CTD-dependent and -independent mechanisms govern co-transcriptional capping of Pol II transcripts

  • Nat Commun. 2018 Aug 23;9(1):3392. doi: 10.1038/s41467-018-05923-w.
Melvin Noe Gonzalez  1 ,  Shigeo Sato  1 ,  Chieri Tomomori-Sato  1 ,  Joan W Conaway  1  2 ,  Ronald C Conaway  3  4
Affiliations
  • 1. Stowers Institute for Medical Research, 1000 E 50 th Street, Kansas City, MO, 64110, USA.
  • 2. Department of Biochemistry and Molecular Biology, Kansas University Medical Center, Kansas City, KS, 66160, USA.
  • 3. Stowers Institute for Medical Research, 1000 E 50 th Street, Kansas City, MO, 64110, USA. [email protected].
  • 4. Department of Biochemistry and Molecular Biology, Kansas University Medical Center, Kansas City, KS, 66160, USA. [email protected].
PMID: 30139934 DOI: 10.1038/s41467-018-05923-w
Abstract

Co-transcriptional capping of RNA polymerase II (Pol II) transcripts by capping enzyme proceeds orders of magnitude more efficiently than capping of free RNA. Previous studies brought to light a role for the phosphorylated Pol II carboxyl-terminal domain (CTD) in activation of co-transcriptional capping; however, CTD phosphorylation alone could not account for the observed magnitude of activation. Here, we exploit a defined Pol II transcription system that supports both CTD phosphorylation and robust activation of capping to dissect the mechanism of co-transcriptional capping. Taken together, our findings identify a CTD-independent, but Pol II-mediated, mechanism that functions in parallel with CTD-dependent processes to ensure optimal capping, and they support a "tethering" model for the mechanism of activation.

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