Impact of iASPP knockout on p63 genome occupancy in mouse keratinocytes

iASPP (PPP1R13L) is an evolutionarily conserved regulator of p53 family members. In mice, iASPP deletion in keratin 14-expressing keratinocytes is sufficient to cause detrimental phenotypes with squamous epithelium abnormalities. In human skin, wild-type nuclear iASPP colocalizes with the key squamous differentiation regulatory factor, TP63, and iASPP mutations are associated with abnormalities in skin development. To clarify how iASPP modulates p63 genome occupancy, p63 ChIP-seq data from iASPP WT and iASPP KO primary mouse keratinocytes (MKC) were compared. Mouse keratinocytes (MKC) were isolated from mice with or without a Krt14-Cre+;Ppp1r13l-/- genotype, which causes a deletion of iASPP exon 8 in Krt14-expressing epithelial cells. ChIP-seq was performed on isolated keratinocytes from Krt14-Cre+;Ppp1r13l-/- (iASPP KO) or iASPP WT mice, using the H129 p63 antibody (Santa Cruz). KO and WT ChIP-seq profiles were then compared using a quantitative method for ChIP-seq sample comparison (MAnorm).