The co-expression of Tsc1^UAS.cGa and gig^UAS.cTa under the control of Scer\GAL4^GMR.long leads to a small but significant decrease in ommatidia area, as compared to controls.

Under standard nutritional conditions, larval fat body clones co-expressing Tsc1^UAS.cPa and gig^UAS.cTa under the control of Scer\GAL4^Act.PU show a significant increase in autophagosomes (identified as mCherry-Atg8 puncta).

Adult females simultaneously expressing Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^fit.PS show significantly weaker suppression of feeding (on standard food) after pre-feeding with tryptone compared to controls.

Co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^phm.PO (using tub-Gal80ts to limit the time of expression to late L2/L3 larval stages) or the Scer\GAL4^P0206 driver results in an almost complete loss of lipid droplets from the prothoracic gland cells in third instar larvae.

The accumulation of lipid droplets observed in prothoracic gland cells of third instar larvae expressing Npc1a^KK101077 under the control of either Scer\GAL4^phm.PO or Scer\GAL4^P0206 is prevented by co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa.

Co-expression of Tsc1^Scer\UAS.cGa and gig^Scer\UAS.cTa driven by Scer\GAL4^GMR.PF (to induce autophagy) partially suppresses age-dependent retinal degeneration (loss of rhabdomeres from photoreceptors) in trp^P365/+ flies.

The co-expression of Tsc1^Scer\UAS.cPa and gig^Scer\UAS.cTa under the control of Scer\GAL4^{E(spl)m6-BFM.PF} leads to significantly decreased numbers of abdominal lateral, dorsal and ventral adult muscle precursor cells in mid-third instar larvae, as compared to controls.

Oenocytes of larvae expressing both Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of the Scer\GAL4^Adh.PF driver accumulate lipid droplets regardless of their fed/starved status.

Co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa suppresses the enlarged bouton phenotype seen when Vap-33A^{P58S.cRa.Scer\UAS} is expressed under the control of Scer\GAL4^elav-C155.

Co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa has no effect on bouton size.

Reduction of TORC1 through expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa (under the control of Scer\GAL4^GMR.PU) suppresses the overgrowth of Pten¹¹⁷ mutant tissue.

Expression of Tsc1^Scer\UAS.cPa and gig^Scer\UAS.cTa suppresses the dendrite pruning defects seen in ddaC neurons expressing lin19^GD9650 under the control of Scer\GAL4^ppk.PG at 16 hours after pupariation.

Scer\GAL4^{Myo31DF-NP0001}-mediated co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa results in smaller midguts at 0h relative puparium formation (RPF) compared to controls. These midguts appear to undergo rapid degradation and are particularly fragile.

The midgut phenotype seen in Tsc1^Scer\UAS.cTa, gig^Scer\UAS.cTa Scer\GAL4^{Myo31DF-NP0001} animals is suppressed by co-expression of Atg1^GL00047.

The midgut phenotype seen in Tsc1^Scer\UAS.cTa, gig^Scer\UAS.cTa Scer\GAL4^{Myo31DF-NP0001} animals is suppressed by co-expression of Atg18^VDRC.cUa.

Central nervous system neuroblasts of fed larvae co-expressing gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cTa under the control of either Scer\GAL4^Cg.PA or Scer\GAL4^nab show a reduction in EdU incorporation compared to controls.

Central nervous system neuroblasts of fed second instar larvae co-expressing gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cTa under the control of Scer\GAL4^n-syb.PS show no significant difference in EdU incorporation compared to controls.

Central nervous system neuroblasts of fed second instar larvae co-expressing gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cTa under the control of Scer\GAL4^repo.PU show a reduction in EdU incorporation compared to controls.

Coexpression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^arm.PS rescues the aberrant heart phenotypes normally caused by a high-fat diet.

Coexpression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^Lsp2.PH rescues the increase in triglyceride levels and the heart defects normally caused by a high-fat diet.

Coexpression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the simultaneous control of both Scer\GAL4^Scer\UAS.cHa and Scer\GAL4^tin.cBa does not rescue the increase in triglyceride levels caused by a high-fat diet. The heart defects that are normally caused by a high-fat diet are also not robustly rescued in these animals.

Co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa (together forming the tuberous sclerosis complex) under the control of Scer\GAL4^e22c does not affect cell death in the posterior compartment of the wing discs seen upon expression of hppy^Scer\UAS.cLa.

Ectopic expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^ey.PH suppresses the growth of the developing eye.

Co-expression of S6k^Scer\UAS.cMa suppresses the reduction in growth of the developing eye seen upon expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^ey.PH.

Ectopic expression of Hr46^EY05451, combined with Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa, in the developing eye under the control of Scer\GAL4^ey.PH, largely counteracts the growth-suppressive effects of Tsc1 and gig.

Ectopic expression of Hr46^EY10268, combined with Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa, in the developing eye under the control of Scer\GAL4^ey.PH, largely counteracts the growth-suppressive effects of Tsc1 and gig.

norpA³⁶ -mediated photoreceptor degeneration is significantly suppressed by overexpression of gig^Scer\UAS.cTa under the control of Scer\GAL4^GMR.PU.

Overexpression of gig^Scer\UAS.cTa under the control of Scer\GAL4^GMR.PU does not attenuate photoreceptor cell death in ninaE^RH27 flies and even has converse effects.

Expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^Act5C.PP results in a significant reduction in fat-body cell size. This reduction in cell size is also observed in a Pi3K59F^Δm22 background.

Co-overexpression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in fat-body cells under the control of Scer\GAL4^Act5C.PP induces the formation of autolysosomes in fed conditions. Over-expression in a Pi3K59F^Δm22 mutant animal does not result in the induction of autolysosome formation.

