FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Lsd-11
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General Information
Symbol
Dmel\Lsd-11
Species
D. melanogaster
Name
FlyBase ID
FBal0247947
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Associated Insertion(s)
Cytology
Description

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.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

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.

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
model of  obesity
is exacerbated by AkhR1
is exacerbated by bmm1
is ameliorated by bmmUAS.cGa
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement
Reference
Other
Phenotype Manifest In
NOT suppressed by
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

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.

Xenogenetic Interactions
Statement
Reference

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.

Complementation and Rescue Data
Comments

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.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (2)