| First Author | Almada AE | Year | 2021 |
| Journal | Cell Rep | Volume | 34 |
| Issue | 4 | Pages | 108656 |
| PubMed ID | 33503437 | Mgi Jnum | J:312035 |
| Mgi Id | MGI:6716734 | Doi | 10.1016/j.celrep.2020.108656 |
| Citation | Almada AE, et al. (2021) FOS licenses early events in stem cell activation driving skeletal muscle regeneration. Cell Rep 34(4):108656 |
| abstractText | Muscle satellite cells (SCs) are a quiescent (non-proliferative) stem cell population in uninjured skeletal muscle. Although SCs have been investigated for nearly 60 years, the molecular drivers that transform quiescent SCs into the rapidly dividing (activated) stem/progenitor cells that mediate muscle repair after injury remain largely unknown. Here we identify a prominent FBJ osteosarcoma oncogene (Fos) mRNA and protein signature in recently activated SCs that is rapidly, heterogeneously, and transiently induced by muscle damage. We further reveal a requirement for FOS to efficiently initiate key stem cell functions, including cell cycle entry, proliferative expansion, and muscle regeneration, via induction of "pro-regenerative" target genes that stimulate cell migration, division, and differentiation. Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration. This work uncovers an early-activated FOS/ART1/mono-ADP-ribosylation (MARylation) pathway that is essential for stem cell-regenerative responses. |
