The conserved protein Seb1 drives transcription termination by binding RNA polymerase II and nascent RNA
Sina Wittmann,
Max Renner,
Beth R. Watts,
Oliver Adams,
Miles Huseyin,
Carlo Baejen,
Kamel El Omari,
Cornelia Kilchert,
Dong-Hyuk Heo,
Tea Kecman,
Patrick Cramer,
Jonathan M. Grimes and
Lidia Vasiljeva ()
Additional contact information
Sina Wittmann: University of Oxford
Max Renner: Wellcome Trust Centre for Human Genetics, University of Oxford
Beth R. Watts: University of Oxford
Oliver Adams: University of Oxford
Miles Huseyin: University of Oxford
Carlo Baejen: Max Planck Institute for Biophysical Chemistry
Kamel El Omari: Diamond Light Source Ltd, Harwell Science & Innovation Campus
Cornelia Kilchert: University of Oxford
Dong-Hyuk Heo: University of Oxford
Tea Kecman: University of Oxford
Patrick Cramer: Max Planck Institute for Biophysical Chemistry
Jonathan M. Grimes: Wellcome Trust Centre for Human Genetics, University of Oxford
Lidia Vasiljeva: University of Oxford
Nature Communications, 2017, vol. 8, issue 1, 1-15
Abstract:
Abstract Termination of RNA polymerase II (Pol II) transcription is an important step in the transcription cycle, which involves the dislodgement of polymerase from DNA, leading to release of a functional transcript. Recent studies have identified the key players required for this process and showed that a common feature of these proteins is a conserved domain that interacts with the phosphorylated C-terminus of Pol II (CTD-interacting domain, CID). However, the mechanism by which transcription termination is achieved is not understood. Using genome-wide methods, here we show that the fission yeast CID-protein Seb1 is essential for termination of protein-coding and non-coding genes through interaction with S2-phosphorylated Pol II and nascent RNA. Furthermore, we present the crystal structures of the Seb1 CTD- and RNA-binding modules. Unexpectedly, the latter reveals an intertwined two-domain arrangement of a canonical RRM and second domain. These results provide important insights into the mechanism underlying eukaryotic transcription termination.
Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14861
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DOI: 10.1038/ncomms14861
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