GSE192776
The SWI/SNF subunit Dpf2 licenses Nrf2-dependent gene expression to enforce multilineage control of inflammation [ATAC-seq]
Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For ATACseq, Lin- cKit+ cells were processed following the OMIM-ATAC-seq protocol (Corces MR et al., Nature Methods 2017). Libraries were sequenced on a NextSeq (75bp, paired end reads) to obtain more than 40 million reads/sample. Results: For ATACseq, we obtained more than 40 million reads per sample. ATAC-Seq chromatin accessible regions were determined using ENCODE pipeline standards (https://github.com/ENCODE-DCC/atac-seq-pipeline; git commit 2b693ab). Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells. Overall design: Samples were obtained from primary bone marrow or spleen cells isolated or sorted from Dpf2f/f and Dpf2D/D mice of approximately 28 days of age. For RNAseq and ATACseq datasets, each file corresponds to data from 1 independent mouse/genotype. At least 3 mice (independent biological replicates) per condition and genotype were used. CUT&RUN samples were obtained from a pool of LK cells