PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

Under inflammatory conditions the extravasation of monocytes into tissues through trans-endothelial migration is a fundamental immunological process underlying innate inflammatory responses across multiple organ systems contributing to tissue injury and the progression of autoimmunity, cardiovascular disease and particularly chronic lung disease. Methylation of protein arginine residues via protein arginine methyltransferases (PRMTs) is a post-translational epigenetic modification implicated in inflammatory responses. How PRMTs, particularly PRMT7, epigenetically regulates monocyte-driven inflammatory response in disease remains unclear. Here, we perform ATAC-seq analysis on an MHS macrophage cell line in which PRMT7 has been disrupted by CRISPR/Cas9 to examine chromatin accessibility regulated by PRMT7. ATAC-Seq analysis of MHS WT and PRMT7null cells.