Muscle stem cells, also called satellite cells, reside in skeletal muscle and maintain a G0 state (quiescent state) in resting muscles. Satellite cells are the main player of muscle regeneration and they could exit quiescent state and undergo lineage progression. Cell fate commitment during this process is tightly regulated by various factors. Muscle specific transcription factor, MyoD, has been shown to act as the master regulator of satellite cell fate. MyoD overexpression could initiate myogenic program in fibroblast cells. An upstream lncRNA, termed lncMyoD, could physically interact with MyoD and facilitate MyoD function. Our truncation study of MyoD indicates that this interaction may occur at N-terminal of MyoD protein. We also explored the potential role of epigenetic modi...[ Read more ]

Muscle stem cells, also called satellite cells, reside in skeletal muscle and maintain a G0 state (quiescent state) in resting muscles. Satellite cells are the main player of muscle regeneration and they could exit quiescent state and undergo lineage progression. Cell fate commitment during this process is tightly regulated by various factors. Muscle specific transcription factor, MyoD, has been shown to act as the master regulator of satellite cell fate. MyoD overexpression could initiate myogenic program in fibroblast cells. An upstream lncRNA, termed lncMyoD, could physically interact with MyoD and facilitate MyoD function. Our truncation study of MyoD indicates that this interaction may occur at N-terminal of MyoD protein. We also explored the potential role of epigenetic modification, Histone 3 lysine 4 crotonylation (H3K4cr) in satellite cell fate regulation. Different levels of H3K4cr in cultured myogenic cells could be detected, indicating that H3K4cr may be related to cell heterogeneity and cell fate. Data from fiber-associated satellite cells suggested that the correlation and, further, genome-wide reprogramming event were observed with satellite cell activation, proliferation, and differentiation. This is also supported by in vivo regeneration study. We also captured cell pairs with asymmetric levels of H3K4cr and it has been shown to be correlated to asymmetric expression of MyoD.