Sox9 directs divergent epigenomic states in brain tumor subtypes (ChIP-Seq)

The goal of this study was to profile active H3K27ac marks between autochthonous mouse models of high-grade glioma (HGG) and ependymoma (EPN). Furthermore, with the objective of how transcription factor Sox9 affect H3K27ac states in these two models, we also profiled H3K27ac status between HGG and EPN after Sox9 overexpression (Sox9-GOF) or deletion (Sox9-LOF) in each of these models. In addition, we extended our studies to evaluate both H3K27ac and Sox9 states in human HGG and mouse EPN derived tumor cells. Chromatin immunoprecipitation (ChIP-seq) for H3K27ac in tumors from mouse models HGG, EPN and human HGG; ChIP-Seq for Sox9 in human HGG; ChIP-Seq for Sox9 from mouse EPN derived tumor cells. All experiments performed in independent biological replicates except for human HGG and mouse EPN derived cells.