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General Information
Symbol
Dmel\Sesn8A11
Species
D. melanogaster
Name
FlyBase ID
FBal0246585
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dSesn8A11
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

Deletion of Sesn resulting from the imprecise excision of P{XP}Sesnd04539 reported at Sesn[8A11]

2R:19601349..19621707 in R5 coordinates.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Deletion that removes the entire Sesn coding sequence (the deletion also removes the CG18128 gene that is nested in intron of Sesn). Generated by imprecise excision of P{XP}Sesnd04539.

Caused by aberration
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 ( 0 )
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

Homozygous Sesn8A11 mutants do not exhibit developmental abnormalities.

Fat bodies of homozygous Sesn8A11 mutant larvae contain more lipids than do those of wild-type animals.

The heart function of homozygous Sesn8A11 mutants is compromised, as manifested in arrhythmia and decreased heart rate. Sesn8A11 mutant hearts are dilated during both the diastolic and systolic phases. Myofibrils of Sesn8A11 mutant hearts display structural disorganisation.

20-day old Sesn8A11/Sesn3F6 mutant flies show degeneration of thoracic muscles with loss of sarcomeric structure, including discontinued Z discs, disappearance of M bands, scrambled actomyosin arrays, and diffused sarcomere boundaries. Such defects are only partially observed in very old wild-type flies (~90 days).

Despite its normal appearance, muscle from 5-day-old Sesn8A11/Sesn3F6 mutant flies exhibit mitochondrial abnormalities, including rounded shape, occasional enlargement, and disorganisation of cistae, which are also observed in 20-day old mutants.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Sesn8A11 is a non-enhancer of visible phenotype of S6kKQ.UAS, Scer\GAL4ap-md544

Phenotype Manifest In
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The growth-promoting effect of InRScer\UAS.Exel overexpression via Scer\GAL4ap-md544 is enhanced in a homozygous Sesn8A11-mutant background

The growth-promoting effect of Akt1Scer\UAS.Exel overexpression via Scer\GAL4ap-md544 is enhanced in a homozygous Sesn8A11-mutant background

Sesn8A11 does not enhance the Scer\GAL4ap-md544-driven S6kSTDETE.Scer\UAS-stimulated cell growth in the wing.

Sesn8A11 does not enhance the growth suppression resulting from Scer\GAL4ap-md544-driven InRK1409A.Scer\UAS expression in the wing.

Sesn8A11 does not enhance the growth suppression resulting from Scer\GAL4ap-md544-driven S6kKQ.Scer\UAS expression in the wing.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of SesnC86S.Scer\UAS.T:Hsap\MYC via Scer\GAL4hs.PB in Sesn8A11/Sesn3F6 mutants prevents muscle degradation.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (3)