FB2024_03 , released June 25, 2024
Allele: Dmel\Sema1aΔ5.UAS
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General Information
Symbol
Dmel\Sema1aΔ5.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0335706
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 an internally deleted form of Sema1a.

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 Sema1aΔ5.Scer\UAS under the control of Scer\GAL4elav.PLu in embryos does not induce significant increase in axon pathfinding defects relative to controls.

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

The moderate axon pathfinding defects (defasciculation defects in intersegmental nerve b, ISNb, motor axons very infrequent lateral axon tract disruptions in the central nervous system) characteristic for embryos expressing pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu are partially exacerbated by co-expression of Sema1aΔ5.Scer\UAS (it increases the frequency of defects in the central nervous system but not in the ISNb) and in addition, the embryos also display midline crossing defects.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Sema1aΔ5.Scer\UAS under the control of Scer\GAL4sca-537.4 strongly rescues the axon guidance defects characteristic for Sema1ak13702 homozygous embryos - the defects in the central nervous system are almost completely suppressed but the frequency of defasciculation irregularities in the intersegmental nerve b is only partially decreased and remains elevated compared to wild-type controls.

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
Sema1aΔ5.Scer\UAS
Sema1aΔ5.UAS
Name Synonyms
Secondary FlyBase IDs
    References (1)