Expression of Tsc1^Scer\UAS.cGa and gig^Scer\UAS.cGa under the control of Scer\GAL4^arm.PS rescues lethality in 40% of Pten³/Df(2L)flp170B animals.

Co-expression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa under the control of Scer\GAL4^ppl.PP results in a marked accumulation of large lipid droplets in the oenocytes of 100% of fed larvae (this contrasts with wild-type larvae, where oenocytes accumulate lipid droplets specifically under starvation conditions).

Overexpression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in a specific subset of cells within the wing imaginal discs (under the control of Scer\GAL4^{Scer\FRT.Act5C} decreases the clone size compared to wild-type controls. This overexpression results in a dramatic reduction in wing marginal bristle size.

Overexpression of Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in a specific subset of cells within the wing imaginal discs (under the control of Scer\GAL4^Bx-MS1096 decreases the clone size compared to wild-type controls. This overexpression results in a dramatic reduction in wing marginal bristle size.

Co-expression of gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cTa under the control of Scer\GAL4^ey.PH results in flies with smaller eyes than normal. This small eye phenotype is enhanced if the flies are also mutant for one of hiw^ND8, hiw^EP1305, hiw^ND42, hiw^ND69 or hiw^EMS.

When Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa are driven together by Scer\GAL4^ppl.PP in the fat body, vesicle aggregation and restricted endoreduplication is seen in the fat body and a growth defect is also seen.

When Tsc1^Scer\UAS.cGa and gig^Scer\UAS.cTa are driven together by Scer\GAL4^ppl.PP in the fat body, vesicle aggregation and restricted endoreduplication is seen in the fay body and a growth defect is also seen.

Tsc1^Scer\UAS.cPa; gig^Scer\UAS.cTa; Scer\GAL4^GMR.PF animals have small eyes. This growth suppression is partially reversed by Rheb^Scer\UAS.cSa.

Ommatidial size in Scer\GAL4^GMR.PF/+; Tsc1^Scer\UAS.cTa, gig^Scer\UAS.cTa/+ flies is reduced to 0.68 of wild-type. The large size and disorganisation of ommatidia in Scer\GAL4^GMR.PF/+; Rheb^EP50.084/+ flies is largely suppressed by Tsc1^Scer\UAS.cTa with gig^Scer\UAS.cTa (ommatidial are = 0.95 of wild-type size and are only slightly disorganised.

Co-expression of gig^Scer\UAS.cGa and Tsc1^Scer\UAS.cGa when driven by Scer\GAL4^Bx-MS1096 leads to a dramatic reduction in wing size. There is a 72% reduction in wing size and a 65% reduction in cell size.

Coexpression of gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cPa under the control of Scer\GAL4^ey.PH results in a significant decrease in overall eye size and number of ommatidia. Coexpression of gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cPa under the control of Scer\GAL4^GMR.PF results in eyes that are flatter and smaller than normal but which contain normal numbers of ommatidia. These ommatidia are 30% smaller than normal. The small ommatidium size caused by coexpression of gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cPa under the control of Scer\GAL4^GMR.PF is suppressed by coexpression of S6k^Scer\UAS.cWa. Coexpression of gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cPa in the posterior compartment of the wing under the control of Scer\GAL4^en-e16E results in a significant decrease in cell size (48% reduction), cell number (15% reduction) and size of the wing. The changes in cell size and number are limited to the posterior compartment of the wing. This combination results in 65% pupal lethality. Coexpression of both gig^Scer\UAS.cTa and Tsc1^Scer\UAS.cPa (but not either gig^Scer\UAS.cTa or Tsc1^Scer\UAS.cPa alone) rescues the lethality and extra ommatidia phenotype of flies expressing InR^Scer\UAS.cHa under the control of Scer\GAL4^ey.PH.

Expression of both Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in the eye under the control of Scer\GAL4^ey.PH results in a much smaller eye than normal. Coexpression of BacA\p35^Scer\UAS.cHa does not alter this phenotype. Coexpression of both CycD^Scer\UAS.cDa and Cdk4^Scer\UAS.cMa fully suppresses the phenotype. Coexpression of CycD^Scer\UAS.cDa partially suppresses the phenotype. Coexpression of CycE^Scer\UAS.cLa fully suppresses the phenotype. Coexpression of dm^Scer\UAS.cZa or S6k^Scer\UAS.cWa suppresses the phenotype. Addition of one copy of Cdk4³, CycE⁰⁵²⁰⁶, CycA⁰³⁹⁴⁶, Ras85D^e1B enhances the phenotype. Coexpression of Pten^Scer\UAS.cGb enhances the phenotype. Expression of both Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in the developing eye under the control of Scer\GAL4^GMR.PF reduces the growth of postmitotic cells. Expression of both Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in the posterior compartment of the wing under the control of Scer\GAL4^en-e16E reduces its size by approximately 2-fold. Cell density in the posterior compartment is approximately 60% higher than in control wings. Expression of both Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in clones in the wing imaginal disc under the control of Scer\GAL4^Act5C.PP results in a reduction in the size of cycling cells. These cells also show an increase in the population of cells in G1 at the expense of those in S phase. The proportion of cells in G2 is unchanged. All phases of the cell cycle are lengthened; G1 is lengthened by 75%, G2 by 47% and S phase by 12%. Expression of both Tsc1^Scer\UAS.cTa and gig^Scer\UAS.cTa in the wing imaginal disc under the control of Scer\GAL4^Act5C.PP results in clones that are smaller than control clones. Coexpression of BacA\p35^Scer\UAS.cHa does not alter this phenotype.