Cell density-dependent acetylation of Δnp63α is associated with p53-dependent cell cycle arrest

ΔNp63α is a p63 isoform that is predominantly expressed in the epidermal stem cells and in cancer. To find the regulatory pathways of ΔNp63α, we assessed whether ΔNp63α is acetylated and determined the functional implications of acetylation. First, the hinge region of p63 was shown to be acetylated by PCAF, similarly to other p53 family members. Second, acetylation synergistically induced cytoplasmic localization of ΔNp63α. Finally, acetyl-ΔNp63α was induced during high-density culture, suggesting that acetylation of ΔNp63α may reinforce cell cycle arrest upon cell contact. Altogether, these findings suggest that acetylation of ΔNp63α contributes to the epidermal homeostasis. Structured summary of protein interactions: PCAF acetylates ΔNp63α by acetylation assay (View Interaction: 1, 2, 3) ΔNp63α physically interacts with ΔNp63α by anti tag coimmunoprecipitation (View interaction) ΔNp63α physically interacts with p53 by anti bait coimmunoprecipitation (View interaction).