RNA-Seq analysis of isolated satellite cells in Prmt5 deficient mice.

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SCs are mononuclear and are located between the basal lamina and the plasma membrane of myofibers. They are typically characterized by presence of the transcription factor paired-box 7 (PAX7) that is widely used as a satellite cell marker. Under normal physiological conditions SCs are quiescent but are activated by insults such as injury, disease or exercise. Once activated, satellite cells proliferate and subsequently differentiate into myoblasts to finally fuse to form new myofibers or with preexisting myofibers to repair or rebuild the skeletal muscle. A minority of SCs retains stem cell characteristics and self-renews to assure future bouts of regeneration throughout most of adult life. While a comprehensive picture of the regulatory events controlling SC fate has not yet been achieved, several factors were recently identified playing important roles in functional processes. One example is the arginine methyltransferase Prmt5 that is known to have multiple roles in germ cells and is involved in the maintenance of ES cell pluripotency. We have previously shown that Prmt5 is required for muscle stem cell proliferation and regenerative myogenesis due to direct epigenetic regulation of the cell cycle inhibitor p21. Here we provide a dataset that investigates the loss of Prmt5 in isolated Pax7(+) primary SCs using the Pax7(CreERT2)/Prmt5(loxP/loxP) knockout mouse model. 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