| First Author | Talluri S | Year | 2010 |
| Journal | Mol Cell Biol | Volume | 30 |
| Issue | 4 | Pages | 948-60 |
| PubMed ID | 20008551 | Mgi Jnum | J:160500 |
| Mgi Id | MGI:4454529 | Doi | 10.1128/MCB.01168-09 |
| Citation | Talluri S, et al. (2010) A G1 checkpoint mediated by the retinoblastoma protein that is dispensable in terminal differentiation but essential for senescence. Mol Cell Biol 30(4):948-60 |
| abstractText | Terminally differentiated cell types are needed to live and function in a postmitotic state for a lifetime. Cellular senescence is another type of permanent arrest that blocks the proliferation of cells in response to genotoxic stress. Here we show that the retinoblastoma protein (pRB) uses a mechanism to block DNA replication in senescence that is distinct from its role in permanent cell cycle exit associated with terminal differentiation. Our work demonstrates that a subtle mutation in pRB that cripples its ability to interact with chromatin regulators impairs heterochromatinization and repression of E2F-responsive promoters during senescence. In contrast, terminally differentiated nerve and muscle cells bearing the same mutation fully exit the cell cycle and block E2F-responsive gene expression by a different mechanism. Remarkably, this reveals that pRB recruits chromatin regulators primarily to engage a stress-responsive G(1) arrest program. |
