FB2025_01 , released February 20, 2025
Allele: Dmel\GstO2A.UAS
Open Close
General Information
Symbol
Dmel\GstO2A.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0267936
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of GstO2-A coding sequences.

Allele components
Component
Use(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
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
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
NOT Suppressor of
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Expression of GstO2A.Scer\UAS under the control of Scer\GAL4phm.PO does not rescue the embryonic lethality associated with homozygous GstE14KO mutants.

Expression of GstO2A.Scer\UAS under the control of Scer\GAL4Mef2.PU significantly decreases the penetrance of the collapsed thorax phenotype seen in Pink1B9 adults. The increased cell death seen in the flight muscles of 3 day old Pink1B9 adults is also suppressed.

The loss of dopaminergic neurons in the PPL1 cluster of the brain which is seen in 20 day old Pink1B9 flies is significantly suppressed by expression of GstO2A.Scer\UAS under the control of Scer\GAL4ple.PF.

Expression of GstO2A.Scer\UAS using the muscle-specific driver Scer\GAL4how-24B significantly suppresses both the thorax and downturned wing phenotypes found in park1 mutants.

Overexpression of GstO2A.Scer\UAS under the control of Scer\GAL4αTub84B.PL, a ubiquitous driver, suppresses the degeneration of IFMs in park1 mutants. Overexpression results in regular and compact muscle tissues in the dorsal longitudinal IFMs, which are similar to those of wild-type flies except for occasional vacuoles. Overexpression of GstO2A.Scer\UAS appears to prevent degeneration of the IFMs by blocking the activation of the JNK pathway and apoptosis in park1 mutants.

Overexpression of GstO2A.Scer\UAS under the control of Scer\GAL4ple.PF results in significant restoration of the lost DA neurons in 20-day-old park1 mutant flies.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Paraquat sensitivity in GstO21 mutants is rescued through Scer\GAL4αTub84B.PL-driven expression of GstO2A.Scer\UAS.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
CG6673A.Scer\UAS
GstO1A.Scer\UAS
GstO2A.Scer\UAS
GstO2A.UAS
Name Synonyms
Secondary FlyBase IDs
    References (4)