G9a regulated chromatin accessibility programs during B cell differentiation [ATAC-seq]
B cell differentiation is tightly regulated through coordinated changes in metabolism, division, expression of transcription factors, and epigenetic programming mediated by histone modifying enzymes.  In this study, we examined the role of an epigenetic writer, the histone H3K9 mono and dimethyltransferse G9a, in regulating the chromatin accessibility programs during B-cell development and plasma cell (PC) formation.  Utilizing a B-cell specific G9afl/flCd19Cre/+ conditional mouse model we performed ATAC-seq on naive and activated B cells and plasma cells that formed in response to LPS. Overall design: Differential chromatin accessibility analysis of ATAC-seq data for naïve, activated B and plasma cells from Ctrl and  G9a KO samples