FB2024_03 , released June 25, 2024
Allele: Dmel\apttdf-PΔ3
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General Information
Symbol
Dmel\apttdf-PΔ3
Species
D. melanogaster
Name
FlyBase ID
FBal0082192
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
aptPΔ3
Key Links
Allele class
Nature of the Allele
Allele class
Cytology
Description

Deletion of the first exon and about 1kb of the first intron.

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

Heterozygous flies show a dramatic reduction in ethanol sedation sensitivity compared to wild type.

Egg chambers containing homozygous apttdf-PΔ3 mutant clones in stage 10 egg chambers contain 1-7 additional invasive "stretched border cells", often dramatically stretched out and trailing behind the main cluster. This phenotype is observed even if only a few anterior follicle cells are mutant, but no stretched border cells are seen in wild type cells. No egg chambers are seen where the border cells are the only mutant cells.

apttdf-PΔ3 homozygous embryos have breakages in the CNS axon tracts and tracheal networks.

Egg chambers of females with homozygous germline clones arrest development in early oogenesis (approximately stage 6) and the oocyte fails to differentiate, with all nuclei becoming polyploid. The egg chambers then degenerate. Some egg chambers have an abnormal number of nuclei.

Stereotypic outgrowth of tracheal branches is severely disrupted in mutant embryos. Mutants show variable tracheal defects. Embryos fail to perform germ band retraction. Embryos derived from germline clones exhibit a severe and consistent tracheal phenotype: lack of tracheal branch outgrowth and tracheal pit formation. Mutant embryos also show specific defects in the central nervous system, stalled germ band retraction and defects during head formation.

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

Embryos derived from a cross of wild-type males to females heterozygous for aretQB and also heterozygous for apttdf-PΔ3 occasionally have head defects (these defects are not seen in embryos derived from females singly heterozygous for aretQB or apttdf-PΔ3). This phenotype is largely suppressed if the females are also heterozygous for nosL7.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of aptScer\UAS.cEa under the control of Scer\GAL4Crz.PU completely rescues the reduced ethanol sedation sensitivity of apttdf-PΔ3/+ flies.

Mutant phenotype can be rescued by Scer\GAL4btl.PS-mediated expression of aptScer\UAS.cEa : tracheal branches grow out and develop the tracheal network including a dorsal trunk. Lack of germ band retraction is not rescued.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (6)