The P{Mae-UAS.6.11} is inserted in the first intron of the slif gene. The orientation of the insert is opposite to the direction of transcription.
lipid droplet & larval fat body, with Scer\GAL4ppl.PP
lipid droplet & larval oenocyte, with Scer\GAL4Lsp2.PH
lipid droplet & larval oenocyte, with Scer\GAL4ppl.PP
wing (with Df(3L)Δ1AK), with Scer\GAL4Bx-MS1096
Adult females expressing slifUY681 under the control of Scer\GAL4fit.PS show significantly weaker suppression of feeding (on standard food) after pre-feeding with tryptone compared to controls.
Expression of slifUY681, throughout development, under the control of Scer\GAL4ple.PF, but not Scer\GAL4NPF.PU, Scer\GAL4Trh.PB, Scer\GAL4Tdc2.PU, Scer\GAL4ChAT.PU, Scer\GAL4Gad1.3.098, Scer\GAL4Hug.PU or Scer\GAL4386Y, results in a significant reduction in larval food intake, compared to controls; this effect also occurs when a Gal80[ts] transgene is used to restrict expression under the control of Scer\GAL4ple.PF to the 16 hours prior to analysis.
Expression of slifUY681 under the control of Scer\GAL4ple.TH-D', but not Scer\GAL4ple.TH-C, in combination with a Gal80[ts] transgene to restrict expression to the 16 hours prior to analysis, reduces larval food intake and body size, compared to controls.
Central nervous system neuroblasts of fed larvae expressing slifUY681 under the control of Scer\GAL4Cg.PA show a reduction in EdU incorporation compared to controls.
Larvae expressing slifUY681 under the control of Scer\GAL4ppl.PP and raised to the third instar on a standard diet resemble starved wild-type larvae in that lipid droplets aggregate in the fat body. Oenocytes in third instar larvae expressing slifUY681 under the control of Scer\GAL4ppl.PP contain numerous lipid droplets, both in larvae that have been fed on a standard diet or those that have been food-deprived for 14 hours (this contrasts with wild-type larvae, where oenocytes accumulate lipid droplets specifically under starvation conditions).
Expression of slifUY681 under the control of Scer\GAL4Lsp2.PH results in an accumulation of lipid droplets in the oenocytes of fed larvae.
Colored food is present in the gut of Scer\GAL4ppl.PP>slifUY681 animals, showing that these mutants are able to swallow and process food.
When slifUY681 is driven by Scer\GAL4Bx-MS1096 a reduction in size is seen. The animals have phenotypes mimicking amino acid deprivation, exhibiting storage vesicle aggregation in the fat body. When slifUY681 is driven by Scer\GAL4ppl.PP in the fat bodies, despite normal feeding behaviour and processing of food along the digestive tract, larval development is delayed and accompanied by significant growth defects. Growth rate is strongly reduced throughout larval life. When induced at 18oC emerging adults are reduced in size and body weight (54% of wild-type). Stronger induction (at 25oC) provokes a longer developmental delay associated with pupal lethality. Unlike for wild-type flies, a 90% reduction of arginine concentration in the food leads to a dramatic aggravation of the growth defect, with most animals dying as small L2 larvae. This aggravation is not seen after starvation for valine. growth in the salivary glands (a larval endoreduplicating tissue) are less affected than growth in imaginal discs. These larvae also displayed remobilisation of lipid vesicles in fat body cells, as well as a reduction in cell size and endoreduplication levels comparable to the effect of a diet lacking protein.
Flies expressing slifUY681 under the control of Scer\GAL4en-e16E show a significant difference in growth between the posterior compartment of the wing (which expresses Scer\GAL4en-e16E) and the anterior compartment of the wing (internal control).
Pten117, Scer\GAL4Act5C.PP, slifUY681 has increased cell death | somatic clone phenotype, non-enhanceable by Atg5RNAi.UAS, Scer\GAL4Act5C.PP
Pten117, Scer\GAL4Act5C.PP, slifUY681 has increased cell growth rate | somatic clone phenotype, non-enhanceable by Atg5RNAi.UAS, Scer\GAL4Act5C.PP
Scer\GAL4ple.PF, slifUY681 has abnormal feeding behavior | larval stage phenotype, suppressible | partially by Gcn2RNAi.UAS.cUa, Scer\GAL4ple.PF
slifUY681/Scer\GAL4Act5C.PP is an enhancer of increased cell death | somatic clone phenotype of Pten117
slifUY681, Scer\GAL4Act5C.CoinFLP-FRT is a suppressor | somatic clone of neoplasia | somatic clone | third instar larval stage phenotype of Ras85DV12.UAS, Scer\GAL4Act5C.CoinFLP-FRT, dlg1GD4689
slifUY681, Scer\GAL4Act5C.CoinFLP-FRT is a suppressor | somatic clone of abnormal size | somatic clone | third instar larval stage phenotype of Ras85DV12.UAS, Scer\GAL4Act5C.CoinFLP-FRT, dlg1GD4689
slifUY681, Scer\GAL4Act5C.CoinFLP-FRT is a suppressor | somatic clone of eye-antennal disc | somatic clone | third instar larval stage phenotype of Ras85DV12.UAS, Scer\GAL4Act5C.CoinFLP-FRT, dlg1GD4689
slifUY681/Scer\GAL4Act5C.PP is a suppressor of eye | somatic clone phenotype of Pten117
Third instar larval eye-antennal imaginal disc clones co-expressing dlg1GD4689 and Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.CoinFLP-FRT, in combination with Dicer-2 for efficient RNAi, form invasive tumors, whose size is significantly reduced by the additional clonal co-expression of slifUY681.
Expression of slifUY681 in Pten117 mutant clones results in a slight reduction of the mutant tissue under normal conditions. Under starvation conditions (10g/l yeast), these double mutant cells are almost completely eliminated. This loss of Pten117 mutant tissue is accompanied by a massive increase in apoptosis. The structure of adult eyes in these mutants are wild-type, indicating that the surrounding tissue is able to compensate for the loss of the clones.
Knockdown of Atg5, through expression of Atg5dsRNA.Scer\UAS, does not impact on the initial growth of Pten117 clones with reduced slif function (through expression of slifUY681).
Blocking apoptosis, through expression of BacA\p35Scer\UAS.cHa in Pten117 clones with diminished slif function (through expression of slifUY681), delays the collapse of the clones but they are absent from adult eyes.
slifUY681 is partially rescued by slifUAS.cCa/Scer\GAL4Bx-MS1096