BMAL1 Modulates Senescence Programming via AP-1 (BMAL1-ChIP-seq)
Cellular senescence and circadian dysregulation are biological hallmarks of aging. Whether they are interdependent has not been thoroughly studied. We hypothesize that BMAL1, a pioneer transcription factor and master regulator of the molecular circadian clock, plays a role in the senescence program. In this study, we show that BMAL1 in is uniquely localized to genomic motifs associated with AP-1 in senescent cells and contributes to AP-1 transcriptional control of the senescence program. Overall design: Triplicate samples of control and senescent primary mouse fibroblasts were collected for BMAL1-ChIP-seq 12 hours post-synchronization with dexamethasone.