Type I and II PRMTs inversely regulate post-transcriptional intron detention through Sm and CHTOP methylation.
Ontology highlight
ABSTRACT: Protein arginine methyltransferases (PRMTs) are required for the regulation of RNA processing factors. Type I PRMT enzymes catalyze mono- and asymmetric dimethylation; Type II enzymes catalyze mono- and symmetric dimethylation. To understand the specific mechanisms of PRMT activity in splicing regulation, we inhibited Type I and II PRMTs and probed their transcriptomic consequences. Using the newly developed Splicing Kinetics and Transcript Elongation Rates by Sequencing (SKaTER-seq) method, analysis of co-transcriptional splicing demonstrated that PRMT inhibition resulted in altered splicing rates. Surprisingly, co-transcriptional splicing kinetics did not correlate with final changes in splicing of polyadenylated RNA. This was particularly true for retained introns (RI). By using actinom
SUBMITTER: Maron MI
PROVIDER: S-EPMC8765754 | biostudies-literature | 2022 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA