAS-expressing clones (generated using MARCM and
Scer\GAL4ppk.PG) show relatively mild dendrite growth defects in the large C4da dendritic arbors.
In contrast to wild-type, transgenic flies expressing
Scer\GAL4ppl.PP>
TorTED.Scer\UAS and reared on medium supplemented with Apis mellifera royal jelly do not show increased body size. However, similarly to wild-type flies in response to royal jelly, they display shortened developmental time compared with flies reared on control medium.
Expression of
TorTED.Scer\UAS under the simultaneous control of both
Scer\GAL4Scer\UAS.cHa and
Scer\GAL4tin.cBa does not rescue the increase in triglyceride levels caused by a high-fat diet. However, the heart defects normally caused by a high-fat diet are rescued in these animals.
Expression of
TorTED.Scer\UAS in the eye under the control of
Scer\GAL4GMR.PU results in retinal degeneration. At 14 days old, degenerating photoreceptor cells display large autophagosomes.
When expression is driven by
Scer\GAL4Lsp2.PH, in the larval fat body, autolysosomes show a marked increase in size (up to 10 microns), a 30% increase in autophagic area, a reduction of cytoplasmic area and disappearance of structures labelled with
Hsap\MLP3BScer\UAS.T:Avic\GFP-EGFP alone. Autolysosomal structures are less acidic than in wild type. Fat droplets accumulate, abnormally.
When
TorTED.Scer\UAS is driven by
Scer\GAL4ppl.PP in the fat body vesicle aggregation and restricted endoreduplication is seen. This is associated with a developmental delay and a weak growth defect.