Fig. 8. A modified model for myoblast fusion in Drosophila. (A) Actin regulates the expansion of the FuRMAS and integrates the FCM into the growing myotube. Blow is localized to the middle of the ring that expresses Sns in FCMs and Duf in FCs. Our data suggest that Vrp1 is also present in this location, inducing the branching of F-actin in concert with WASP. The correct localization of these components (Kesper et al., 2007) is required for the formation of a fusion pore, and hence their presence guarantees successful fusion. Transmission electron microscopy studies suggest that wasp and vrp1 mutants are capable of forming a pore. In Arp3 (encoding a subunit of the Arp2/3 complex) mutants, fusion is disrupted after fusion-pore formation. Therefore, we propose that F-actin is required for the integration of FCMs into the FC/growing myotube. (B) Molecular model for regulating F-actin branching during the first and the second step of myoblast fusion. Duf and Sns form a ring in FCs and FCMs, respectively. The fusion pore will be formed in the middle of the ring (indicated in red). We postulate that the SCAR-Kette complex regulates F-actin formation during the first fusion step. The formation of F-actin during the first fusion step might additionally require the activity of Vrp1. During the second fusion step, the signal from the outer membrane in FCs becomes translated by Rols7, which is involved in the localization of Drosophila Titin (Menon and Chia, 2001). Our results suggest that F-actin becomes regulated differently in FCs and FCMs. The activity of the actin regulator WASP might be required in FCMs, in which it acts together with Vrp1. We propose that the actin regulators SCAR and Kette are also involved during the second fusion step, because Kette and WASP act antagonistically during the fusion process. Functions of the proteins involved during the first and second fusion step are described in Table 1.