BMAL1 Modulates Senescence Programming via AP-1 (WT and Bmal1 KO RNA-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, from WT C57BL/6 mice and Bmal1 -/- mice were collected for RNA-seq 12 hours post-synchronization with dexamethasone.