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General Information
Symbol
Dmel\WASp3D3-035
Species
D. melanogaster
Name
FlyBase ID
FBal0246285
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

T28825619A

Amino acid change:

L472term | WASp-PA; L472term | WASp-PB; L439term | WASp-PC; L472term | WASp-PD

Reported amino acid change:

?472term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

WASp3D3-035 alleles carry a point mutation that leads to loss of the CA domain of the VCA module, essential for binding of the Arp2/3 complex.

Amino acid replacement: ?472term.

The premature stop codon is predicted to result in a protein that lacks the CA domain and part of one of the V domains, removing the Arp2/3 complex binding domain and resulting in a dominant negative effect.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

WASp3D3-035 mutants exhibit normal visceral mesoderm development, resulting in normal gut development.

Ultrathin sections of WASp3D3-035 embryos reveal that the membrane breakdown step in myoblast fusion fails to complete.

WASp3D3-035 mutants display a striking myoblast fusion defect. Small mini muscles are surrounded by myoblasts that fail to fuse and often do not attach correctly,

WASp3D3-035/Df(3R)3450 mutants exhibit myoblast fusion as well as attachment defects.

The majority of founder cells are correctly specified in WASp3D3-035/Df(3R)3450 transheterozygous mutants.

An average of 3 to 4 nuclei are found in DA1 mini muscles in WASp3D3-035/Df(3R)3450 mutant embryos compared to up to 14 nuclei in wild-type. WASp3D3-035/Df(3R)3450 transheterozygous mutants appear to often stop fusion after precursor cell formation.

WASp3D3-035/WASp3 and WASp3D3-035/WASp1 transheterozygotes exhibit a myoblast fusion phenotype.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement
Reference

WASp3D3-035 has lethal | embryonic stage phenotype, non-enhanceable by Hem[+]/HemJ4-48

NOT suppressed by
Statement
Reference

WASp3D3-035 has lethal | embryonic stage phenotype, non-suppressible by Hem[+]/HemJ4-48

Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference

WASp3D3-035 has embryonic myoblast phenotype, non-enhanceable by Hem[+]/HemJ4-48

WASp3D3-035 has muscle attachment site phenotype, non-enhanceable by Hem[+]/HemJ4-48

NOT suppressed by
Statement
Reference

WASp3D3-035 has embryonic myoblast phenotype, non-suppressible by Hem[+]/HemJ4-48

WASp3D3-035 has muscle attachment site phenotype, non-suppressible by Hem[+]/HemJ4-48

Enhancer of
NOT Enhancer of
Statement
Reference

WASp3D3-035 is a non-enhancer of embryonic myoblast phenotype of HemJ4-48

Suppressor of
Statement
Reference

WASp3D3-035/WASp[+] is a suppressor | partially of embryonic myoblast phenotype of HemJ4-48

Other
Additional Comments
Genetic Interactions
Statement
Reference

Aberrant migration of the longitudinal visceral muscle founder cells is observed in stage 13 WASp3D3-035;Arp3schwachling double homozygote embryos and many unfused somatic myoblasts are seen at stage 16 but both the longitudinal visceral muscles and gut morphology appear normal.

Arp66Bschwachling WASp3D3-035 double mutants exhibit normal visceral mesoderm development, resulting in normal gut development.

The DA1 muscle in Arp66Bschwachling WASp3D3-035 double mutants is mainly mononucleated, indicating that myoblasts fail to fuse completely.

The myoblast-fusion phenotype found in WASp3D3-035 or Arp66Bschwachling single mutant embryos is strongly enhanced in the double mutant. Analysis of the DA1 muscle in the double mutant reveals only one nucleus per hemisegment, indicating that fusion is completely blocked in the double mutant.

Myoblast fusion does not occur in DA1 muscles in Arp66BEP3640, WASp3D3-035 double mutants.

HemJ4-48/WASp3D3-035 double mutants exhibit a similar myoblast fusion phenotype as HemJ4-48 single mutants. A HemJ4-48 heterozygous background does not influence the WASp3D3-035 homozygous mutant phenotype. A WASp3D3-035 heterozygous background partially suppresses the block of fusion observed in HemJ4-48 homozygous mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of WASpScer\UAS.cBa in WASp3D3-035/Df(3R)3450 mutants under the control of Scer\GAL4twi.PG restores almost the complete muscle pattern.

Expression of WASpScer\UAS.cBa specifically in founder cells (under the control of Scer\GAL4kirre-rP298) in WASp3D3-035/Df(3R)3450 mutants does not restore a wild-type muscle pattern. Instead muscles look thinner compared to wild-type and some muscles are even missing.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)