FB2024_03 , released June 25, 2024
Allele: Dmel\AblKN.UAS
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General Information
Symbol
Dmel\AblKN.UAS
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Hsouna
FlyBase ID
FBal0285361
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-AblKN
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of a kinase-inactive (K417N) Abl mutant.

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

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4insc-Mz1407 has no embryonic commissural phenotype.

Expression of AblKN.Scer\UAS using Scer\GAL4ftz.ng or Scer\GAL4elav.PLu causes at least one axon bundle to cross the midline inappropriately in 11-20% of embryos examined.

Co-expression of AblScer\UAS.cHa and AblKN.Scer\UAS in the Scer\GAL4ftz.ng pattern suppresses all abnormal axonal crossovers.

Co-expression of Ablftz.PH and AblKN.Scer\UAS suppresses all abnormal axonal crossovers.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4insc-Mz1407 in fra3 heterozygotes has no embryonic commissural phenotype.

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4insc-Mz1407 in fra3/fra4 embryos significantly increases the frequency of thin and missing posterior commissure defects.

Less than 10% of fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>AblKN.Scer\UAS exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).

Compared with 26% of heterozygous robo1 mutants exhibiting inappropriate crossovers, expression of AblKN.Scer\UAS in the Scer\GAL4ftz.ng pattern results in almost all (95%) embryos exhibiting several axon bundles crossing the midline.

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.

Expression of AblKN.Scer\UAS in a subset of neurons under the control of Scer\GAL4ftz.ng partially suppresses the comm1 commissure phenotype.

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 (3)
Reported As
Symbol Synonym
AblKN.Scer\UAS
AblKN.UAS
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Hsouna
Secondary FlyBase IDs
    References (2)