Affiliations 

  • 1 Molecular Cancer Research and Regenerative Medicine, University Medical Centre Utrecht, Utrecht, The Netherlands
  • 2 European Molecular Biology Laboratory (EMBL), Grenoble, France
  • 3 Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences and Netherlands Proteomics Centre, Utrecht University, Utrecht, The Netherlands
  • 4 Université Grenoble Alpes, CEA, CNRS, IBS (Institut de Biologie Structurale), Grenoble, France
  • 5 Molecular Cancer Research, Center for Molecular Medicine, University Medical Centre Utrecht, Utrecht, The Netherlands
  • 6 Bristol Synthetic Biology Centre BrisSynBio, Biomedical Sciences, School of Biochemistry, University of Bristol, Bristol, UK
  • 7 Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France
  • 8 Molecular Cancer Research and Regenerative Medicine, University Medical Centre Utrecht, Utrecht, The Netherlands. m.timmers@dkfz-heidelberg.de
  • 9 Bristol Synthetic Biology Centre BrisSynBio, Biomedical Sciences, School of Biochemistry, University of Bristol, Bristol, UK. imre.berger@bristol.ac.uk
Nat Struct Mol Biol, 2018 12;25(12):1119-1127.
PMID: 30510221 DOI: 10.1038/s41594-018-0156-z

Abstract

TFIID is a cornerstone of eukaryotic gene regulation. Distinct TFIID complexes with unique subunit compositions exist and several TFIID subunits are shared with other complexes, thereby conveying precise cellular control of subunit allocation and functional assembly of this essential transcription factor. However, the molecular mechanisms that underlie the regulation of TFIID remain poorly understood. Here we use quantitative proteomics to examine TFIID submodules and assembly mechanisms in human cells. Structural and mutational analysis of the cytoplasmic TAF5-TAF6-TAF9 submodule identified novel interactions that are crucial for TFIID integrity and for allocation of TAF9 to TFIID or the Spt-Ada-Gcn5 acetyltransferase (SAGA) co-activator complex. We discover a key checkpoint function for the chaperonin CCT, which specifically associates with nascent TAF5 for subsequent handover to TAF6-TAF9 and ultimate holo-TFIID formation. Our findings illustrate at the molecular level how multisubunit complexes are generated within the cell via mechanisms that involve checkpoint decisions facilitated by a chaperone.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.