Journal
DEVELOPMENT
Volume 134, Issue 24, Pages 4357-4367Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.010678
Keywords
cell-cell fusion; myoblast fusion; muscle; actin; Kette (Hem, Nap1); SCAR (WAVE); Arp2/3
Categories
Funding
- NIGMS NIH HHS [R01 GM078318-02, R01 GM056989, R01 GM056989-02, R01 GM056989-01A1, R01 GM056989-05, GM 586989, R01 GM078318, R01 GM056989-06A2, R01 GM056989-07, R01 GM078318-03, R01 GM078318-01A1, GM 78318, R01 GM056989-03, R01 GM056989-04] Funding Source: Medline
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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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