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Publication : PRMT7 Preserves Satellite Cell Regenerative Capacity.

First Author  Blanc RS Year  2016
Journal  Cell Rep Volume  14
Issue  6 Pages  1528-1539
PubMed ID  26854227 Mgi Jnum  J:271361
Mgi Id  MGI:6281057 Doi  10.1016/j.celrep.2016.01.022
Citation  Blanc RS, et al. (2016) PRMT7 Preserves Satellite Cell Regenerative Capacity. Cell Rep 14(6):1528-1539
abstractText  Regeneration of skeletal muscle requires the continued presence of quiescent muscle stem cells (satellite cells), which become activated in response to injury. Here, we report that whole-body protein arginine methyltransferase PRMT7(-/-) adult mice and mice conditionally lacking PRMT7 in satellite cells using Pax7-CreERT2 both display a significant reduction in satellite cell function, leading to defects in regenerative capacity upon muscle injury. We show that PRMT7 is preferentially expressed in activated satellite cells and, interestingly, PRMT7-deficient satellite cells undergo cell-cycle arrest and premature cellular senescence. These defects underlie poor satellite cell stem cell capacity to regenerate muscle and self-renew after injury. PRMT7-deficient satellite cells express elevated levels of the CDK inhibitor p21CIP1 and low levels of its repressor, DNMT3b. Restoration of DNMT3b in PRMT7-deficient cells rescues PRMT7-mediated senescence. Our findings define PRMT7 as a regulator of the DNMT3b/p21 axis required to maintain muscle stem cell regenerative capacity.
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