Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodelling complex
Tissue‐specific transcriptional activators initiate differentiation towards specialized cell types by inducing chromatin modifications permissive for transcription at target loci, through the recruitment of SWItch/Sucrose NonFermentable (SWI/SNF) chromatin‐remodelling complex. However, the molecular...
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creator | Forcales, Sonia V Albini, Sonia Giordani, Lorenzo Malecova, Barbora Cignolo, Luca Chernov, Andrei Coutinho, Paula Saccone, Valentina Consalvi, Silvia Williams, Roy Wang, Kepeng Wu, Zhenguo Baranovskaya, Svetlana Miller, Andrew Dilworth, F Jeffrey Puri, Pier Lorenzo |
description | Tissue‐specific transcriptional activators initiate differentiation towards specialized cell types by inducing chromatin modifications permissive for transcription at target loci, through the recruitment of SWItch/Sucrose NonFermentable (SWI/SNF) chromatin‐remodelling complex. However, the molecular mechanism that regulates SWI/SNF nuclear distribution in response to differentiation signals is unknown. We show that the muscle determination factor MyoD and the SWI/SNF subunit BAF60c interact on the regulatory elements of MyoD‐target genes in myoblasts, prior to activation of transcription. BAF60c facilitates MyoD binding to target genes and marks the chromatin for signal‐dependent recruitment of the SWI/SNF core to muscle genes. BAF60c phosphorylation on a conserved threonine by differentiation‐activated p38α kinase is the signal that promotes incorporation of MyoD–BAF60c into a Brg1‐based SWI/SNF complex, which remodels the chromatin and activates transcription of MyoD‐target genes. Our data support an unprecedented two‐step model by which pre‐assembled BAF60c–MyoD complex directs recruitment of SWI/SNF to muscle loci in response to differentiation cues.
The SWI/SNF chromatin‐remodelling complex regulates myogenic gene expression during muscle differentiation. BAF60c, a SWI/SNF subunit, recruits the muscle determinant transcription factor MyoD to target genes, facilitates chromatin remodelling and gene activation after phosphorylation by p38α MAP‐kinase. |
doi_str_mv | 10.1038/emboj.2011.391 |
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The SWI/SNF chromatin‐remodelling complex regulates myogenic gene expression during muscle differentiation. BAF60c, a SWI/SNF subunit, recruits the muscle determinant transcription factor MyoD to target genes, facilitates chromatin remodelling and gene activation after phosphorylation by p38α MAP‐kinase.</description><identifier>ISSN: 0261-4189</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1038/emboj.2011.391</identifier><identifier>PMID: 22068056</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animals ; Cell Line ; Cellular biology ; Chromatin ; Chromatin - genetics ; Chromosomal Proteins, Non-Histone - antagonists & inhibitors ; Chromosomal Proteins, Non-Histone - chemistry ; Chromosomal Proteins, Non-Histone - genetics ; Chromosomal Proteins, Non-Histone - physiology ; DNA Helicases - physiology ; EMBO09 ; EMBO37 ; Fibroblasts - metabolism ; Gene expression ; Gene Expression Regulation - genetics ; HeLa Cells - metabolism ; Humans ; MAP Kinase Signaling System ; Mice ; Molecular biology ; Multiprotein Complexes ; Muscle Development - physiology ; muscle differentiation ; Muscle Proteins - antagonists & inhibitors ; Muscle Proteins - chemistry ; Muscle Proteins - genetics ; Muscle Proteins - physiology ; Myoblasts - metabolism ; myod ; MyoD Protein - physiology ; Nuclear Proteins - physiology ; p38 ; p38 Mitogen-Activated Protein Kinases - physiology ; Phosphorylation ; Phosphothreonine - analysis ; Protein Processing, Post-Translational ; RNA Interference ; RNA, Small Interfering - pharmacology ; Signal transduction ; Transcription Factors - antagonists & inhibitors ; Transcription Factors - chemistry ; Transcription Factors - genetics ; Transcription Factors - physiology ; Two-Hybrid System Techniques</subject><ispartof>The EMBO journal, 2012-01, Vol.31 (2), p.301-316</ispartof><rights>European Molecular Biology Organization 2012</rights><rights>Copyright © 2012 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Jan 18, 2012</rights><rights>Copyright © 2012, European Molecular Biology Organization 2012 European Molecular Biology