MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [scRNA-seq]

Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting and limitation of life. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells significantly contributes to disease progression. Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and muscle stem cell (MuSC) function in dystrophin deficient skeletal muscle using immunohistology, isometric force measurements, transplantation assays, and transcriptomic analysis. Here, we performed single cell RNA-sequencing of wild-type (WT) and mdx myogenic cells before and 5-days following cardiotoxin injury. Overall design: Muscle stem cells from uninjured and 5 days post cardiotoxin-injured WT and mdx Myf5creER;ROSA-mTmG mice were FACS-isolated. Two processed data files on the Series were reanalyzed with a different version of Cell ranger and reference for this study. The files are from GSM7498324 and GSM7498326 of GSE235284.