CLK:BMAL1 is a pioneer-like transcription factor [H2AZ-ChIP]

ABSTRACT: The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-spec

ORGANISM(S): Mus musculus

SUBMITTER: Jerome Menet 

PROVIDER: E-GEOD-47143 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress