RNA-seq analysis of UFM1 deletion effect on gene expression during the RIG-I antiviral response

UFM1 is a post-translational modification that regulates protein function during the ER stress response, DNA damage response, and antiviral response. The goal of this experiment was to determine the role of UFM1 in regulating gene expression induced during RIG-I signaling. We found that deletion of UFM1 broadly decreases transcription of some interferon-stimulated genes during activation of antiviral innate immunity. In subsequent experiments, we found that this is due to UFM1/ufmylation regulation of RIG-I interaction with its trafficking protein 14-3-3epsilon. Overall design: Wild-type or UFM1 CRISPR/CAS9 knock-out 293T cells were seeded in 6-well plates and infected with Sendai virus (SenV) (200HAU) or mock infection for 18 hours. RNA was extracted and RNA-seq was performed. 3 biological replicates were performed for each condition.