GSE111960
Arginine methylation controls cell proliferation by integrating E2F activity with the splicing machinery (RNA-seq data set)
Residue-specific arginine methylation (meR) on the E2F1 subunit plays an essential role in determining whether cell cycle progression or apoptosis ensues, although the molecular pathways underpinning the effects of methylation remain obscure.  We report here that the methylation events on E2F1 have a direct impact on the mechanisms which underpin gene expression control. Specifically, the PRMT5-mediated symR mark not only influences the transcription repertoire of genes targeted by E2F1, but also endows E2F1 with the ability to regulate RNA splicing. This occurs through tudor domain protein p100/TSN which reads the symR mark on E2F1, and thereby enables a distinct set of RNA to be alternatively spliced. The p100/TSN-E2F1 complex binds alternatively spliced RNAs, with many RNAs derived from E2F target genes connected with proliferation and cancer. Overall design: The U2OS Tet-ON inducle, stable cell line system was used to generate cell lines expressing WT E2F1, or meR deficient derivatives R109K and R111/113K (KK).  An empty vector cell line (pTRE) was used as a control, reference sample.  mRNA was enriched from three biological replicates and sequenced by Illumina NextSeq platform.