Journal
JOURNAL OF CELL BIOLOGY
Volume 183, Issue 7, Pages 1259-1274Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200805146
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Funding
- National Health and Medical Research Council ( NHMRC) of Australia
- Cancer Council Victoria
- National Institutes of Health [5R01HL077814]
- NHMRC
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In mammals, the mechanisms regulating the number of active copies of the similar to 200 ribosomal RNA (rRNA) genes transcribed by RNA polymerase I are unclear. We demonstrate that depletion of the transcription factor upstream binding factor (UBF) leads to the stable and reversible methylation-independent silencing of rRNA genes by promoting histone H1-induced assembly of transcriptionally inactive chromatin. Chromatin remodeling is abrogated by the mutation of an extracellular signal-regulated kinase site within the high mobility group box 1 domain of UBF1, which is required for its ability to bend and loop DNA in vitro. Surprisingly, rRNA gene silencing does not reduce net rRNA synthesis as transcription from remaining active genes is increased. We also show that the active rRNA gene pool is not static but decreases during differentiation, correlating with diminished UBF expression. Thus, UBF1 levels regulate active rRNA gene chromatin during growth and differentiation.
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