SAGA Is a General Cofactor for RNA Polymerase II Transcription
Baptista, Tiago; Grünberg, Sebastian; Minoungou, Nadège; Koster, Maria J.E.; Timmers, H. T.Marc; Hahn, Steve; Devys, Didier; Tora, László
(2017) Molecular Cell, volume 68, issue 1, pp. 130 - 143
(Article)
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
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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.
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Keywords: coactivator, RNA polymerase II, SAGA complex, TATA box, TFIID complex, transcription initiation, Molecular Biology, Cell Biology, Journal Article
ISSN: 1097-2765
Publisher: Cell Press
Note: Funding Information: We are grateful to Violaine Alunni and Christelle Thibault (IGBMC) for array hybridization. We thank Vincent Géli and Pierre Luciano (CRCM, Marseille, France) for advice and discussion, Gabe Zentner (Indiana University) for advice on ChEC-seq data analysis, and P. Anthony Weil for antibodies. We thank Farrah El Saafin for critically reading the manuscript. T.B. was supported by a Marie Curie-ITN fellowship ( EU-FP7 PEOPLE-2013 program , PITN-GA-2013-606806 , NR-NET ) and the Fondation ARC . This work was supported by NIH grants GM053451 and GM075114 (to S.H.), funds from the Agence Nationale de la Recherche ( ANR-15-CE11-0022 SAGA2 to D.D.; ANR-13-BSV8-0021-03 DiscoverIID to L.T.), and the European Research Council Advanced grant ( ERC-2013-340551, Birtoaction , to L.T.). This study was also supported by ANR-10-LABX-0030-INRT , a French State fund managed by the Agence Nationale de la Recherche under the frame program Investissements d’Avenir ANR-10-IDEX-0002-02 . N.M. is a student in the Magistère de Génétique Graduate Program at Université Paris Diderot, Sorbonne, Paris Cité. Publisher Copyright: © 2017 Elsevier Inc.
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