STAT1, STAT2 and IRF9 transcription factor binding analysis in wild type mouse embryonic fibroblasts (MEF) in response to type I interferons

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Mechanisms to meet this demand on the relevant molecular machinery include remodeling of chromatin but also changes in transcription factor interaction prior and during the IFN response. Our results show how transcription factors STAT1, STAT2 and IRF9 change binding patterns upon IFNb treatment in wild type mouse embryonic fibroblasts. Overall design: Methods: Genome wide binding of transcription factors STAT1, STAT2 and IRF9 in untreated and 90 min IFNb treated wild-type (WT) mouse embryonic fibroblasts. Samples were analyzed by using Illumina sequencing.