{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Schwer B"],"funding":["HHS | NIH | National Institute of General Medical Sciences","NCI NIH HHS","NIGMS NIH HHS","NIH HHS"],"pagination":["e2108105118"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8379984"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["118(33)"],"pubmed_abstract":["The system of long noncoding RNA (lncRNA)-mediated transcriptional interference that represses fission yeast phosphate homoeostasis gene <i>pho1</i> provides a sensitive readout of genetic influences on cotranscriptional 3'-processing and termination and a tool for discovery of regulators of this phase of the Pol2 transcription cycle. Here, we conducted a genetic screen for relief of transcriptional interference that unveiled a mechanism by which Pol2 termination is enhanced via a gain-of-function mutation, G476S, in the RNA-binding domain of an essential termination factor, Seb1. The genetic and physical evidence for gain-of-function is compelling: 1) <i>seb1-G476S</i> de-represses <i>pho1</i> and <i>tgp1</i>, both of which are subject to lncRNA-mediated transcriptional interference; 2) <"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Genetic screen for suppression of transcriptional interference identifies a gain-of-function mutation in Pol2 termination factor Seb1."],"pmcid":["PMC8379984"],"funding_grant_id":["R35 GM126945","P30 CA008748","P30 GM124165","S10 OD021527","R35-GM126945","R01-GM134021","R01 GM134021"],"pubmed_authors":["Schwer B","Shuman S","Garg A","Jacewicz A"],"additional_accession":[]},"is_claimable":false,"name":"Genetic screen for suppression of transcriptional interference identifies a gain-of-function mutation in Pol2 termination factor Seb1.","description":"The system of long noncoding RNA (lncRNA)-mediated transcriptional interference that represses fission yeast phosphate homoeostasis gene <i>pho1</i> provides a sensitive readout of genetic influences on cotranscriptional 3'-processing and termination and a tool for discovery of regulators of this phase of the Pol2 transcription cycle. Here, we conducted a genetic screen for relief of transcriptional interference that unveiled a mechanism by which Pol2 termination is enhanced via a gain-of-function mutation, G476S, in the RNA-binding domain of an essential termination factor, Seb1. The genetic and physical evidence for gain-of-function is compelling: 1) <i>seb1-G476S</i> de-represses <i>pho1</i> and <i>tgp1</i>, both of which are subject to lncRNA-mediated transcriptional interference; 2) <","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2026-05-31T19:55:26.38Z","creation":"2025-02-18T23:32:35.648Z"},"accession":"S-EPMC8379984","cross_references":{"pubmed":["34389684"],"doi":["10.1073/pnas.2108105118"]}}