cardioblast & adherens junction
embryonic head & embryonic/first instar larval cuticle
The disorganised ommatidial lattice and supernumerary primary pigment cells phenotype observed in either Vav2 or Vav3 homozygotes is strongly enhanced by combination with shgk03401 in heterozygous state but the proportion of ommatidia with extra cone cells is not further increased.
shgk03401; p130CAS1 double homozygotes arrest in late embryogenesis (and thereby do not hatch) and are considered semi-lethal. Athough most of the embryos form at least partial cuticles, absence of p130CAS1 significantly enhances shgk03401 single mutant cuticle defects, with shgk03401; p130CAS1 mutant embryos showing severe defects that essentially eliminate head and ventral cuticle, while incomplete dorsal closure is reflected by the presence of holes in the dorsal cuticle.
shgk03401 mutant larval brain cells expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.PI exhibit a weak invasive phenotype and can invade the ventral nerve cord (this phenotype occurs with 20% penetrance).
shgk03401 mutant larval brain cells expressing both Ras85DV12.Scer\UAS and egrScer\UAS.cIa under the control of Scer\GAL4Act5C.PI generate into invasive tumours that can invade the ventral nerve cord (this phenotype occurs with 88% penetrance).
Expression of Ras85DV12.Scer\UAS, egrScer\UAS.cIa and bskDN.Scer\UAS, under the control of Scer\GAL4Act5C.PI in shgk03401 mutant larval cephalic complexes (brain, eye and antennal discs) induces tumor invasion of the ventral nerve cord.
Overexpression of hepCA.Scer\UAS in shgk03401 mutant cephalic cells (i.e. cells in the larval brain and eye-antennal discs) expressing Ras85DV12.Scer\UAS results in neither enhanced tumour growth nor metastatic behaviour.
shg::α-CatScer\UAS.fl can suppress shgk03401 clone phenotypes such as follicle cell sorting, loss of epithelial integrity, and oocyte mis-positioning, as well as the migration defects of shgk03401 mutant border cell clones.