FB2024_03 , released June 25, 2024
Allele: Dmel\srlKG08646
Open Close
General Information
Symbol
Dmel\srlKG08646
Species
D. melanogaster
Name
FlyBase ID
FBal0148128
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Srl1
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description
Mutations Mapped to the Genome
Curation Data
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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

srlKG08646/srlKG08646 flies exhibit an age-dependent defect in climbing ability, loss of dopaminergic neurons from the PPL1 and PPM3 clusters; mitochondria in dopaminergic neurons from these flies exhibit a significant decrease in size, and mitochondria in the flight muscle are visibly more fragmented, as compared to controls.

srlKG08646/srlKG08646 flies have a significantly reduced lifespan compared to controls. Fecundity in mutant females (but not males) is severely compromised; ovaries develop more slowly and carry about half the number of ovarioles compared to wild type.

Homozygous srlKG08646 mutant adults are viable. srlKG08646 females are sterile. Both mutant males and females have an approximately 25% reduction in wet weight compared with controls. When normalised to body weight, reduced lipid and glycogen levels are observed in adult males demonstrating metabolic defects. Size defects are not observed when external structures derived from imaginal discs, such as wings or legs, are analysed.

A trans-heterozygous combination of srlKG08646 with Df(3R)ED5046 does not lead to a further decrease in adult weight compared with srlKG08646 homozygous animals.

Whereas control larvae enter the third instar 72 h after egg deposition (AED) and pupate 120 h AED, srlKG08646 mutants enter with a 12-14-h delay, and pupate with a 24-h delay.

The larval fat body of homozygous srlKG08646 mutants show normal abundance of mitochondria. The morphology of mitochondria appear normal in srlKG08646 mutants.

Enlarged lipid droplets are observed in srlKG08646 mutant fat body cells.

Mitochondrial DNA content (normalised to nuclear DNA) in srlKG08646 mutants is similar to that of controls.

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

While both single mutants are viable to adulthood, foxounspecified, srlKG08646 double mutants show larval lethality.

There is no further weight reduction in chicoflp147E/chico1, srlKG08646 double mutants.

srlKG08646, Ets97D613 double mutants show a more severe mitochondrial phenotype in the fat body. The abundance of mitochondria in the fat body is further reduced compared with Ets97D613 single mutants. In contrast to the phenotype in the single mutants, the mitochondria in double mutants are rounded in shape and the inner-mitochondrial cristae are either missing or strongly reduced in size.

Mitochondrial DNA content (normalised to nuclear DNA) in srlKG08646, Ets97D613 double mutants is further increased compared to that of Ets97D613 single mutants.

The delay in pupation is increased to four days in srlKG08646, Ets97D613 double mutants.

The effects of Scer\GAL4αTub84B.PP>InRScer\UAS.cHa overexpression on cell growth and lipid droplet size in fat body cell clones are completely abrogated in a srlKG08646 mutant genetic background.

The effect of Scer\GAL4αTub84B.PP>Pi3K92EScer\UAS.T:Hsap\MYC,T:Hsap\CAAX overexpression on cell growth in fat body cell clones is suppressed by srlKG08646.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (7)