MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [bulk RNA-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 bulk RNA-sequencing of wild-type (WT) and mdx myogenic cells in different conditions. Bulk RNA-sequencing of mogenic cells derived from WT and mdx Pax7-nGFP mice was performed in biological triplicate for 4 conditions (24 libraries total). PAX7 expressing MuSCs were isolated from hindlimb muscles before and 3-days after cardiotoxin injury. Myoblasts and 2-day differentiated myotubes were also collected after in vitro culture of WT and mdx PAX7 expressing cells.