Myoblast fusion, which is essential for skeletal muscle development, involves cell recognition and adhesion, followed by cell membrane breakdown and multinucleate syncitia formation. Here, Susan Abmayr and colleagues clarify the molecular mechanism of myoblast fusion in Drosophila embryos (see p. 1551). In Drosophila, the initial myoblast fusion event occurs asymmetrically between a founder cell (which patterns the musculature) and a fusion-competent myoblast (FCM). The researchers report that the non-conventional guanine nucleotide exchange factor Myoblast city (Mbc) is required in the FCMs but not in the founder cells for myoblast fusion, and that Mbc activates the small GTPase Rac1 in the FCMs. Notably, Mbc, active Rac1 and F-actin foci are concentrated in the FCMs at their site of contact with founder cells, and Mbc is essential for the formation and organisation of F-actin foci and the cytoskeleton in the FCMs. The researchers suggest, therefore, that Mbc-dependent actin polymerisation in FCMs may be one of the driving forces behind Drosophila myoblast fusion.