Duplication composed of two non-functional copies of Hr96 which are separated by an Avic\GFPE.3xP3 marker. The 5' copy contains a deletion of exon 4 through the exon 5 splice acceptor. The 3' copy contains a deletion of the start codon and also the deletion of exon 4 through the exon 5 splice acceptor.
Hr961 mutants display elevated levels of cholesterol and decreased levels of triacylglycerol (TAG) compared to controls. Wild type levels of TAG, but not cholesterol, are restored by raising flies on a diet supplemented with pancreatin (a mixture of pancreatic enzymes).
Dp(3;3)Hr961 mutants, comprising Hr961.5' and Hr961.3', display elevated levels of cholesterol and decreased levels of triacylglycerol (TAG) compared to controls. Wild type levels of TAG, but not cholesterol, are restored by raising flies on a diet supplemented with pancreatin (a mixture of pancreatic enzymes).
Hr961 mutants die at a faster rate than wild type controls when transferred to starvation media.
Mutants have wild type levels of glycogen under normal feeding conditions, but have significantly less glycogen upon starvation compared to controls.
Mutants have reduced triacylglycerol (TAG) levels in both fed and starved conditions relative to controls.
Fat body cells of Hr961 mutants are approximately half the size of controls and the size of lipid droplets is reduced. In contrast to controls, no neutral lipids are detected in the midgut epithelium of Hr961 mutants.
Hr961 mutants grown on either low-calorie or high-calorie media display a lean phenotype (as measured by triacylglycerol levels) relative to control animals on the low-calorie diet. These mutants only show a mild decrease in the amount of ingested food relative to controls, and do not appear to have any major defects in dietary fatty acid uptake.
In contrast to control flies, no reduction in fat (triacylglycerol) levels is seen when Hr961 mutants are maintained for 5 days on media supplemented with Orlistat (an over-the-counter weight loss drug). Hr961 mutants do not display detectable neutral lipids in their midgut epithelium either in the presence or absence of Orlistat.
Hr961 mutants maintained on a lipid-depleted medium display a 'lean phenotype' (as measured by triacylglycerol (TAG) levels) compared to controls. The same phenotype is seen when the medium is supplemented with TAG. However, the lean phenotype is effectively rescued by dietary supplementation with free fatty acids.
Hr961.5', Hr961.3' mutants die at a faster rate than wild type controls when transferred to starvation media.
Hr961.5', Hr961.3' mutants have wild type levels of glycogen under normal feeding conditions, but mutants have significantly less glycogen upon starvation compared to controls.
Hr961.5', Hr961.3' mutants have reduced triacylglycerol (TAG) levels in both fed and starved conditions relative to controls.
Fat body cells of Hr961.5', Hr961.3' mutants are approximately half the size of controls and the size of lipid droplets is reduced.
In contrast to controls, no neutral lipids are detected in the midgut epithelium of Hr961.5', Hr961.3' mutants.
Hr961.5', Hr961.3' mutants grown on either low-calorie or high-calorie media display a lean phenotype (as measured by triacylglycerol levels) relative to control animals on the low-calorie diet. These mutants only show a mild decrease in the amount of ingested food relative to controls, and do not appear to have any major defects in dietary fatty acid uptake.
In contrast to control flies, no reduction in fat (triacylglycerol) levels is seen when Hr961.5', Hr961.3' mutants are maintained for 5 days on media supplemented with Orlistat (an over-the-counter weight loss drug). Hr961.5', Hr961.3' mutants do not display detectable neutral lipids in their midgut epithelium either in the presence or absence of Orlistat.
Hr961.5', Hr961.3' mutants maintained on a lipid-depleted medium display a 'lean phenotype' (as measured by triacylglycerol (TAG) levels) compared to controls. The same phenotype is seen when the medium is supplemented with TAG. However, the lean phenotype is effectively rescued by dietary supplementation with free fatty acids.
