Live imaging of rols^T627 mutants, which are capable of some myoblast fusion, indicates that fusion always follows actin focus formation and dissolution, as in wild-type.

Homozygous border cell clones show defects in migration.

In rols^T627 mutant embryos, mature, multinucleated muscle fibers are absent. Instead, a large number of unfused myoblasts are present by late stage 13. These unfused founder cells maintain the ability to differentiate and form elongated mononucleated myocytes. Fusion-competent myoblasts extend filopodia toward elongated mononucleated founder cells, suggesting that adhesion between fusion-competent myoblasts and founder cells is not affected. All skeletal muscles appear to be affected, but visceral muscles exhibit only minor defects in the first midgut constriction, and the dorsal vessel appears to be normal. rols^T321/Df(3L)vin4 embryos also have myoblast fusion defects.