Skeletal muscle has primarily evolved to facilitate coordinated voluntary movement in animals. The functional cells of skeletal muscle are the long, cylindrical shaped, syncytial myofibres. Each is packed with myofibrils composed of thousands of sarcomeres, containing the actin and myosin filaments that interact to generate force. These multinucleated myofibres often contain hundreds of post-mitotic myonuclei, and are formed by the fusion of many myoblasts during developmental myogenesis. Postnatal muscle growth in mouse is initially achieved by both further increasing the number of myonuclei, combined with myofibre hypertrophy. The myoblasts that supply these new myonuclei are generated by muscle satellite cells. After approximately 3 weeks of age though, further muscle growth occurs solely by myofibre hypertrophy. Satellite cells become mitotically quiescent as muscle matures, residing in a niche on the surface of the myofibre. However, these stem cells can be readily activated to enter the cell cycle to provide further myoblasts for the routine needs of myofibre homeostasis and hypertrophy, or the more sporadic demands for muscle fibre repair and regeneration. There are distinct parallels between developmental and regenerative myogenesis, both in the mechanism, myoblasts fusing to damaged myofibres to replace lost myonuclei, or fusing together for de novo formation of new myofibres, and the regulatory networks that control satellite cell function. Here, I will give an overview of the role of satellite cells in skeletal muscle biology and discuss the progress that we have made in understanding how satellite cell function is regulated.