Hr961.5', Hr961.3' mutants die at a faster rate than wild type controls when transferred to starvation media.
Hr961.5', Hr961.3' mutants have wild type levels of glycogen under normal feeding conditions, but mutants have significantly less glycogen upon starvation compared to controls.
Hr961.5', Hr961.3' mutants have reduced triacylglycerol (TAG) levels in both fed and starved conditions relative to controls.
Fat body cells of Hr961.5', Hr961.3' mutants are approximately half the size of controls and the size of lipid droplets is reduced.
In contrast to controls, no neutral lipids are detected in the midgut epithelium of Hr961.5', Hr961.3' mutants.
Hr961.5', Hr961.3' mutants grown on either low-calorie or high-calorie media display a lean phenotype (as measured by triacylglycerol levels) relative to control animals on the low-calorie diet. These mutants only show a mild decrease in the amount of ingested food relative to controls, and do not appear to have any major defects in dietary fatty acid uptake.
In contrast to control flies, no reduction in fat (triacylglycerol) levels is seen when Hr961.5', Hr961.3' mutants are maintained for 5 days on media supplemented with Orlistat (an over-the-counter weight loss drug). Hr961.5', Hr961.3' mutants do not display detectable neutral lipids in their midgut epithelium either in the presence or absence of Orlistat.
Hr961 mutants are viable and fertile when raised under standard conditions.
Hr961 mutants are sensitive to 1% phenobarbital, displaying significantly less activity in a negative geotaxis assay than control flies. The mutants are also more sensitive to chronic exposure to the pesticide DDT compared to controls.
Dp(3;3)Hr961 mutants (carrying both Hr961.5' and Hr961.3') are viable and fertile when raised under standard conditions.
Dp(3;3)Hr961 mutants (carrying both Hr961.5' and Hr961.3') are sensitive to 1% phenobarbital, displaying significantly less activity in a negative geotaxis assay than control flies. The mutants are also more sensitive to chronic exposure to the pesticide DDT compared to controls.
Scer\GAL4mex1.2.1-mediated expression of magScer\UAS.cSa in Dp(3;3)Hr961 mutants (comprising Hr961.5' and Hr961.3') is sufficient to reduce the elevated cholesterol levels in these animals.
Scer\GAL4bab1-Agal4-5-mediated expression of magScer\UAS.cSa in Dp(3;3)Hr961 mutants (comprising Hr961.5' and Hr961.3') is sufficient to rescue the reduced triacylglycerol levels, but not the elevated cholesterol levels, in these animals.
Scer\GAL4mex1.2.1-mediated expression of magScer\UAS.cSa in Hr961 mutants is sufficient to reduce the elevated cholesterol levels in these animals.
Scer\GAL4bab1-Agal4-5-mediated expression of magScer\UAS.cSa in Hr961 mutants is sufficient to rescue the reduced triacylglycerol levels, but not the elevated cholesterol levels, in these animals.
Expression of magScer\UAS.cSa using Scer\GAL4mex1.2.1 rescues the lean phenotype (reduced levels of whole-animal triacylglycerol) of Hr961 mutants.
Expression of CG5932Scer\UAS.cSa using Scer\GAL4mex1.2.1 rescues the lean phenotype (reduced levels of whole-animal triacylglycerol) of Hr961.5', Hr961.3' mutants.
Hr961 is rescued by Scer\GAL4mex1.2.1/Hr96UAS.cHa
Hr961 is not rescued by Scer\GAL4Cg.PA/Hr96UAS.cHa
Expression of Hr96Scer\UAS.cHa in the midgut using Scer\GAL4mex1.2.1, but not in the fat body using Scer\GAL4Cg.PA, effectively rescues the lean phenotype of Hr961 animals.
Expression of Hr96Scer\UAS.cHa in the midgut using Scer\GAL4mex1.2.1, but not in the fat body using Scer\GAL4Cg.PA, effectively rescues the lean phenotype of Hr961.5', Hr961.3' animals.
