Identify WT and p53 3KR target in basal progenitor cells of epidermis
Unbalanced and growth promoting cell fate dynamics that follow p53 loss, and the inability of canonical p53 functions to restrict clonal expansion, suggest the existence of a non-canonical p53 transcriptional program that controls key cell fate regulators. We hypothesized that these cell fate genes are among the shared targets of p53WT and p533KR. Overall design: p53 ChIP-seq performed in isolated epidermal basal progenitor cells of  p53WT and p533KR animals, 25uM of Nutlin-3a were added to digestion medium to stabilize p53