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.