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General Information
Symbol
Dmel\AP-2α3
Species
D. melanogaster
Name
FlyBase ID
FBal0060816
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
α-Ada3
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

3kb deletion encompassing the nontranscribed upstream sequences, the two first introns and the N-terminal region of the protein encoded by both transcripts.

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

AP-2α3 ddaC and ddaD/E neuron clones within mosaic individuals present severe and fully penetrant dendrite pruning defects at 16h and 18h after puparium formation, respectively, as compared to controls; mutant ddaC neurons also exhibit simplified dendrite arbors at the white prepupal stage, as compared to controls. ddaF neuron clones, however, are eliminated by 16h after puparium formation, similarly to controls; AP-2α3 heterozygotes do not show these defects.

Salivary gland cell growth (which normally occurs in the third larval instar, starting at the distal end of the gland) is defective in α-Adaptin06694/α-Adaptin3 third instar larvae.

The α-Adaptin3/α-Adaptin4 combination causes a temperature-dependent wing phenotype. At 18oC the mutant wings are normal. At 25oC wings are reduced in size and show vein pattern defects, truncations, along the A/P axis. At 29oC only wing remnants are left. The remnants develop diagnostic dorsoventral pattern elements, indicating that only A/P axis is affected. Homozygous clones induced during early larval development do not survive. Clones induced late in larval development do survive but at a growth disadvantage compared to wild type twin spots.

Muscle contractions are sporadic and larvae fail to hatch from the egg shell. Architecture of the nervous system of the embryos is not affected by lack of α-Adaptin. Ultrastructure of the presynaptic terminal shows absence of synaptic boutons and deep folds in the presynaptic membrane.

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

AP-2alpha[+]/AP-2α3 is an enhancer of abnormal size | pupal stage P5 phenotype of Df(3R)Exel7310, unc-104GD16406

AP-2alpha[+]/AP-2α3 is an enhancer of abnormal size | pupal stage P5 phenotype of Df(3R)Exel7310/prd1M56

AP-2α3/alpha-Adaptin[+] is an enhancer of visible | recessive phenotype of lqfFDD9

Other
Statement
Reference

AP-2α3, Chc[+]/Chc1 has visible | dominant | heat sensitive phenotype

AP-2α3/alpha-Adaptin[+], Chc1 has visible | dominant | heat sensitive phenotype

Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

AP-2alpha[+]/AP-2α3 is an enhancer of dendritic tree | pupal stage P5 phenotype of Df(3R)Exel7310/prd1M56

AP-2α3/alpha-Adaptin[+] is an enhancer of dendrite | larval stage phenotype of NakdsRNA.UAS, Scer\GAL4elav-C155

AP-2α3/alpha-Adaptin[+] is an enhancer of eye phenotype of lqfFDD9

AP-2α3/alpha-Adaptin[+] is an enhancer of wing phenotype of lqfFDD9

Other
Additional Comments
Genetic Interactions
Statement
Reference

Heterozygosity for AP-2α3 enhances the ddaC neuron pruning defects observed in prd1M56/Df(3R)Exel7310 transheterozygous or upon expression of unc-104GD16406 under the control of Scer\GAL4ppk.PU (and Dicer-2, for efficient RNAi); specifically, the persisting dendrites become significantly longer.

α-Adaptin3/+ enhances the reduction in the number of dendritic endpoints of dorsal dendritic arborisation neurons which is seen in larvae expressing NakdsRNA.Scer\UAS under the control of Scer\GAL4elav-C155. In addition, clusters of shortened terminals are more often seen.

The eye and wing defects of lqfFDD9 homozygotes are dominantly enhanced by α-Adaptin3.

Double heterozygotes of α-Adaptin3/+ with Chc1/+ have a reduced wing with vein defects at 25oC and the wing remnant phenotype at 29oC. Double heterozygotes of α-Adaptin3/+ with Chc1/+ at 18oC show a thickened posterior crossvein phenotype, reminiscent of the tkv mutant phenotype.

shi2; α-Adaptin3/α-Adaptin+ males are indistinguishable from wild type at 18oC but at 25oC males can neither fly or walk and they show sporadic and uncoordinated movements.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (11)