The aurora B kinase and the polycomb protein ring1B combine to regulate active promoters in quiescent lymphocytes.
Mol Cell, 2013/9/12;51(5):647-61.
Frangini A[1], Sjöberg M, Roman-Trufero M, Dharmalingam G, Haberle V, Bartke T, Lenhard B, Malumbres M, Vidal M, Dillon N
Affiliations
PMID: 24034696
Impact factor: 19.328
Abstract
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.
MeSH terms
Animals; Aurora Kinase B; B-Lymphocytes; Cell Survival; Cells, Cultured; Gene Expression Regulation; Gene Knockout Techniques; Histones; Mice; Polycomb Repressive Complex 1; Promoter Regions, Genetic; RNA Polymerase II; Ribosomal Protein S6 Kinases, 90-kDa; T-Lymphocytes; Ubiquitin Thiolesterase; Ubiquitin-Conjugating Enzymes; Ubiquitin-Protein Ligases; Ubiquitination
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