期刊
JOURNAL OF CELL SCIENCE
卷 125, 期 16, 页码 3790-3800出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.101048
关键词
CKIP-1; Arp2/3; Actin cytoskeleton; Myoblast fusion; Zebrafish muscle development
类别
资金
- NICHD
- Association francaise contre les Myopathies [AFM-12130]
- Ministere de la Recherche et de l'Enseignement Superieur
- Fondation pour la Recherche Medicale [FDT20101221104]
- Association pour la Recherche contre le Cancer [ARC-3853]
- Ministere de la Recherche et de la Technologie [ANR-11-BSV2-017-01]
Multinucleated muscle fibres arise by fusion of precursor cells called myoblasts. We previously showed that CKIP-1 ectopic expression in C2C12 myoblasts increased cell fusion. In this work, we report that CKIP-1 depletion drastically impairs C2C12 myoblast fusion in vitro and in vivo during zebrafish muscle development. Within developing fast-twich myotome, Ckip-1 localises at the periphery of fast precursor cells, closed to the plasma membrane. Unlike wild-type myoblasts that form spatially arrayed multinucleated fast myofibres, Ckip-1-deficient myoblasts show a drastic reduction in fusion capacity. A search for CKIP-1 binding partners identified the ARPC1 subunit of Arp2/3 actin nucleation complex essential for myoblast fusion. We demonstrate that CKIP-1, through binding to plasma membrane phosphoinositides via its PH domain, regulates cell morphology and lamellipodia formation by recruiting the Arp2/3 complex at the plasma membrane. These results establish CKIP-1 as a regulator of cortical actin that recruits the Arp2/3 complex at the plasma membrane essential for muscle precursor elongation and fusion.
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