Regulation of Avian Skeletal Muscle Development and Maturation

Abstract

The chick has served as a useful model for studies on vertebrate development. Easy access to the embryo through the shell and the ready availability of large numbers of embryos at known developmental stages have contributed to the avian egg's popularity as a research model. Early research with the avian embryo described the differentiation and morphogenesis of the single cell egg into a free living chick (1). In the case of skeletal muscle, the origin and timing of mesodermal tissue differentiation and migration into somites and then skeletal muscle was followed. More recently, embryonic skeletal muscle precursors have been removed and cultured in vitro. Using combinations of in vivo and in vitro approaches, it has become apparent that the progenitors of muscle, the myoblasts, divide repeatedly and then cease making DNA and fuse with adjacent myoblasts to produce extended multicellular myotubes. DNA synthesis and nuclear division are not seen in multinucleated myotubes. After fusion, the myotubes begin to synthesize muscle-specific proteins such as creatine kinase, actin, tropomyosin, and myosin heavy chain. During the maturation process, there is an orderly progression in the type of myosin expressed until adult forms predominate. Once adult-type muscle is present, a cell similar to an embryonic myoblast, the satellite cell, is responsible for adding new DNA to existing myotubes to permit growth and for forming new myotubes following injury.

Many questions remain to be answered. Our current view of skeletal muscle development is mostly descriptive, with little appreciation for the signals and mechanisms which are responsible for the steady transition in cell number, morphology and function, the diversity of muscle types, and the growth and repair of existing muscle. This symposium addresses several areas of progress in understanding muscle development at the cellular level.