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General Information
Symbol
Dmel\Arp3schwachling
Species
D. melanogaster
Name
FlyBase ID
FBal0247673
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:

G8115589A

Comment:

G to A nucleotide transition at the splice acceptor site of the first intron.

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

Arp66Bschwachling flies exhibit a G to A nucleotide transition at the splice acceptor site of the first intron. This point mutation possibly leads to an aberrantly spliced transcript, retaining the first intron, that becomes translated into a truncated protein of 15 amino acids.

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

Mutant stage 16 embryos show a severe myoblast fusion defect in the dorsal pharyngeal muscle. Fusion competent myoblasts show a significant decrease in the volume of F-actin foci and a corresponding increase in the frequency of filopodia emanating from an F-actin focus compared to wild type.

Longitudinal muscle development is not strongly disturbed in Arp3schwachling homozygote embryos, although fewer nuclei are observed in the longitudinal muscles at stage 13, the muscle and gut morphology appears normal at stage 16.

Homozygous Arp66Bschwachling and Arp66Bschwachling/Df(3L)ZP1 trans-heterozygous mutants display a severe defect in myoblast fusion.

The determination of founder cells and fusion-competent myoblasts in Arp66Bschwachling mutant embryos occurs normally. The DA1 muscles in Arp66Bschwachling embryos are formed to contain, on average, three nuclei, indicating that the first fusion step, forming a bi- to trinucleated precursor cell, has completed.

Ultrathin sections of Arp66Bschwachling embryos reveal the formation of fusion pores between growing muotubes and fusion-competent myoblasts. However, no plasma membrane remnants are found between the cells, as seen in wild-type cells, indicating that Arp66Bschwachling embryos stop fusion after membrane breakdown, when a fusion pore has been formed.

Trans-heterozygous Arp66BEP3640/Arp66Bschwachling exhibit a clear myoblast-fusion defect.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
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.

Myoblast fusion does not occur in DA1 muscles in Arp66Bschwachling, WASp3 double mutants.

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.

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

Separated from pnt3D2-026 by meiotic recombination.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (6)