FlyBase Allele Report: Dmel\AP-2α[3]

General Information

Symbol

Dmel\AP-2α³

Species

D. melanogaster

Name

FlyBase ID

FBal0060816

Feature type

allele

Associated gene

Dmel\AP-2α

Associated Insertion(s)

Carried in Construct

Also Known As

α-Ada³

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Gonzalez-Gaitan and Jackle, 1997)

Mutagen

Delta2-3 transposase

(Gonzalez-Gaitan and Jackle, 1997)

Progenitor genotype

AP-2α⁰⁶⁶⁹⁴

(Gonzalez-Gaitan and Jackle, 1997)

Cytology

Description

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

(Gonzalez-Gaitan and Jackle, 1997)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

abnormal locomotor behavior | heat sensitive

(Gonzalez-Gaitan and Jackle, 1997)

abnormal neuroanatomy

(Gonzalez-Gaitan and Jackle, 1997)

abnormal neuroanatomy | prepupal stage P1 | somatic clone

(Zong et al., 2018)

abnormal neuroanatomy | pupal stage P5 | somatic clone

(Zong et al., 2018)

abnormal neurophysiology

(Gonzalez-Gaitan and Jackle, 1997)

abnormal size | prepupal stage P1 | somatic clone

(Zong et al., 2018)

abnormal size | pupal stage P5 | somatic clone

(Zong et al., 2018)

lethal | somatic clone

(Gonzalez-Gaitan and Jackle, 1999)

lethal - all die before end of larval stage | recessive

(Gonzalez-Gaitan and Jackle, 1997)

some die during larval stage | recessive

(Gonzalez-Gaitan and Jackle, 1997)

uncoordinated | heat sensitive

(Gonzalez-Gaitan and Jackle, 1997)

visible | heat sensitive (with AP-2α⁴)

(Gonzalez-Gaitan and Jackle, 1999)

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.

(Zong et al., 2018)

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.

(Peng et al., 2009)

The α-Adaptin³/α-Adaptin⁴ combination causes a temperature-dependent wing phenotype. At 18^oC the mutant wings are normal. At 25^oC wings are reduced in size and show vein pattern defects, truncations, along the A/P axis. At 29^oC 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.

(Gonzalez-Gaitan and Jackle, 1999)

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.

(Gonzalez-Gaitan and Jackle, 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

AP-2α³ has abnormal neuroanatomy | somatic clone | pupal stage P5 phenotype, suppressible by Nrg^GL00656/Scer\GAL4^ppk.PU

(Zong et al., 2018)

AP-2α³ has abnormal size | somatic clone | pupal stage P5 phenotype, suppressible by Nrg^GL00656/Scer\GAL4^ppk.PU

(Zong et al., 2018)

Enhancer of

Statement

Reference

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

(Zong et al., 2018)

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

(Zong et al., 2018)

AP-2alpha[+]/AP-2α³ is an enhancer of abnormal neuroanatomy | pupal stage P5 phenotype of Df(3R)Exel7310/prd1^M56

(Zong et al., 2018)

AP-2alpha[+]/AP-2α³ is an enhancer of abnormal size | pupal stage P5 phenotype of Df(3R)Exel7310/prd1^M56

(Zong et al., 2018)

AP-2α³/alpha-Adaptin[+] is an enhancer of abnormal neuroanatomy | larval stage phenotype of Nak^RNAi.UAS, Scer\GAL4^elav-C155

(Yang et al., 2011)

AP-2α³/alpha-Adaptin[+] is an enhancer of visible | recessive phenotype of lqf^FDD9

(Cadavid et al., 2000)

Other

Statement

Reference

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

(Gonzalez-Gaitan and Jackle, 1999)

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

(Gonzalez-Gaitan and Jackle, 1999)

Phenotype Manifest In

Suppressed by

Statement

Reference

AP-2α³ has dendritic tree | somatic clone | pupal stage P5 phenotype, suppressible by Nrg^GL00656/Scer\GAL4^ppk.PU

(Zong et al., 2018)

AP-2α³ has larval dorsal multidendritic neuron ddaC | somatic clone | pupal stage P5 phenotype, suppressible by Nrg^GL00656/Scer\GAL4^ppk.PU

(Zong et al., 2018)

Enhancer of

Statement

Reference

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

(Zong et al., 2018)

