ParkinsonFranceV1, Hal, Corpus, bibRecord, 000325

Dopamine Signaling Leads to Loss of Polycomb Repression and Aberrant Gene Activation in Experimental Parkinsonism

Identifieur interne : 000325 ( Hal/Corpus ); précédent : 000324; suivant : 000326

Dopamine Signaling Leads to Loss of Polycomb Repression and Aberrant Gene Activation in Experimental Parkinsonism

Auteurs : Erik Södersten ; Michael Feyder ; Mads Lerdrup ; Ana-Luisa Gomes ; Hanna Kryh ; Giada Spigolon ; Jocelyne Caboche ; Gilberto Fisone ; Klaus Hansen

Source :

PLoS Genetics [ 1553-7390 ] ; 2014-09.

RBID : Hal:hal-01342715

Abstract

Polycomb group (PcG) proteins bind to and repress genes in embryonic stem cells through lineage commitment to the terminal differentiated state. PcG repressed genes are commonly characterized by the presence of the epigenetic histone mark H3K27me3, catalyzed by the Polycomb repressive complex 2. Here, we present in vivo evidence for a previously unrecognized plasticity of PcG-repressed genes in terminally differentiated brain neurons of parkisonian mice. We show that acute administration of the dopamine precursor, L-DOPA, induces a remarkable increase in H3K27me3S28 phosphorylation. The induction of the H3K27me3S28p histone mark specifically occurs in medium spiny neurons expressing dopamine D1 receptors and is dependent on Msk1 kinase activity and DARPP-32-mediated inhibition of protein phosphatase-1. Chromatin immunoprecipitation (ChIP) experiments showed that increased H3K27me3S28p was accompanied by reduced PcG binding to regulatory regions of genes. An analysis of the genome wide distribution of L-DOPA-induced H3K27me3S28 phosphorylation by ChIP sequencing (ChIP-seq) in combination with expression analysis by RNA-sequencing (RNA-seq) showed that the induction of H3K27me3S28p correlated with increased expression of a subset of PcG repressed genes. We found that induction of H3K27me3S28p persisted during chronic L-DOPA administration to parkisonian mice and correlated with aberrant gene expression. We propose that dopaminergic transmission can activate PcG repressed genes in the adult brain and thereby contribute to long-term maladaptive responses including the motor complications, or dyskinesia, caused by prolonged administration of L-DOPA in Parkinson's disease.

Url:

