<?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>2026-04-17T11:26:01Z</responseDate><request verb="GetRecord" identifier="oai:www.recercat.cat:10230/54061" metadataPrefix="marc">https://recercat.cat/oai/request</request><GetRecord><record><header><identifier>oai:recercat.cat:10230/54061</identifier><datestamp>2025-12-18T01:14:22Z</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">Fraile Beneitez, Rodrigo</subfield>
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      <subfield code="a">Sánchez Mir, Laura</subfield>
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      <subfield code="a">Murciano-Julià, Guillem</subfield>
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      <subfield code="a">Ayté del Olmo, José</subfield>
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      <subfield code="a">Hidalgo Hernando, Elena</subfield>
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      <subfield code="c">2022-09-14T06:49:42Z</subfield>
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      <subfield code="c">2022-09-14T06:49:42Z</subfield>
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      <subfield code="c">2022</subfield>
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      <subfield code="a">The MAP kinase Sty1 phosphorylates and activates the transcription factor Atf1 in response to several stress conditions, which then shifts from a transcriptional repressor to an activator. Atf1 also participates in heterochromatin assembly at the mat locus, in combination with the RNA interference (RNAi) machinery. Here, we study the role of signal-dependent phosphorylation of Atf1 in heterochromatin establishment at mat, using different Atf1 phospho mutants. Although a hypo-phosphorylation Atf1 mutant, Atf1.10M, mediates heterochromatin assembly, the phosphomimic Atf1.10D is unable to maintain silencing. In a minimal mat locus, lacking the RNAi-recruiting cis elements and displaying intermediate silencing, Atf1.10M restores full heterochromatin and silencing. However, evolution experiments with this stress-blinded Atf1.10M show that it is unable to facilitate switching between the donor site mat3 and mat1. We propose that the unphosphorylated, inactive Atf1 contributes to proper heterochromatin assembly by recruiting repressive complexes, but its stress-dependent phosphorylation is required for recombination/switching to occur.</subfield>
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      <subfield code="a">This work is supported by grant PGC2018-093920-B-I00 to E.H, funded by MCIN/AEI/10.13039/501100011033 and by “ERDF A way of making Europe,” by the “European Union.” The Oxidative Stress and Cell Cycle group is also supported by Generalitat de Catalunya (Spain) (2017-SGR-539) and by Excellence Unit «María de Maeztu» Grant CEX2018-000792-M funded by MCIN/AEI/10.13039/501100011033. E.H. is recipient of an ICREA Academia Award (Generalitat de Catalunya, Spain). R.F. was recipient of a FPI contract from the Ministerio de Ciencia, Innovación y Universidades (Spain).</subfield>
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      <subfield code="a">Epigenetics</subfield>
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      <subfield code="a">Functional aspects of cell biology</subfield>
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      <subfield code="a">Molecular biology</subfield>
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      <subfield code="a">Molecular mechanism of gene regulation</subfield>
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      <subfield code="a">A stress-blinded Atf1 can fully assemble heterochromatin in a RNAi-independent minimal mat locus but impairs directionality of mat2/3 switching</subfield>
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