Co-expression of both vgScer\UAS.T:Ivir\HA1 and sdΔ88-159.Scer\UAS in developing muscles under the control of Scer\GAL4Mef2.PR results in fewer ectopic muscle attachments (24.5% compared with 81.8% when vgScer\UAS.T:Ivir\HA1 is expressed alone).
Ectopic expression of vg2.Scer\UAS within the lateral transverse muscles with sdΔ88-159.Scer\UAS (with both under the control of Scer\GAL4C23 leads to partial suppression of the vg2.Scer\UAS-induced muscle phenotype.
Blocking vg function through expression of sdΔ88-159.Scer\UAS in ventral longitudinal muscle cells (under the control of Scer\GAL4Mef2.PR) that abnormally migrate along the midline owing to a sli2 mutant background, leads to fewer and smaller muscle-muscle adhesions.
Mesodermal expression of constitutively active btl::EgfrScer\UAS.T:λ\cI-DD in sli2 mutants (under the control of Scer\GAL4Mef2.PR) produces many small adhesion sites between midline-crossing ventral longitudinal muscles. This ectopic attachment phenotype is vg-specific as interfering with vg function through coexpression of sdΔ88-159.Scer\UAS results in fewer of these adhesion sites.