Satellite cells, or muscle stem cells, are resident somatic stem cells responsible for skeletal muscle regeneration. In resting, uninjured adult muscles, majority of satellite cells are quiescent. Upon stimulation such as acute injury, satellite cells are activated and subsequently proliferate, differentiate and finally fuse to form new muscle fibers. The whole process of muscle regeneration is tightly regulated. Emerging evidence shows that alternative splicing plays important roles in stem cell pluripotency maintenance and cell fate determination. However, the role of alternative splicing in satellite cell is still largely unknown. To better understand the role of alternative splicing in satellite cell, we investigate the role of Rbfox2 in muscle regeneration. Rbfox2 is a major spl...[ Read more ]

Satellite cells, or muscle stem cells, are resident somatic stem cells responsible for skeletal muscle regeneration. In resting, uninjured adult muscles, majority of satellite cells are quiescent. Upon stimulation such as acute injury, satellite cells are activated and subsequently proliferate, differentiate and finally fuse to form new muscle fibers. The whole process of muscle regeneration is tightly regulated. Emerging evidence shows that alternative splicing plays important roles in stem cell pluripotency maintenance and cell fate determination. However, the role of alternative splicing in satellite cell is still largely unknown. To better understand the role of alternative splicing in satellite cell, we investigate the role of Rbfox2 in muscle regeneration. Rbfox2 is a major splicing regulator. Previous studies have showed that Rbfox2 regulates alternative splicing in several kinds of stem cells such as embryonic stem cells. In addition, Rbfox2 was also found to be important regulator of myoblast fusion. These findings make it a good candidate for us to study the role of alternative splicing in satellite cell. To investigating the role of Rbfox2, expression level of Rbfox2 in different stages of postnatal myogenesis was characterized using immunostaining approach. The result showed that Rbfox2 was upregulated after satellite cell activation. To further study the function of Rbfox2, we used siRNA to knock down Rbfox2 in satellite cells and also generated an Rbfox2 conditional knock out mouse line. Our study will help to understand the role of Rbfox2 in satellite cell and provide insight as to how transcripts are differentially regulated during skeletal muscle regeneration.