Chromatin associated RNA sequencing during the IFN response induced by poly(I:C)

Type-I Interferons (IFNs) are central components of the antiviral response in vertebrates. Most cell types have the ability to respond to viral infection by secreting IFNs, however, the mechanisms that regulate correct expression of these cytokines are still not completely understood. Here, we show that activation of the IFN response regulates the expression of miRNAs in a post-transcriptional manner. Specifically, IFN impairs the binding of the nuclear Microprocessor complex to pri-miRNAs, which leads to a transient accumulation of unprocessed pri-miRNAs and consequently, decreased levels of specific miRNAs. We propose a model by which the inhibition of Microprocessor activity is an essential step to induce a robust type-I IFN response in mammalian cells. Comparison between RNA samples from mock and poly(I:C) transfected HeLa cells