Organization</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5041-9573d29ba34024259b41cf7dcd859e92fcfd137f7299fa2c6fad80bd170373463</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261556/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261556/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27929,27930,41125,42194,45579,45580,46414,46838,51581,53796,53798</link.rule.ids><linktorsrc>$$Uhttps://doi.org/10.1038/emboj.2011.391$$EView_record_in_Springer_Nature$$FView_record_in_$$GSpringer_Nature</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22068056$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Forcales, Sonia V</creatorcontrib><creatorcontrib>Albini, Sonia</creatorcontrib><creatorcontrib>Giordani, Lorenzo</creatorcontrib><creatorcontrib>Malecova, Barbora</creatorcontrib><creatorcontrib>Cignolo, Luca</creatorcontrib><creatorcontrib>Chernov, Andrei</creatorcontrib><creatorcontrib>Coutinho, Paula</creatorcontrib><creatorcontrib>Saccone, Valentina</creatorcontrib><creatorcontrib>Consalvi, Silvia</creatorcontrib><creatorcontrib>Williams, Roy</creatorcontrib><creatorcontrib>Wang, Kepeng</creatorcontrib><creatorcontrib>Wu, Zhenguo</creatorcontrib><creatorcontrib>Baranovskaya, Svetlana</creatorcontrib><creatorcontrib>Miller, Andrew</creatorcontrib><creatorcontrib>Dilworth, F Jeffrey</creatorcontrib><creatorcontrib>Puri, Pier Lorenzo</creatorcontrib><title>Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodelling complex</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><addtitle>EMBO J</addtitle><description>Tissue‐specific transcriptional activators initiate differentiation towards specialized cell types by inducing chromatin modifications permissive for transcription at target loci, through the recruitment of SWItch/Sucrose NonFermentable (SWI/SNF) chromatin‐remodelling complex. However, the molecular mechanism that regulates SWI/SNF nuclear distribution in response to differentiation signals is unknown. We show that the muscle determination factor MyoD and the SWI/SNF subunit BAF60c interact on the regulatory elements of MyoD‐target genes in myoblasts, prior to activation of transcription. BAF60c facilitates MyoD binding to target genes and marks the chromatin for signal‐dependent recruitment of the SWI/SNF core to muscle genes. BAF60c phosphorylation on a conserved threonine by differentiation‐activated p38α kinase is the signal that promotes incorporation of MyoD–BAF60c into a Brg1‐based SWI/SNF complex, which remodels the chromatin and activates transcription of MyoD‐target genes. Our data support an unprecedented two‐step model by which pre‐assembled BAF60c–MyoD complex directs recruitment of SWI/SNF to muscle loci in response to differentiation cues.
The SWI/SNF chromatin‐remodelling complex regulates myogenic gene expression during muscle differentiation. BAF60c, a SWI/SNF subunit, recruits the muscle determinant transcription factor MyoD to target genes, facilitates chromatin remodelling and gene activation after phosphorylation by p38α MAP‐kinase.</description><subject>Animals</subject><subject>Cell Line</subject><subject>Cellular biology</subject><subject>Chromatin</subject><subject>Chromatin - genetics</subject><subject>Chromosomal Proteins, Non-Histone - antagonists & inhibitors</subject><subject>Chromosomal Proteins, Non-Histone - chemistry</subject><subject>Chromosomal Proteins, Non-Histone - genetics</subject><subject>Chromosomal Proteins, Non-Histone - physiology</subject><subject>DNA Helicases - physiology</subject><subject>EMBO09</subject><subject>EMBO37</subject><subject>Fibroblasts - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - genetics</subject><subject>HeLa Cells - metabolism</subject><subject>Humans</subject><subject>MAP Kinase Signaling System</subject><subject>Mice</subject><subject>Molecular biology</subject><subject>Multiprotein Complexes</subject><subject>Muscle Development - physiology</subject><subject>muscle differentiation</subject><subject>Muscle Proteins - antagonists & inhibitors</subject><subject>Muscle Proteins - chemistry</subject><subject>Muscle Proteins - genetics</subject><subject>Muscle Proteins - physiology</subject><subject>Myoblasts - metabolism</subject><subject>myod</subject><subject>MyoD Protein - physiology</subject><subject>Nuclear Proteins - physiology</subject><subject>p38</subject><subject>p38 Mitogen-Activated Protein Kinases - physiology</subject><subject>Phosphorylation</subject><subject>Phosphothreonine - analysis</subject><subject>Protein Processing, Post-Translational</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Signal transduction</subject><subject>Transcription Factors - antagonists & inhibitors</subject><subject>Transcription Factors - chemistry</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><subject>Two-Hybrid System