Effect of ILF3 depletion in HeLa cells on RNA steady state levels

Upon detection of viral infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines to control viral dissemination. As part of their antiviral response, cells also trigger the translational shutoff response which prevents translation of viral mRNAs and cellular mRNAs in a non-selective manner. Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, suggesting the presence of additional regulatory mechanisms enabling expression of the self-defence genes. Here, we identified the dsRNA binding protein ILF3 as an essential host factor required for efficient translation of the central antiviral cytokine, IFNB1, and a subset of interferon-stimulated genes. By combining polysome profiling and next-generation sequencing, ILF3 was also found to be necessary to establish the dsRNA-induced transcriptional and translational programs. We propose a central role for the host factor ILF3 in enhancing expression of the antiviral defence mRNAs in cellular conditions where cap-dependent translation is compromised. HeLa cells were depleted of ILF3 using a pool of siRNAs that target ILF3 (siILF3) and a pool of non targeting siRNAs as a control (Mock) for 72 hours. the cells were then transfected with or without poly(I:C) for 4 hours and harvested using Trizol. For each experimental condition we used 3 biological replicates. The RNA was the sequenced using the Illumina Platform