AP-2alpha[+]/AP-2α³ is an enhancer of larval dorsal multidendritic neuron ddaC | pupal stage P5 phenotype of Df(3R)Exel7310, unc-104^GD16406

(Zong et al., 2018)

AP-2alpha[+]/AP-2α³ is an enhancer of dendritic tree | pupal stage P5 phenotype of Df(3R)Exel7310/prd1^M56

(Zong et al., 2018)

AP-2alpha[+]/AP-2α³ is an enhancer of larval dorsal multidendritic neuron ddaC | pupal stage P5 phenotype of Df(3R)Exel7310/prd1^M56

(Zong et al., 2018)

AP-2α³/alpha-Adaptin[+] is an enhancer of dendritic arborizing neuron | larval stage phenotype of Nak^RNAi.UAS, Scer\GAL4^elav-C155

(Yang et al., 2011)

AP-2α³/alpha-Adaptin[+] is an enhancer of dendrite | larval stage phenotype of Nak^RNAi.UAS, Scer\GAL4^elav-C155

(Yang et al., 2011)

AP-2α³/alpha-Adaptin[+] is an enhancer of eye phenotype of lqf^FDD9

(Cadavid et al., 2000)

AP-2α³/alpha-Adaptin[+] is an enhancer of wing phenotype of lqf^FDD9

(Cadavid et al., 2000)

Other

Statement

Reference

AP-2α³, Chc[+]/Chc¹ has wing phenotype

(Gonzalez-Gaitan and Jackle, 1999)

AP-2α³, Chc[+]/Chc¹ has wing vein phenotype

(Gonzalez-Gaitan and Jackle, 1999)

AP-2α³, Chc[+]/Chc¹ has posterior crossvein phenotype

(Gonzalez-Gaitan and Jackle, 1999)

AP-2α³/alpha-Adaptin[+], Chc¹ has wing phenotype

(Gonzalez-Gaitan and Jackle, 1999)

AP-2α³/alpha-Adaptin[+], Chc¹ has wing vein phenotype

(Gonzalez-Gaitan and Jackle, 1999)

AP-2α³/alpha-Adaptin[+], Chc¹ has posterior crossvein phenotype

(Gonzalez-Gaitan and Jackle, 1999)

Additional Comments

Genetic Interactions

Statement

Reference

Heterozygosity for AP-2α³ enhances the ddaC neuron pruning defects observed in prd1^M56/Df(3R)Exel7310 transheterozygous or upon expression of unc-104^GD16406 under the control of Scer\GAL4^ppk.PU (and Dicer-2, for efficient RNAi); specifically, the persisting dendrites become significantly longer.

(Zong et al., 2018)

α-Adaptin³/+ enhances the reduction in the number of dendritic endpoints of dorsal dendritic arborisation neurons which is seen in larvae expressing Nak^{dsRNA.Scer\UAS} under the control of Scer\GAL4^elav-C155. In addition, clusters of shortened terminals are more often seen.

(Yang et al., 2011)

The eye and wing defects of lqf^FDD9 homozygotes are dominantly enhanced by α-Adaptin³.

(Cadavid et al., 2000)

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

(Gonzalez-Gaitan and Jackle, 1999)

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

(Gonzalez-Gaitan and Jackle, 1997)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

AP-2α^ear26

(Berdnik et al., 2002)

AP-2α^ear4

(Berdnik et al., 2002)

AP-2α^ear5

(Berdnik et al., 2002)

Rescued by

AP-2α³ is rescued by Scer\GAL4^ppk.PU/AP-2α^UAS.GFP

(Zong et al., 2018)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

99484

AP-2α³ P{neoFRT}40A/CyO, P{GAL4-twi.G}2.2, P{UAS-2xEGFP}AH2.2

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

AP-2α³

(Lin et al., 2015)

D-Ada³

(Gonzalez-Gaitan and Jackle, 1999)

D-αAda³

(Boehm and Bonifacino, 2002, Gonzalez-Gaitan and Jackle, 1997)

ada³

(Gui et al., 2016)

α-Ada³

(Cadavid et al., 2000)

α-Adaptin³

(Yang et al., 2011)

α-ada³

(Zong et al., 2018, Chance and Bashaw, 2015, Peng et al., 2009, Peng et al., 2009)

Name Synonyms

Secondary FlyBase IDs

References (12)

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