Downstream promoter interactions of TFIID TAFs facilitate transcription reinitiation

  1. Stephen Buratowski1
  1. 1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA;
  2. 2Department of Cancer Biology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
  3. 3Blais Proteomics Center, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
  1. Corresponding author: steveb{at}hms.harvard.edu

Abstract

TFIID binds promoter DNA to recruit RNA polymerase II and other basal factors for transcription. Although the TATA-binding protein (TBP) subunit of TFIID is necessary and sufficient for in vitro transcription, the TBP-associated factor (TAF) subunits recognize downstream promoter elements, act as coactivators, and interact with nucleosomes. In yeast nuclear extracts, transcription induces stable TAF binding to downstream promoter DNA, promoting subsequent activator-independent transcription reinitiation. In vivo, promoter responses to TAF mutations correlate with the level of downstream, rather than overall, Taf1 cross-linking. We propose a new model in which TAFs function as reinitiation factors, accounting for the differential responses of promoters to various transcription factor mutations.

Keywords

Footnotes

  • Received August 21, 2017.
  • Accepted November 9, 2017.

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