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.
G8115589A
G to A nucleotide transition at the splice acceptor site of the first intron.
myoblast | embryonic stage (with Arp3EP3640)
myoblast | embryonic stage (with Df(3L)ZP1)
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.
Arp3schwachling has dorsal acute muscle cell | embryonic stage phenotype, enhanceable by WASp3D3-035
Arp3schwachling has myoblast | embryonic stage phenotype, enhanceable by WASp3D3-035
Arp3schwachling has dorsal acute muscle cell | embryonic stage phenotype, enhanceable by WASp3
Arp3schwachling has myoblast | embryonic stage phenotype, enhanceable by WASp3
Arp3schwachling is an enhancer of dorsal acute muscle cell | embryonic stage phenotype of WASp3D3-035
Arp3schwachling is an enhancer of myoblast | embryonic stage phenotype of WASp3D3-035
Arp3schwachling, WASp3D3-035 has embryonic myoblast | embryonic stage 16 phenotype
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.
Separable from: pnt3D2-026.
Separated from pnt3D2-026 by meiotic recombination.