Tip60-mediated H2A.Z acetylation is required for neuronal fate specification and bivalent gene activation [ATAC-Seq]

Examination of the effects of Tip60/Kat5 depletion on chromatin accessibility dynamics during Ascl1-mediated direct reprogramming of mouse embryonic fibroblasts (MEFs) into induced neuronal cells. Overall design: Genome-wide chromatin accessibility (ATAC-seq) determined for rtTA control or Ascl1-transduced MEFs co-expressing shRNA targeting Tip60 (shTip60), shRNA targeting H2A.Z (shH2AZ), or non-targetng control shRNA (shNTC) at day2 and/or day5 of iN cell reprogramming.