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. 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.

固有免疫系统介导的宿主防御，需先建立抗菌状态，使细胞能在适应性免疫应答启动前抵御微生物侵袭。干扰素（Interferons, IFN）在细胞自主性抗菌免疫的建立过程中发挥至关重要的作用。因此，应答速率是细胞对干扰素产生应答的关键特性之一。由于多数抗菌应答需从头构建，这一过程首要聚焦于基因表达——即宿主防御基因在静息状态与激活状态转录间的快速切换。为满足相关分子机器的此类需求，其调控机制包括染色质重塑，以及干扰素应答前后转录因子相互作用的改变。本研究结果阐明了转录因子STAT1、STAT2与IRF9在野生型小鼠胚胎成纤维细胞经干扰素β（IFNb）处理后结合模式的变化规律。实验方法：在未处理与经IFNb处理90分钟的野生型（wild-type, WT）小鼠胚胎成纤维细胞中，开展转录因子STAT1、STAT2与IRF9的全基因组结合检测。所有样本均采用Illumina测序技术进行分析。