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Coactivator-Dependent Oscillation of Chromatin Accessibility Dictates Circadian Gene Amplitude via REV-ERB Loading.
- Source :
-
Molecular Cell . Dec2015, Vol. 60 Issue 5, p769-783. 15p. - Publication Year :
- 2015
-
Abstract
- Summary A central mechanism for controlling circadian gene amplitude remains elusive. We present evidence for a “facilitated repression (FR)” model that functions as an amplitude rheostat for circadian gene oscillation. We demonstrate that ROR and/or BMAL1 promote global chromatin decondensation during the activation phase of the circadian cycle to actively facilitate REV-ERB loading for repression of circadian gene expression. Mechanistically, we found that SRC-2 dictates global circadian chromatin remodeling through spatial and temporal recruitment of PBAF members of the SWI/SNF complex to facilitate loading of REV-ERB in the hepatic genome. Mathematical modeling highlights how the FR model sustains proper circadian rhythm despite fluctuations of REV-ERB levels. Our study not only reveals a mechanism for active communication between the positive and negative limbs of the circadian transcriptional loop but also establishes the concept that clock transcription factor binding dynamics is perhaps a central tenet for fine-tuning circadian rhythm. [ABSTRACT FROM AUTHOR]
- Subjects :
- *DNA condensation
*NUCLEOPROTEINS
*CHROMOSOMES
*CHROMATIN
*GENOMES
Subjects
Details
- Language :
- English
- ISSN :
- 10972765
- Volume :
- 60
- Issue :
- 5
- Database :
- Academic Search Index
- Journal :
- Molecular Cell
- Publication Type :
- Academic Journal
- Accession number :
- 111303215
- Full Text :
- https://doi.org/10.1016/j.molcel.2015.10.024