GSE125182
System-wide profiling of RNA-binding proteins uncovers key regulators of virus infection
The compendium of RNA-binding proteins (RBPs) has been greatly expanded by the development of RNA interactome capture (RIC). However, it remained unknown if the complement of RBPs changes in response to environmental perturbations and whether these rearrangements are important. To answer these questions, we developed 'comparative RIC' and applied it to cells challenged with an RNA virus, called sindbis (SINV). Over two hundred RBPs display differential interaction with RNA upon SINV infection. These alterations are mainly driven by the loss of cellular mRNAs and the emergence of viral RNA. RBPs stimulated by the infection redistribute to viral replication factories and regulate the capacity of the virus to infect. For example, ablation of XRN1 causes cells to be refractory to SINV, while GEMIN5 moonlights as a regulator of SINV gene expression. In summary, RNA availability controls RBP localisation and function in SINV-infected cells. Overall design: RNA-seq and iCLIP-seq in SINV infected human cells.