Fig. 2. A model describing the main events of myogenesis in teleost skeletal muscle. In this scheme pleuripotent stems cells become myoblasts, which are committed to a myogenic fate to form the Myogenic Progenitor Cell (MPC) population, involving the expression of the myogenic regulatory factors (MRFs) myoD (myoblast determination factor; there are at least two paralogues in teleosts) and myf-5. Following activation by Hepatocyte Growth Factor/Scatter Factor (HGF/SF) the MPCs are thought to undergo an asymmetric division to regenerate the MPC and provide a daughter cell committed to terminal differentiation. MPC markers (boxed) include c-met (the receptor for HGF/SF), paired-box protein 7 (Pax-7), and the transcription factors, sox-8 and Fox-K1. The MPC progeny undergo a proliferation phase [when proliferating cell nuclear antigen (PCNA), a DNA polymerase associated peptide, is upregulated] controlled by positive and negative signalling pathways. Myostatin-II is an important negative regulator of muscle growth and may also negatively regulate the activation of MPCs (cf. satellite cells in mammals) (McCroskery et al., 2003). Following cell cycle exit (and upregulation of p21), the MPC progeny initiate the differentiation programme involving the expression of the MRFs, myogenin and MRF-4 and MEF-2 gene family members. The MPC progeny can migrate through the muscle and have several fates. Until around 44% of the ultimate fish length, myoblasts in fast muscle can fuse to form short myotubes in a myoblast–myoblast fusion event, which probably involves calpain. Short myotubes can be extended by the fusion of additional myoblasts in a myoblast–myotube fusion event. Once formed myotubes initiate the programme of myofibrillargenesis and mature into muscle fibres. The regulation of fibre mass is thought to be controlled by signalling pathways involving insulin-like growth factor I (IGF-I) and IGF-II. At all stages of growth the MPC progeny can fuse with muscle fibres (myoblast–muscle fibre fusion) in the process of nuclear accretion. As muscle fibres increase in diameter and length additional nuclei are required to maintain the myonuclear domain (the volume of cytoplasm controlled by each nuclei) within certain limits.