http://hal.upmc.fr/hal-01342715

DOI: 10.1371/journal.pgen.1004574

Links to Exploration step

Hal:hal-01342715

Le document en format XML

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<front><div type="abstract" xml:lang="en">Polycomb group (PcG) proteins bind to and repress genes in embryonic stem cells through lineage commitment to the terminal differentiated state. PcG repressed genes are commonly characterized by the presence of the epigenetic histone mark H3K27me3, catalyzed by the Polycomb repressive complex 2. Here, we present in vivo evidence for a previously unrecognized plasticity of PcG-repressed genes in terminally differentiated brain neurons of parkisonian mice. We show that acute administration of the dopamine precursor, L-DOPA, induces a remarkable increase in H3K27me3S28 phosphorylation. The induction of the H3K27me3S28p histone mark specifically occurs in medium spiny neurons expressing dopamine D1 receptors and is dependent on Msk1 kinase activity and DARPP-32-mediated inhibition of protein phosphatase-1. Chromatin immunoprecipitation (ChIP) experiments showed that increased H3K27me3S28p was accompanied by reduced PcG binding to regulatory regions of genes. An analysis of the genome wide distribution of L-DOPA-induced H3K27me3S28 phosphorylation by ChIP sequencing (ChIP-seq) in combination with expression analysis by RNA-sequencing (RNA-seq) showed that the induction of H3K27me3S28p correlated with increased expression of a subset of PcG repressed genes. We found that induction of H3K27me3S28p persisted during chronic L-DOPA administration to parkisonian mice and correlated with aberrant gene expression. We propose that dopaminergic transmission can activate PcG repressed genes in the adult brain and thereby contribute to long-term maladaptive responses including the motor complications, or dyskinesia, caused by prolonged administration of L-DOPA in Parkinson's disease.</div>
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                  <affiliation ref="#struct-302344"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Michael</forename>
                    <surname>Feyder</surname>
                  </persName>
                  <idno type="halauthorid">1169179</idno>
                  <affiliation ref="#struct-302344"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Mads</forename>
                    <surname>Lerdrup</surname>
                  </persName>
                  <idno type="halauthorid">1361408</idno>
                  <affiliation ref="#struct-182755"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Ana-Luisa</forename>
                    <surname>Gomes</surname>
                  </persName>
                  <idno type="halauthorid">1361409</idno>
                  <affiliation ref="#struct-182755"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Hanna</forename>
                    <surname>Kryh</surname>
                  </persName>
                  <idno type="halauthorid">1361410</idno>
                  <affiliation ref="#struct-182755"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Giada</forename>
                    <surname>Spigolon</surname>
                  </persName>
                  <idno type="halauthorid">1361411</idno>
                  <affiliation ref="#struct-302344"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Jocelyne</forename>
                    <surname>Caboche</surname>
                  </persName>
                  <idno type="halauthorid">161870</idno>
                  <affiliation ref="#struct-81502"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Gilberto</forename>
                    <surname>Fisone</surname>
                  </persName>
                  <idno type="halauthorid">224336</idno>
                  <affiliation ref="#struct-302344"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Klaus</forename>
                    <surname>Hansen</surname>
                  </persName>
                  <idno type="halauthorid">1361412</idno>
                  <affiliation ref="#struct-182755"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">1957</idno>
                <idno type="issn">1553-7390</idno>
                <idno type="eissn">1553-7404</idno>
                <title level="j">PLoS Genetics</title>
                <imprint>                  <publisher>Public Library of Science</publisher>
                  <biblScope unit="volume">10</biblScope>
                  <biblScope unit="issue">9</biblScope>
                  <biblScope unit="pp">e1004574</biblScope>
                  <date type="datePub">2014-09</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1371/journal.pgen.1004574</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="halDomain" n="sdv.gen">Life Sciences [q-bio]/Genetics</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">Polycomb group (PcG) proteins bind to and repress genes in embryonic stem cells through lineage commitment to the terminal differentiated state. PcG repressed genes are commonly characterized by the presence of the epigenetic histone mark H3K27me3, catalyzed by the Polycomb repressive complex 2. Here, we present in vivo evidence for a previously unrecognized plasticity of PcG-repressed genes in terminally differentiated brain neurons of parkisonian mice. We show that acute administration of the dopamine precursor, L-DOPA, induces a remarkable increase in H3K27me3S28 phosphorylation. The induction of the H3K27me3S28p histone mark specifically occurs in medium spiny neurons expressing dopamine D1 receptors and is dependent on Msk1 kinase activity and DARPP-32-mediated inhibition of protein phosphatase-1. Chromatin immunoprecipitation (ChIP) experiments showed that increased H3K27me3S28p was accompanied by reduced PcG binding to regulatory regions of genes. An analysis of the genome wide distribution of L-DOPA-induced H3K27me3S28 phosphorylation by ChIP sequencing (ChIP-seq) in combination with expression analysis by RNA-sequencing (RNA-seq) showed that the induction of H3K27me3S28p correlated with increased expression of a subset of PcG repressed genes. We found that induction of H3K27me3S28p persisted during chronic L-DOPA administration to parkisonian mice and correlated with aberrant gene expression. We propose that dopaminergic transmission can activate PcG repressed genes in the adult brain and thereby contribute to long-term maladaptive responses including the motor complications, or dyskinesia, caused by prolonged administration of L-DOPA in Parkinson's disease.</abstract>
          </profileDesc>
        </hal>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Dopamine Signaling Leads to Loss of Polycomb Repression and Aberrant Gene Activation in Experimental Parkinsonism

Dopamine Signaling Leads to Loss of Polycomb Repression and Aberrant Gene Activation in Experimental Parkinsonism

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