Dependence of myoblast fusion on a cortical actin wall and nonmuscle myosin IIA

Duan, Rui; Gallagher, Patricia J.

doi:10.1016/j.ydbio.2008.10.035

Cited by 69 publications

(63 citation statements)

References 39 publications

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“…Importantly, a discrete actin-based structure associated with the fusion process in mammalian muscles is still missing. Indications that such structures may exist come from myogenic cell-culture studies (25,33), but have not been reported in vivo or in primary culture studies, and we were not able to identify them in the course of the current study.…”

Section: Discussionmentioning

confidence: 87%

The actin regulator N-WASp is required for muscle-cell fusion in mice

Gruenbaum-Cohen

Harel²,

Umansky³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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A fundamental aspect of skeletal myogenesis involves extensive rounds of cell fusion, in which individual myoblasts are incorporated into growing muscle fibers. Here we demonstrate that N-WASp, a ubiquitous nucleation-promoting factor of branched microfilament arrays, is an essential contributor to skeletal muscle-cell fusion in developing mouse embryos. Analysis both in vivo and in primary satellite-cell cultures, shows that disruption of N-WASp function does not interfere with the program of skeletal myogenic differentiation, and does not affect myoblast motility, morphogenesis and attachment capacity. N-WASp-deficient myoblasts, however, fail to fuse. Furthermore, our analysis suggests that myoblast fusion requires N-WASp activity in both partners of a fusing myoblast pair. These findings reveal a specific role for N-WASp during mammalian myogenesis. WASp-family elements appear therefore to act as universal mediators of the myogenic cell-cell fusion mechanism underlying formation of functional muscle fibers, in both vertebrate and invertebrate species.actin nucleation | myotube formation

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Section: Discussionmentioning

confidence: 87%

The actin regulator N-WASp is required for muscle-cell fusion in mice

Gruenbaum-Cohen

Harel²,

Umansky³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…Visualization of the actin cytoskeleton revealed dynamic changes in fusing mouse myoblasts in vitro, as described for flies (Swailes et al, 2006;Duan and Gallagher, 2009;Nowak et al, 2009;Stadler et al, 2010). A dense actin wall forms in one cell, paralleling the long axis of aligned myoblasts (Duan and Gallagher, 2009), and is hypothesized to provide the membrane rigidity needed for cell fusion. As fusion proceeds, gaps appear in this actin wall at sites of vesicle accumulation, vesicles pair in both cells along the membrane, and fusion pores then form.…”

Section: Actin Cytoskeletal Remodeling In Mouse Myoblastsmentioning

confidence: 83%

Myoblast fusion: lessons from flies and mice

2012

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The fusion of myoblasts into multinucleate syncytia plays a fundamental role in muscle function, as it supports the formation of extended sarcomeric arrays, or myofibrils, within a large volume of cytoplasm. Principles learned from the study of myoblast fusion not only enhance our understanding of myogenesis, but also contribute to our perspectives on membrane fusion and cell-cell fusion in a wide array of model organisms and experimental systems. Recent studies have advanced our views of the cell biological processes and crucial proteins that drive myoblast fusion. Here, we provide an overview of myoblast fusion in three model systems that have contributed much to our understanding of these events: the Drosophila embryo; developing and regenerating mouse muscle; and cultured rodent muscle cells. IntroductionThe process of fusing two adjacent membranes accomplishes many goals that are crucial to the development and maintenance of living organisms. Broadly, membrane fusion can occur intracellularly, as with synaptic vesicles, or between cells, as for sperm-egg fusion. Cell fusion occurs in a broad range of organisms, including Saccharomyces cerevisiae and Caenorhabditis elegans, and between several cell types, such as macrophages, placental trophoblasts and myoblasts. Experimental analysis of fusion in these systems has revealed the involvement of a diverse array of specialized molecules.Myoblast fusion, a fundamental step in the differentiation of muscle in most organisms, can involve tens of thousands of myoblasts, Given the complexity of the musculature, fusion must be a regulated process in which the appropriate number of cells fuse at the appropriate time and place. Often these cells migrate long distances prior to fusion, and fusion can involve multiple cell types, necessitating cell recognition and adhesion, which are crucial to accurate and efficient fusion. In addition to the early fusion events that occur during embryogenesis, vertebrate muscle tissue is able to regenerate in response to damage and disease. This regeneration involves proliferation of muscle satellite cells (see Glossary, Box 1) and their subsequent fusion to repair the damaged muscles. The focus of this review is the process of myoblast fusion, which involves cell migration, adhesion and signaling transduction pathways leading up to the actual fusion event. We review the crucial role of the actin cytoskeleton and actin polymerizing proteins, and recently revealed membrane protrusions that may drive fusion itself. We describe three powerful systems for this analysis: Drosophila embryogenesis; mouse embryogenesis and regeneration; and rodent tissue culture. We highlight the genes and morphological events involved in myoblast fusion, as revealed by each system. With the emergence of Danio rerio as another model for myoblast fusion, we also list relevant homologs in this system (Tables 1, 2). Experimental systems for the analysis of myoblast fusionThe ability to isolate and propagate mammalian myoblasts that could differentiate and fuse in...

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“…siRNA knockdown of WASP and Vrp1 as well as Latrunculinmediated F-actin destabilization leads to a lower fusion index in C2C12 murine myoblast cell culture (Kim et al, 2007). In murine myoblast cell culture models, F-actin seems to play a role in the alignment of cells, and fusion pores have been suggested to appear in the actin-free regions (Duan and Gallagher, 2009), a suggestion also made by Kim et al (2007) for Drosophila myoblast fusion. Chen et al (2008) report for the viral fusogene gp64 that fusion pore expansion during syncytium formation in a cell culture assay is also restricted by an actin network, suggesting again a common mechanism.…”

Section: Functional Conservation Between Drosophila and Vertebrate Mymentioning

confidence: 87%

FuRMAS: triggering myoblast fusion in Drosophila

Önel

Renkawitz‐Pohl

2009

Developmental Dynamics

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In Drosophila, as in mammals, myoblast fusion is fundamental for development. This fusion process has two distinct phases that share common ultrastructural features and at least some molecular players between Drosophila and vertebrates. Here, we integrate the latest data on the key molecular players and ultrastructural features found during myoblast fusion into a new working model to explain this fundamental cellular process. At cell-cell contact sites, a protein complex (

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Dependence of myoblast fusion on a cortical actin wall and nonmuscle myosin IIA

Cited by 69 publications

References 39 publications

The actin regulator N-WASp is required for muscle-cell fusion in mice

The actin regulator N-WASp is required for muscle-cell fusion in mice

Myoblast fusion: lessons from flies and mice

FuRMAS: triggering myoblast fusion in Drosophila

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