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.
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.
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.