Key result
Mutations in kette, SCAR, and Arp2/3 block myoblast fusion and prevent the dissolution of actin foci at the site of fusion in Drosophila.
The Kette-SCAR-Arp2/3 pathway is crucial for actin cytoskeletal remodeling and subsequent myoblast fusion in Drosophila.
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Extends cytoskeletal insights into myoblast fusion; leaves open conservation in mammalian cardiogenesis.
Myoblast fusion is crucial for formation and repair of skeletal muscle. Here we show that active remodeling of the actin cytoskeleton is essential for fusion in Drosophila. Using live imaging, we have identified a dynamic F-actin accumulation (actin focus) at the site of fusion. Dissolution of the actin focus directly precedes a fusion event. Whereas several known fusion components regulate these actin foci, others target additional behaviors required for fusion. Mutations in kette/Nap1, an actin polymerization regulator, lead to enlarged foci that do not dissolve, consistent with the observed block in fusion. Kette is required to positively regulate SCAR/WAVE, which in turn activates the Arp2/3 complex. Mutants in SCAR and Arp2/3 have a fusion block and foci phenotype, suggesting that Kette-SCAR-Arp2/3 participate in an actin polymerization event required for focus dissolution. Our data identify a new paradigm for understanding the mechanisms underlying fusion in myoblasts and other tissues.
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Richardson et al. (2007) studied Myoblast fusion. Mutations in kette/Nap1, SCAR, and Arp2/3 vs. Wild-type (implied) was evaluated on Myoblast fusion and actin focus dissolution. Mutations in kette, SCAR, and Arp2/3 block myoblast fusion and prevent the dissolution of actin foci at the site of fusion in Drosophila.
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