Epigenetics and transcription regulation during eukaryotic diversification: the saga of TFIID
- 1Molecular Cancer Research and Regenerative Medicine, University Medical Centre Utrecht, 3584 CT Utrecht, The Netherlands;
- 2Department of Developmental Biology, Erasmus MC, 3015 CN Rotterdam, The Netherlands;
- 3Department of Urology, Medical Centre-University of Freiburg, 79106 Freiburg, Germany;
- 4Deutsches Konsortium für Translationale Krebsforschung (DKTK) Standort Freiburg, Deutsches Krebsforschungszentrum (DKFZ), 69120 Heidelberg, Germany;
- 5Theoretical Biology and Bioinformatics, Department of Biology, Utrecht University, 3584 CH Utrecht, The Netherlands
- Corresponding authors: m.timmers@dfkz-heidelberg.de, b.snel@uu.nl
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↵6 These authors contributed equally to this work.
Abstract
The basal transcription factor TFIID is central for RNA polymerase II-dependent transcription. Human TFIID is endowed with chromatin reader and DNA-binding domains and protein interaction surfaces. Fourteen TFIID TATA-binding protein (TBP)-associated factor (TAF) subunits assemble into the holocomplex, which shares subunits with the Spt–Ada–Gcn5–acetyltransferase (SAGA) coactivator. Here, we discuss the structural and functional evolution of TFIID and its divergence from SAGA. Our orthologous tree and domain analyses reveal dynamic gains and losses of epigenetic readers, plant-specific functions of TAF1 and TAF4, the HEAT2-like repeat in TAF2, and, importantly, the pre-LECA origin of TFIID and SAGA. TFIID evolution exemplifies the dynamic plasticity in transcription complexes in the eukaryotic lineage.
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Footnotes
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Supplemental material is available for this article.
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Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.300475.117.
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