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Conserved protein Seb1 that interacts with RNA polymerase II and RNA is an antipausing transcription elongation factor

Lookup NU author(s): Dr Soren NielsenORCiD, Professor Nikolay ZenkinORCiD

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

© 2026 Kuś et al. Published by Cold Spring Harbor Laboratory Press for the RNA Society. Maturation of protein-coding precursor messenger RNA (pre-mRNA) is closely linked to RNA polymerase II (Pol II) transcription. However, the mechanistic understanding of how pre-mRNA processing is coordinated with transcription remains incomplete. Conserved proteins interacting with the C-terminal domain of the largest catalytic subunit of Pol II and nascent RNA (CID-RRM factors) were demonstrated to play a role in pre-mRNA 3'-end processing and termination of Pol II transcription. Here, we use a fully reconstituted system to demonstrate that the fission yeast CID-RRM factor Seb1 acts as a bona fide elongation factor. Our analyses show that Seb1 exhibits context-dependent regulation of Pol II pausing, capable of either promoting or inhibiting pause site entry. We propose that CID-RRM factors coordinate Pol II transcription and pre-mRNA 3'-end processing by modulating the rate of Pol II transcription.


Publication metadata

Author(s): Kus K, Nielsen S, Zenkin N, Vasiljeva L

Publication type: Article

Publication status: Published

Journal: RNA

Year: 2025

Volume: 32

Pages: 71-81

Online publication date: 24/10/2025

Acceptance date: 04/10/2025

Date deposited: 05/01/2026

ISSN (print): 1355-8382

ISSN (electronic): 1469-9001

Publisher: Cold Spring Harbor Laboratory Press

URL: https://doi.org/10.1261/rna.080765.125

DOI: 10.1261/rna.080765.125

Data Access Statement: Supplemental material is available for this article at https://rnajournal.cshlp.org/content/32/1/71/suppl/DC1

PubMed id: 41136340


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Funding

Funder referenceFunder name
217189/Z/19/ZWellcome Trust
BBSRC grant BB/Y00194X/1
Wellcome Trust Senior Research Fellowship (WT106994/Z/15/Z)

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