L472term | WASp-PA; L472term | WASp-PB; L439term | WASp-PC; L472term | WASp-PD
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
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.
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.
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.
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.