GSE211976
Transcriptome and chromatin accessibility mapping reveals a type I Interferon response triggered by Mycobacterium tuberculosis infection [ATAC-Seq]
Currently there is limited knowledge of changes in genome-wide chromatin accessibility during Mycobacterium tuberculosis (Mtb) infection and whether host phosphatases such as PPM1A play a role in this process. Using combinatorial chromatin accessibility (ATAC-seq) and transcriptomics (RNA-seq) profiling of wild-type (WT), PPM1A knockout (?PPM1A) and PPM1A overexpressing (PPM1A+) macrophages, we demonstrate that Mtb infection induces global chromatin remodeling consistent with changes in gene expression signatures. The strongest concordant chromatin accessibility and gene expression signature triggered by Mtb infection was enriched for genes involved in the type I interferon (IFN) signaling pathways. Modulation of PPM1A expression results in altered chromatin accessibility signatures during Mtb infection that are reflected in the total number, chromosome location and directionality of change. Overall design: ATAC-seq and RNA-seq for non-infected (NI) and Mtb infected wild-type (WT) THP-1, PPM1A knockout THP-1 (?PPM1A),  and PPM1A overexpressing THP-1 (PPM1A+) macrophages.