Mechanisms of muscle development and responses to temperature change in fish larvae

Three phases of myogenesis have been identified in the myotomal muscles of larval teleosts. The commitment of embryonic slow and fast muscle lineages is determined prior to segmentation (embryonic myogenesis) and involves notochord and floorplate derived signaling pathways, which drive the adaxial cells to a slow muscle fate. The adaxial cells elongate to span the entire somite width and subsequently migrate through the myotome to form a superficial layer of slow muscle fibers. The remaining cells of the lateral mesoderm adopt the default fast muscle phenotype. The second phase of fiber expansion in the myotomes involves recruitment from discrete germinal zones for both slow and fast muscle fibers (stratified hyperplasia). Finally, myogenic precursor cells are activated throughout the myotome (mosaic hyperplasia). The progeny of these cells either fuse to form additional fibers on the surface of existing muscle fibers or are absorbed by fibers as they expand in diameter (hypertrophic growth). There is considerable species diversity with respect to the timingofinnervation of the embryonic muscle fibers in relation to other developmental events, the degree of maturation of the muscle fibers at hatching, and the onset and relative importance of stratified and mosaic hyperplasia to growth during larval life. A subset of myogenic cells specified by their position in the anterior myotomes are thought to migrate out and populate the pectoral fin buds leading to the differentiation of the pectoral fin muscles. Little is known about the mechanism of formation of the unpaired fin muscles, which occurs after the differentiation of the myotomes and is often delayed until relatively late in larval life. During ontogeny, embryonic isoforms of the myofibrillar proteins are replaced by larval and adult isoforms, and the adult multiterminal pattern of slow muscle innervation gradually develops, reflecting changes in swimming style and performance as body size increases. The body length at which particular protein isoforms are switched on varies for each myofibrillar component and with temperature. In general, early larval stages show a greater reliance on aerobic metabolic pathways and a lower capacity for anaerobic glycolysis than later larval and juvenile stages. Temperature has a marked effect on the ultrastructure, number, and phenotype of larval muscle fibers. Recent evidence suggests that egg incubation temperature can influence myogenic cell commitment, producing long-term consequences for fiber recruitment and growth performance during subsequent stages of the life cycle. The ecological significance of the phenotypic plasticity of muscle growth and some potential applications to fisheries science are briefly discussed.