Growth signaling promotes H2A.Z deposition by SRCAP to sustain somatic tissue regeneration [ChIP-Seq]

In this study, we find that H2A.Z expression and chromatin occupancy dramatically decrease during normal epidermal differentiation. While the chromatin remodeler SRCAP is necessary and sufficient to maintain H2A.Z deposition in epidermal progenitors, EP400 is dispensable. Growth factor signaling mediated by the MAPK and PI3K signaling pathways is necessary to maintain both the expression and deposition of H2A.Z. Loss of SRCAP, H2AZ1, or H2AZ2 induces nuclear deformation and cytoplasmic DNA in progenitor keratinocytes which impairs DNA repair and proliferation. Additional H2A.Z ChIP-sequencing data performed in the progenitor or differentiated state with H2AZ1, H2AZ2, or SRCAP knockdown. We also include wild-type progenitor H3K9ac Cut&Run samples.