FB2025_01 , released February 20, 2025
Allele: Dmel\fogUAS.cRa
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General Information
Symbol
Dmel\fogUAS.cRa
Species
D. melanogaster
Name
FlyBase ID
FBal0296413
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-fog
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of 1.6kb of fog cDNA sequences (full-length).

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 ( 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

Expression of fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096 results in a strong wing defect in male flies, with complete penetrance. The wings appear short, sometimes stub-like, and at times necrotic. By contrast, female flies appear normal. However, increasing the dosage of fog by either increasing the copy number of Scer\GAL4Bx-MS1096 or fogScer\UAS.cRa leads to wing defects in these females as well.

Animals expressing fogScer\UAS.cRa under the control of Scer\GAL4Mhc.PU exhibit small mitochondria that are spherical or elliptical in shape, indicating fragmentation. This effect is observed in animals raised at both 25[o]C and 28[o]C.

Overexpression of fogScer\UAS.cRa in the developing glia, under the control of Scer\GAL4repo results in 1st or 2nd instar lethality. Mutant embryos exhibit severe glial defects. The longitudinal glia exhibit a disorganised and clumped appearance, and the extension of glial processes appears abnormal.

Overexpression of fogScer\UAS.cRa in neurons under the control of Scer\GAL4elav.PLu or Scer\GAL4elav-C155 generates strong central nervous system defects. The three pairs of 1D4-positive longitudinal axon bundles in the CNS display multiple breaks and fusions and fail to extend along straight pathways. Ectopic midline crossing by 1D4-positive longitudinal axon bundles is observed in 27% of segments. In embryos carrying both Scer\GAL4elav.PLu and Scer\GAL4elav-C155, the percentage of segments with ectopic midline crossing increases to 44%. SNa defects are also observed.

Overexpression of fogScer\UAS.cRa in glia, under the control of Scer\GAL4repo, causes axon guidance defects, producing ectopic midline crossing phenotypes in 23% of segments.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

Scer\GAL4Bx-MS1096, fogUAS.cRa has wing phenotype, suppressible by cta5/cta[+]

Scer\GAL4Bx-MS1096, fogUAS.cRa has wing | male limited phenotype, suppressible by cta5/cta[+]

Scer\GAL4Bx-MS1096, fogUAS.cRa has wing phenotype, suppressible by Ptp52F[+]/Ptp52F18.3

Scer\GAL4Bx-MS1096, fogUAS.cRa has wing | male limited phenotype, suppressible by Ptp52F[+]/Ptp52F18.3

Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of rho-7GD3775 results in a 66-74% suppression of the wing phenotype found upon expression of fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096.

The presence of cta5 strongly suppresses the wing defects seen in male flies expressing fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096.

The presence of Ptp52F18.3 strongly suppresses the wing defects seen in male flies expressing fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096.

Approximately 43.5% of Scer\GAL4Bx-MS1096>fogScer\UAS.cRa/rho-7pΔ1 males show rescue of the wing phenotype whereas 37% show only a partial rescue, indicating that rho-7 is a suppressor of fog signalling.

Expression of Drp1GD10456 results in a 77-83% suppression of the wing phenotype found in male flies expressing fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096, suggesting that loss of mitochondrial fission inhibits fog signalling.

Overexpression of Drp1Scer\UAS.cDa under the control of Scer\GAL4Bx-MS1096, enhances the wing phenotype of Scer\GAL4Bx-MS1096>fogScer\UAS.cRa flies, with males appearing similar to Scer\GAL4Bx-MS1096>fogScer\UAS.cRa males, with corresponding females showing strong wing defects ranging from relatively mild margin defects to strong wing defects that are similar to those in males.

Expression of MarfScer\UAS.cDa under the control of Scer\GAL4Bx-MS1096 suppresses the wing phenotype found upon expression of fogScer\UAS.cRa : in >80% of F1 males, the wings appear normal, whereas the F1 females do not show any wing defects.

Expression of MarfJF01650 under the control of Scer\GAL4Bx-MS1096, leads to a clear enhancement of the wing phenotype found in flies expressing fogScer\UAS.cRa, with complete penetrance: in males, the wings appear small or stub-like, similar to parental males, and all females show short and abnormal wings, indicating that inhibiting mitochondrial fusion through down-regulation of Marf potentiates fog signalling.

Expression of Drp1GD10456 suppresses the mitochondrial defects found upon expression of fogScer\UAS.cRa under the control of Scer\GAL4Mhc.PU.

Expression of WASpScer\UAS.cUa in Scer\GAL4Bx-MS1096->fogScer\UAS.cRa animals suppresses the wing phenotype in approximately 53.3% of animals.

Co-expression of WASpScer\UAS.cUa and fogScer\UAS.cRa, under the control of Scer\GAL4Mhc.PU results in long filamentous mitochondria as opposed to the fragmented forms associated with fogScer\UAS.cRa.

Removal of Ptp52F function in fogScer\UAS.cRa overexpression mutants, through a Ptp52F18.3 mutant background, results in a strong suppression of the CNS phenotype. Only 3% of segments exhibit ectopic midline crossing, as compared to 44% for fogScer\UAS.cRa overexpression (under the control of Scer\GAL4elav-C155 and Scer\GAL4elav.PLu) in a wild-type background. For embryos with one copy of the driver (Scer\GAL4elav.PLu), the phenotype was suppressed from 27% to 5%. The longitudinal tracts appear normal in fogScer\UAS.cRa, Ptp52F18.3 embryos, resembling those seen in Ptp52F18.3 single mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
fogScer\UAS.cRa
fogUAS.cRa
Name Synonyms
Secondary FlyBase IDs
    References (2)