SPOP mutation reshapes chromatin landscape and transcriptional response to androgens [ChIP-seq]. SPOP mutation reshapes chromatin landscape and transcriptional response to androgens [ChIP-seq]

To define the epigenomic response to AR activation, we employed the 3D organoid model of murine prostate tissue. Control and SPOP-mutant prostate organoids were stimulated with 10 nM dihydrotestosterone (DHT) or vehicle. Next, we performed the transcriptomic analysis (mRNA-seq) together with profiling of the accessibility landscape (ATAC-seq), transcription factor (AR, and FOXA1) binding and H3K4me2 modified nucleosomes. Overall design: Examination of H3K4me2 histone modifications, and AR and FOXA1 binding in Control (normal) and SPOP-mutant mouse prostate organoids. In case of H3K4me2 and FOXA1 ChIP-seq cells we performed ChIP-seq on DHT and EtOH treated cells . In case of AR ChIP-eq, only on DHT-treated cells.