Imprecise excision of the progenitor insertion, resulting in partial deletion of nucleotides -509 to +82 relative to the putative Lsd-1 start site (this deletes sequences encoding amino acid residues 1-28). 2.2kb of the original inserted element remains.
Estimated boundaries of a deletion resulting from the imprecise excsion of P{EP}Lsd-1G4304, which removes sequences from -509 relative to the Lsd-1 translation start site up through amino acid 28. 2.2 kb of residual P element sequences remain.
Homozygotes develop into obese but otherwise normal-looking adults. The obesity phenotype progressively manifests, starting at day 2 of adult life. The obesity phenotype is nutrition dependent; on a high-sugar diet, the cumulative food intake of the mutant flies during the first 6 days of adult life is approximately one-third higher than that of controls and their body fat content is doubled. On a low-sugar diet, both mutant and wild-type controls show a similar food intake, but the mutant flies accumulate up to 50% more body fat than the controls. Activity patterns and total cumulative locomotor activity of mutant and control flies are comparable during obesity development.
Fat body cells of mutant animals have a giant lipid droplet phenotype typical for unilocular fat cells. This phenotype is cell autonomous. The phenotype develops during larval stages, prior to the onset of obesity.
Homozygous, Lsd-11/Lsd-12 and Lsd-11/Df(3R)mbc-30 flies have double the fat content of control flies.
Homozygous and Lsd-11/Lsd-12 flies show increased resistance to starvation compared to control flies. Homozygous flies show incomplete storage fat mobilisation under starvation conditions.
Lsd-11 has increased body size phenotype, non-suppressible by Scer\GAL4fat/Hsap\PLIN1UAS.cBa
Lsd-11, bmm1 has abnormal stress response phenotype
AkhR1, Lsd-11 has abnormal stress response phenotype
Lsd-11 has lipid droplet phenotype, non-suppressible by Scer\GAL4fat/Hsap\PLIN1UAS.cBa
Lsd-11, Lsd-251 has lipid droplet phenotype
Lsd-11 bmm1 double mutant flies are more obese than either single mutant and the double mutants fail to mobilise their fat storage under starvation conditions are hypersensitive to starvation.
Lsd-11 GRHR1 double mutant flies are more obese than either single mutant. The double mutants show resistance to starvation compared to controls.
Expression of bmmScer\UAS.cGa under the control of Scer\GAL4fat suppresses the increase in fat content which is seen in Lsd-11 flies and the double mutant flies are leaner than flies expressing bmmScer\UAS.cGa under the control of Scer\GAL4fat in a Lsd-1[+] background.
Expression of Pka-C1Scer\UAS.cKa under the control of Scer\GAL4fat suppresses the increased fat content seen in Lsd-11 flies.
Lsd-11 Lsd-251 double mutant adults have strongly reduced body fat stores at hatching (in contrast to the normal levels seen in newly hatched single mutants). The double mutants recover to have levels of stored body fat which are similar to those seen in the lean Lsd-251 single mutants within the first 6 days after eclosion. The fat body cells contain large lipid droplets. During aging, the fat content of the double mutants is adjusted to a level between the level seen in each single mutant. Under a starvation/re-feeding scheme, the double mutant flies show attenuated lipid metabolism and re-accumulation compared to controls flies.
The giant lipid droplet and obesity phenotypes seen in Lsd-11 mutants are not rescued by expression of Hsap\PLIN1Scer\UAS.cBa under the control of Scer\GAL4fat.
Lsd-11 is rescued by Lsd-1+t3.5
Lsd-11 is rescued by Scer\GAL4fat/Lsd-1UAS.cBa
Lsd-1+t3.5 rescues the increased body fat content of Lsd-11 flies.
Expression of Lsd-1Scer\UAS.cBa under the control of Scer\GAL4fat rescues the increased starvation resistance seen in Lsd-11 flies. Lipid droplet size is reduced in these animals compared to Lsd-11 single mutants.
One copy of Lsd-1+t3.5 partially rescues the increased starvation resistance seen in Lsd-11 flies.