Key result
Mutations in either jamb or jamc genes prevented myocyte fusion in vivo, reducing fusion rates from 96.9% in wild-type to 5.1% in jamb mutants.
Absolute Event Rate: 5.1% vs 96.9%
The zebrafish orthologues of JAM-B and JAM-C receptors are identified as an essential in vivo-validated cell surface heterophilic receptor pair required for myocyte fusion.
Zebrafish findings do not inform human practice; leaves open JAM-B/C conservation and roles in mammalian myogenesis.
Cellular fusion is required in the development of several tissues, including skeletal muscle. In vertebrates, this process is poorly understood and lacks an in vivo-validated cell surface heterophilic receptor pair that is necessary for fusion. Identification of essential cell surface interactions between fusing cells is an important step in elucidating the molecular mechanism of cellular fusion. We show here that the zebrafish orthologues of JAM-B and JAM-C receptors are essential for fusion of myocyte precursors to form syncytial muscle fibres. Both jamb and jamc are dynamically co-expressed in developing muscles and encode receptors that physically interact. Heritable mutations in either gene prevent myocyte fusion in vivo, resulting in an overabundance of mononuclear, but otherwise overtly normal, functional fast-twitch muscle fibres. Transplantation experiments show that the Jamb and Jamc receptors must interact between neighbouring cells (in trans) for fusion to occur. We also show that jamc is ectopically expressed in prdm1a mutant slow muscle precursors, which inappropriately fuse with other myocytes, suggesting that control of myocyte fusion through regulation of jamc expression has important implications for the growth and patterning of muscles. Our discovery of a receptor-ligand pair critical for fusion in vivo has important implications for understanding the molecular mechanisms responsible for myocyte fusion and its regulation in vertebrate myogenesis.
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Powell et al. (2011) studied Myocyte fusion defect. jamb and jamc loss-of-function mutations vs. Wild-type was evaluated on Percentage of fused (multinucleated) fast muscle fibers in transplanted hosts. Mutations in either jamb or jamc genes prevented myocyte fusion in vivo, reducing fusion rates from 96.9% in wild-type to 5.1% in jamb mutants.
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