GSE42728
Genome wide maps of p53 binding in IMR90 cells
Oncogene-induced senescence is an anti-proliferative stress response program that acts as a fail-safe mechanism to  limit oncogenic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor  pathways. We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently upregulated  during oncogene-induced senescence, a setting where it acts in response to p53 as a direct transcriptional  target. Once induced, E2F7 binds and represses a series of E2F target genes and cooperates with RB to efficiently  promote cell cycle arrest and limit oncogenic transformation. Disruption of RB triggers a further increase in E2F7,  which induces a second cell cycle checkpoint that prevents unconstrained cell division despite aberrant DNA  replication. Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes. Overall design: Examination of p53 binding in either growing or senescent IMR90 cells with different hairpins.