SAGA Is a General Cofactor for RNA Polymerase II Transcription

Publication date

2017-10-05

Authors

Baptista, Tiago
Grünberg, Sebastian
Minoungou, Nadège
Koster, Maria P. H.
Timmers, MarcISNI 0000000389187205
Hahn, Steve
Devys, Didier
Tora, László

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Supervisors

Document Type

Article

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taverne

Abstract

Prior studies suggested that SAGA and TFIID are alternative factors that promote RNA polymerase II transcription, with about 10% of genes in S. cerevisiae dependent on SAGA. We reassessed the role of SAGA by mapping its genome-wide location and role in global transcription in budding yeast. We find that SAGA maps to the UAS elements of most genes, overlapping with Mediator binding and irrespective of previous designations of SAGA- or TFIID-dominated genes. Disruption of SAGA through mutation or rapid subunit depletion reduces transcription from nearly all genes, measured by newly synthesized RNA. We also find that the acetyltransferase Gcn5 synergizes with Spt3 to promote global transcription and that Spt3 functions to stimulate TBP recruitment at all tested genes. Our data demonstrate that SAGA acts as a general cofactor required for essentially all RNA polymerase II transcription and is not consistent with the previous classification of SAGA- and TFIID-dominated genes. Baptista et al. show that SAGA, a transcriptional coactivator conserved in all eukaryotes, is involved in overall RNA polymerase II transcription in budding yeast. Using ChEC-seq, SAGA was shown to be recruited to both TATA-containing and TATA-less genes. In agreement, inactivation of SAGA leads to dramatic effects on nascent transcription.

Keywords

coactivator, RNA polymerase II, SAGA complex, TATA box, TFIID complex, transcription initiation, Taverne, Molecular Biology, Cell Biology, Journal Article

Citation

Baptista, T, Grünberg, S, Minoungou, N, Koster, M J E, Timmers, H T M, Hahn, S, Devys, D & Tora, L 2017, 'SAGA Is a General Cofactor for RNA Polymerase II Transcription', Molecular Cell, vol. 68, no. 1, pp. 130-143.e5. https://doi.org/10.1016/j.molcel.2017.08.016