Techniques</subject><issn>0261-4189</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkcFv0zAUxi0EYmVw5YgiceDk9tmO4_iCtG7r2GiLUEE7Wo7tdClJHJwU1v8el45qIE629X2_5_feh9BrAmMCLJ-4pvCbMQVCxkySJ2hE0gwwBcGfohHQjOCU5PIEvej7DQDwXJDn6IRSyHLg2QiZVbVudY2t61xrXTskVWt86HzQQ-XbxJfJYucv8PRsloGJ4uCTaVgTXOje2WR1ez1ZLWeJuQu-iUSLg2u8dXVdtevE-Kar3f1L9KzUde9ePZyn6Ovs8sv5Bzz_dHV9fjbHhkNKsOSCWSoLzVKgKeWySIkphTU259JJWprSEiZKQaUsNTVZqW0OhSUCmGBpxk7R-0Pdbls0zpo4TdC16kLV6LBTXlfqb6Wt7tTa_1As7onzfYF3DwWC_751_aCaqjdxGN06v-2VJFnOAVKIzrf_ODd-G-Iie0WA5JnkDFh0vXnc0LGTP-uPBnEw_KxqtzvqBNQ-XPU7XLUPV8Vw1eVierN_xHskJweyj1C7duFxA_-jI4EPRNUP7v74lw7fVCaY4Op2eaVuxMf54vNSqgv2C4j-ttk</recordid><startdate>20120118</startdate><enddate>20120118</enddate><creator>Forcales, Sonia V</creator><creator>Albini, Sonia</creator><creator>Giordani, Lorenzo</creator><creator>Malecova, Barbora</creator><creator>Cignolo, Luca</creator><creator>Chernov, Andrei</creator><creator>Coutinho, Paula</creator><creator>Saccone, Valentina</creator><creator>Consalvi, Silvia</creator><creator>Williams, Roy</creator><creator>Wang, Kepeng</creator><creator>Wu, Zhenguo</creator><creator>Baranovskaya, Svetlana</creator><creator>Miller, Andrew</creator><creator>Dilworth, F Jeffrey</creator><creator>Puri, Pier Lorenzo</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><general>Nature Publishing Group</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120118</creationdate><title>Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodelling complex</title><author>Forcales, Sonia V ; Albini, Sonia ; Giordani, Lorenzo ; Malecova, Barbora ; Cignolo, Luca ; Chernov, Andrei ; Coutinho, Paula ; Saccone, Valentina ; Consalvi, Silvia ; Williams, Roy ; Wang, Kepeng ; Wu, Zhenguo ; Baranovskaya, Svetlana ; Miller, Andrew ; Dilworth, F Jeffrey ; Puri, Pier Lorenzo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5041-9573d29ba34024259b41cf7dcd859e92fcfd137f7299fa2c6fad80bd170373463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Cell Line</topic><topic>Cellular biology</topic><topic>Chromatin</topic><topic>Chromatin - 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However, the molecular mechanism that regulates SWI/SNF nuclear distribution in response to differentiation signals is unknown. We show that the muscle determination factor MyoD and the SWI/SNF subunit BAF60c interact on the regulatory elements of MyoD‐target genes in myoblasts, prior to activation of transcription. BAF60c facilitates MyoD binding to target genes and marks the chromatin for signal‐dependent recruitment of the SWI/SNF core to muscle genes. BAF60c phosphorylation on a conserved threonine by differentiation‐activated p38α kinase is the signal that promotes incorporation of MyoD–BAF60c into a Brg1‐based SWI/SNF complex, which remodels the chromatin and activates transcription of MyoD‐target genes. Our data support an unprecedented two‐step model by which pre‐assembled BAF60c–MyoD complex directs recruitment of SWI/SNF to muscle loci in response to differentiation cues.
The SWI/SNF chromatin‐remodelling complex regulates myogenic gene expression during muscle differentiation. BAF60c, a SWI/SNF subunit, recruits the muscle determinant transcription factor MyoD to target genes, facilitates chromatin remodelling and gene activation after phosphorylation by p38α MAP‐kinase.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>22068056</pmid><doi>10.1038/emboj.2011.391</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cell Line Cellular biology Chromatin Chromatin - genetics Chromosomal Proteins, Non-Histone - antagonists & inhibitors Chromosomal Proteins, Non-Histone - chemistry Chromosomal Proteins, Non-Histone - genetics Chromosomal Proteins, Non-Histone - physiology DNA Helicases - physiology EMBO09 EMBO37 Fibroblasts - metabolism Gene expression Gene Expression Regulation - genetics HeLa Cells - metabolism Humans MAP Kinase Signaling System Mice Molecular biology Multiprotein Complexes Muscle Development - physiology muscle differentiation Muscle Proteins - antagonists & inhibitors Muscle Proteins - chemistry Muscle Proteins - genetics Muscle Proteins - physiology Myoblasts - metabolism myod MyoD Protein - physiology Nuclear Proteins - physiology p38 p38 Mitogen-Activated Protein Kinases - physiology Phosphorylation Phosphothreonine - analysis Protein Processing, Post-Translational RNA Interference RNA, Small Interfering - pharmacology Signal transduction Transcription Factors - antagonists & inhibitors Transcription Factors - chemistry Transcription Factors - genetics Transcription Factors - physiology Two-Hybrid System Techniques |
title | Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodelling complex |
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