Effect of ∆Np63 deletion on epigenomic rewiring via differential H3K27ac and H3K27me3 enrichment

Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT) for 48 hours. Technical triplicates of ∆Np63 WT and ∆Np63 KO treated in parallel were harvested for each IP for p63 and each histone modification for ChIP-seq. Comparative ChIP-seq of ±∆Np63 post-injury basal cell monolayers for H3K27ac, H3K27me3, and p63