Open Close
General Information
Symbol
Dmel\awdj2A4
Species
D. melanogaster
Name
FlyBase ID
FBal0010910
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{lacW} insertion in the 5' untranslated region.

Insertion components
P{lacW}awdj2A4
Product class / Tool use(s)
Encoded product / tool
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 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Homozygous embryos show tracheal defects including ectopic branches. Abnormal sprouting of filopodium-like projections can be seen in some cells.

Tracheal cells of heterozygotes show moderate ectopic migration defects in 71% of embryos, and show severe ectopic migration defects in 10% of embryos.

Mutant embryos have tracheal lumen defects, with a dilated dorsal trunk and ectopic, tortuous tracheal branches.

Homozygous follicle cell clones show defects in epithelial integrity, with the severity of the defect depending on the size of the clone. Cells in smaller clones become flattened but remain adhered to their neighbours. As the clone size increases, gaps in the epithelium and adenoma-like piling up of epithelial cells becomes more common. In the most severe cases, large regions of the epithelium become composed of multiple cell layers and invade deep into the germ cell complex.

Homozygous embryos show ectopic branching in the tracheal network.

81% of heterozygous embryos show ectopic tracheal migration.

awdj2A4 homozygous embryos exhibit major disruption of the tracheal network accompanied by ectopic branching and looping, appearance of a few extra branches or "knobs", and migration abnormalities. By stage 16 in the most severely effected embryos, fragments of the dorsal trunks are scattered throughout the embryo with random, ectopic branches sprouting out. (Note patterning of other late embryonic structures such as midgut are appears normal.). awdj2A4 heterozygous embryos have similar but milder tracheal phenotypes: Segments of dorsal trunk are often mis-positioned and sprout ectopic projections. In addition the dorsal trunks may be fused at the stalk. The fusion is usually accompanied by thickening at the base. In other instances, dorsal branches from adjacent subunits are linked, rather than connecting with their counterparts across the embryonic midline. During the tubule migration phase of tracheal development, the tips of migrating forsal branches in these embryos extend many more stable filopodia like projections than wild-type. These extensions often do not point in the direction of the wild-type migratory path.

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

awdj2A4/awd[+] is an enhancer of embryonic/larval tracheal system phenotype of PuZ22

awdj2A4/awd[+] is an enhancer of presumptive embryonic/larval tracheal system | heat sensitive phenotype of shi1

awdj2A4/awd[+] is an enhancer of dorsal trunk primordium | heat sensitive phenotype of shi1

Suppressor of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Vhl1/+ ; awdj2A4/+ double heterozygous embryos have a severely disrupted tracheal tree with ectopic filopodia and isolated, round cells.

The penetrance and severity of the ectopic tracheal migration phenotype is increased in PurAA17 awdj2A4 double heterozygous embryos compared to either single heterozygote.

The opposing tracheal phenotypes of awdj2A4/+ and Catsup26/+ single heterozygous embryos (ectopic migration and lack of migration respectively) are both partially suppressed in awdj2A4/+ Catsup26/+ double heterozygous embryos.

The penetrance and severity of the ectopic tracheal migration phenotype is increased in PuZ22/+ awdj2A4 double mutant embryos compared to either single mutant.

A awdj2A4 heterozygous background strongly enhances both the penetrance (from 46% of embryos to greater than 80% of embryos) of the ago1/ago3 mutant dorsal trunk phenotype and its expressivity among affected embryos. These embryos also show a much more severe disruption of the entire tracheal system compared to ago1/ago3 mutants.

68.8% of btlH82Δ3/+; awdj2A4/+ transheterozygous embryos have normal tracheal systems, compared to 33.3% in awdj2A4/+ embryos. 17.5% of these transheterozygotes have tracheal phenotypes resembling those seen in 66.7% of awdj2A4/+ embryos, with the remainder having tracheal phenotypes resembling those seen in btlH82Δ3/+. The tracheal system phenotypes of shi1 homozygous embryos (collected at the permissive temperature (25oC) for 7 h and then shifted to 34oC for another 7 hours) are dominantly enhanced by awdj2A4 : the penetrance of the most severe phenotypic class is increased from 1.2% to 33.2% by the presence of awdj2A4/+. (Note, these sever phenotypes are never observed in awdj2A4/+ embryos raised under the same conditions). The relatively mild tracheal phenotypes seen in awdj2A4/+ embryos are enhanced by btlScer\UAS.T:Avic\GFP-S65T with Scer\GAL4btl.PS so that 20% have tracheal phenotypes as severe as the majority awdj2A4 homozygotes compared to none with awdj2A4/+ alone.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

L. and Y. Jan.

Comments
Comments

Excision of the P{lacW} element reverts the failure of awdj2A4 to complement awdMSM95.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (13)