Protect-seq: Genome-wide profiling of nuclease inaccessible domains reveals physical properties of chromatin

We compare histone modifications, chromatin accessibility, and replication timing domain genome-wide in HCT116 colon cancer cells with its genetic derivative DKO cells which lack DNMT3B and DNMT1 activity and the fibrosarcoma cell line HT1080. This submission contains the following experiments on HCT116, DKO (DNMT1-/-;DNMT3b-/-), and HT1080 cells: 3 biological replicates of Protect-seq for each cell lines using Illumina and 1 Oxford Nanopore run on HCT116, 1 replicate of WGS on DKO and HT1080 for Protect-seq input, 2 biological replicates of H3K9me2, H3K9me3, H3K27me3, HP1alpha, CTCF, and input ChIP-seq and Early and Late fractions of Repli-seq for HT1080 cells. 1 biological replicate of H3K9me2, H3K9me3, HP1beta, HP1alpha, H3, and input ChIP-seq for HCT116 and DKO cells.