H3K9ac data from mouse models suggest structural changes in the murine brain epigenome that involve the nuclear lamina

To explore whether tau-related epigenomic changes that we found human brain H3K9ac data (Synapse ID: syn4896408) are recapitulated in mouse models known to accumulate tau, we generated hippocampal H3K9ac ChIP-seq profiles from two different mouse models each at an early and a late stage of neurodegeneration. Specifically, we studied 6 and 11 months old mutant tau mice (MAPT P301S), which start to accumulate phosphorylated tau in neurons by 6 months. Wild-type mice of the same age were used as controls. The second mouse model was the CK-p25 model, which is characterized by increased amyloid-β levels early after p25 induction followed by increased tau phosphorylation and neuronal loss at later stages. Three months old CK-p25 mice were studied 2 weeks and 6 weeks after p25 induction and compared with CK littermate controls. H3K9ac profiles were generated for mutant tau mice at the ages of 6 and 11 months and compared with wild type controls. H3K9ac profiles of the CK-p25 mouse model were generated 2 and 6 weeks after p25 induction and compared with controls. The main purpose of the study was to detect differential H3K9 acetylation between AD mice and control mice. Therefore, a common set of peaks was defined, then the number of reads in these peaks was counted, finally peaks were tested for different read counts between AD mice and controls. The processed data provided under this series contains a bed file with peak locations and a matrix file with read counts for each sample and peak. Samples of input DNA (without ChIP) were sequenced and used as negative controls during peak calling, but are not represented in the matrix file.