LaminB1 ChIP-seq of DP thymocytes from wildtype and Suv39h1 and Suv39h2 double knockout mice

H3K9me3-dependent heterochromatin is critical for the silencing of repeat-rich pericentromeric regions and also has key roles in repressing lineage-inappropriate protein-coding genes for healthy cellular function. Within all eukaryotic nuclei, heterochromatin and euchromatin are spatially segregated, with euchromatin typically located in the nuclear interior and heterochromatin at the nuclear periphery. Here we investigate the disruption of lamina-association in the absence of H3K9me3-dependent heterochromatin by performing LaminB1 ChIP-seq in primary immune cells deficient in both Suv39h1 and Suv39h2 (Suv39DKO), the major mammalian histone methyltransferase enzymes which catalyse heterochromatic H3K9me3 deposition. Overall design: CD4+CD8+ double positive mouse thymocyte cells were analysed. ChIP and whole-cell extract (WCE) libraries from two replicates from Suv39h1+/y Suv39h2+/- (control) mice and two replicates from Suv39h1-/y Suv39h2-/- double knock-out (Suv39DKO) mice were independently prepared and sequenced to confirm successful immunoprecipitation. For the bioinformatics analysis, the replicate FASTQ files were merged. LaminB1 peaks were then called separately for the knockout and control mice using WCE as the input control in each case.