| First Author | Frangini A | Year | 2013 |
| Journal | Mol Cell | Volume | 51 |
| Issue | 5 | Pages | 647-61 |
| PubMed ID | 24034696 | Mgi Jnum | J:203428 |
| Mgi Id | MGI:5527017 | Doi | 10.1016/j.molcel.2013.08.022 |
| Citation | Frangini A, et al. (2013) The aurora B kinase and the polycomb protein ring1B combine to regulate active promoters in quiescent lymphocytes. Mol Cell 51(5):647-61 |
| abstractText | Reversible cellular quiescence is critical for developmental processes in metazoan organisms and is characterized by a reduction in cell size and transcriptional activity. We show that the Aurora B kinase and the polycomb protein Ring1B have essential roles in regulating transcriptionally active genes in quiescent lymphocytes. Ring1B and Aurora B bind to a wide range of active promoters in resting B and T cells. Conditional knockout of either protein results in reduced transcription and binding of RNA Pol II to promoter regions and decreased cell viability. Aurora B phosphorylates histone H3S28 at active promoters in resting B cells as well as inhibiting Ring1B-mediated ubiquitination of histone H2A and enhancing binding and activity of the USP16 deubiquitinase at transcribed genes. Our results identify a mechanism for regulating transcription in quiescent cells that has implications for epigenetic regulation of the choice between proliferation and quiescence. |
