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               <dc:title>Gcn5-mediated acetylation at MBF-regulated promoters induces the G1/S transcriptional wave</dc:title>
               <dc:creator>González Medina, Alberto, 1990-</dc:creator>
               <dc:creator>Hidalgo Hernando, Elena</dc:creator>
               <dc:creator>Ayté del Olmo, José</dc:creator>
               <dc:subject>Gene regulation</dc:subject>
               <dc:subject>Chromatin and epigenetics</dc:subject>
               <dc:description>In fission yeast, MBF-dependent transcription is inactivated at the end of S phase through a negative feedback loop that involves the co-repressors, Yox1 and Nrm1. Although this repression system is well known, the molecular mechanisms involved in MBF activation remain largely unknown. Compacted chromatin constitutes a barrier to activators accessing promoters. Here, we show that chromatin regulation plays a key role in activating MBF-dependent transcription. Gcn5, a part of the SAGA complex, binds to MBF-regulated promoters through the MBF co-activator Rep2 in a cell cycle-dependent manner and in a reverse correlation to the binding of the MBF co-repressors, Nrm1 or Yox1. We propose that the co-repressors function as physical barriers to SAGA recruitment onto MBF promoters. We also show that Gcn5 acetylates specific lysine residues on histone H3 in a cell cycle-regulated manner. Furthermore, either in a gcn5 mutant or in a strain in which histone H3 is kept in an unacetylated form, MBF-dependent transcription is downregulated. In summary, Gcn5 is required for the full activation and correct timing of MBF-regulated gene transcription.</dc:description>
               <dc:description>Spanish Ministerio de Economia y Competitividad, PLAN E, and Feder [BFU2015-66347, PGC2018-097248-B-I00]; MEIONet [BFU2015-71786-REDT]; Unidad de Excelencia Maria de Maeztu [MDM-2014-0370]; ICREA Academia Award (Generalitat de Catalunya) (to E.H.). Funding for open access charge: Spanish Ministerio de Economia y Competitividad [BFU2015-66347, PGC2018-097248-B-I00].</dc:description>
               <dc:date>2019-11-06T10:51:36Z</dc:date>
               <dc:date>2019-11-06T10:51:36Z</dc:date>
               <dc:date>2019</dc:date>
               <dc:type>info:eu-repo/semantics/article</dc:type>
               <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
               <dc:relation>Nucleic Acids Research. 2019;47(16):8439-51</dc:relation>
               <dc:relation>info:eu-repo/grantAgreement/ES/1PE/BFU2015-66347</dc:relation>
               <dc:relation>info:eu-repo/grantAgreement/ES/2PE/PGC2018-097248-B-I00</dc:relation>
               <dc:relation>info:eu-repo/grantAgreement/ES/1PE/BFU2015-71786-REDT</dc:relation>
               <dc:rights>© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com</dc:rights>
               <dc:rights>http://creativecommons.org/licenses/by-nc/4.0/</dc:rights>
               <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
               <dc:publisher>Oxford University Press</dc:publisher>
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