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Artificial RNA Polymerase II Elongation Complexes for Dissecting Co-transcriptional RNA Processing Events
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Super elongation complex contains a TFIIF-related subcomplex.

Bruce A Knutson1, Marissa L Smith1, Nancy Walker-Kopp1

  • 1a Department of Biochemistry and Molecular Biology , SUNY Upstate Medical University , Syracuse , NY , USA.

Transcription
|May 26, 2016
PubMed
Summary

The Super Elongation Complex (SEC) shares functional similarities with TFIIF, a transcription factor, despite lacking structural homology. Researchers discovered an evolutionarily related TFIIF-like subcomplex within SEC, revealing new insights into its function.

Keywords:
EAFELLSECTFIIFelongationpausing

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Area of Science:

  • Molecular Biology
  • Gene Transcription
  • Protein Complexes

Background:

  • The Super Elongation Complex (SEC) is an RNA polymerase II (Pol II) elongation factor.
  • SEC exhibits functional similarities to TFIIF, a general transcription factor that enhances transcription elongation and reduces pausing.
  • Despite functional parallels, SEC and TFIIF lack apparent sequence and structural homology.

Purpose of the Study:

  • To investigate the evolutionary relationship between SEC and TFIIF.
  • To elucidate the mechanism by which SEC functions as a Pol II elongation factor.
  • To understand how SEC suppresses Pol II pausing.

Main Methods:

  • Utilized HHpred for homology searches.
  • Investigated the interaction between SEC subunit ELL and Pol II subunit Rbp2.

Main Results:

  • Identified an evolutionarily related TFIIF-like subcomplex within SEC using HHpred.
  • Demonstrated that the SEC subunit ELL interacts with the Pol II Rbp2 subunit.
  • Confirmed SEC's role as a TFIIF-like factor through subunit interactions.

Conclusions:

  • SEC possesses a TFIIF-like subcomplex, explaining its functional similarities to TFIIF.
  • The interaction between ELL and Rbp2 supports SEC's role in Pol II elongation.
  • These findings propose a novel model for SEC's function in regulating transcription elongation and suppressing Pol II pausing.