<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-14T02:47:36Z</responseDate><request verb="GetRecord" identifier="oai:www.recercat.cat:10230/42752" metadataPrefix="marc">https://recercat.cat/oai/request</request><GetRecord><record><header><identifier>oai:recercat.cat:10230/42752</identifier><datestamp>2025-12-22T13:37:13Z</datestamp><setSpec>com_2072_6</setSpec><setSpec>col_2072_452952</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">González Medina, Alberto, 1990-</subfield>
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      <subfield code="a">Hidalgo Hernando, Elena</subfield>
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      <subfield code="a">Ayté del Olmo, José</subfield>
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      <subfield code="c">2019-11-06T10:51:36Z</subfield>
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      <subfield code="c">2019-11-06T10:51:36Z</subfield>
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      <subfield code="c">2019</subfield>
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      <subfield code="a">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.</subfield>
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      <subfield code="a">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].</subfield>
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      <subfield code="a">Gene regulation</subfield>
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      <subfield code="a">Chromatin and epigenetics</subfield>
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      <subfield code="a">Gcn5-mediated acetylation at MBF-regulated promoters induces the G1/S transcriptional wave</subfield>
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