Dual Chromatin Remodeling Roles for RSC during DNA Double Strand Break Induction and Repair at the Yeast MAT Locus
DNA double strand breaks (DSBs) are potentially serious chromosomal lesions. However, cells sometimes deliberately cleave their own DNA to facilitate certain chromosomal processes, and there is much interest in how such self-inflicted breaks are effectively managed. Eukaryotic DSBs occur in the cont...
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Veröffentlicht in: | The Journal of biological chemistry 2007-09, Vol.282 (38), p.27693-27701 |
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creator | Kent, Nicholas A. Chambers, Anna L. Downs, Jessica A. |
description | DNA double strand breaks (DSBs) are potentially serious chromosomal lesions. However, cells sometimes deliberately cleave their own DNA to facilitate certain chromosomal processes, and there is much interest in how such self-inflicted breaks are effectively managed. Eukaryotic DSBs occur in the context of chromatin and the RSC chromatin-remodeling ATPase complex has been shown to promote DSB repair at the budding yeast MAT locus DSB, created by the HO endonuclease during mating type switching. We show that the role of RSC at MAT is highly specialized. The Rsc1p subunit of RSC directs nucleosome sliding immediately after DSB creation at both MAT and generally and is required for efficient DNA damage-induced histone H2A phosphorylation and strand resection during repair by homologous recombination. However, the Rsc2p and Rsc7p subunits are additionally required to set up a basal MAT locus structure. This RSC-dependent chromatin structure at MAT ensures accessibility to the HO endonuclease. The RSC complex therefore has chromatin remodeling roles both before and after DSB induction at MAT, promoting both DNA cleavage and subsequent repair. |
doi_str_mv | 10.1074/jbc.M704707200 |
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The RSC complex therefore has chromatin remodeling roles both before and after DSB induction at MAT, promoting both DNA cleavage and subsequent repair.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M704707200</identifier><identifier>PMID: 17652077</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Chromatin - metabolism ; Chromosomal Proteins, Non-Histone - metabolism ; DNA Damage ; DNA Repair ; Fungal Proteins ; Gene Expression Regulation, Fungal ; Histones - chemistry ; Models, Biological ; Models, Genetic ; Nucleosomes - metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Recombination, Genetic ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - metabolism ; Saccharomyces cerevisiae Proteins - metabolism</subject><ispartof>The Journal of biological chemistry, 2007-09, Vol.282 (38), p.27693-27701</ispartof><rights>2007 © 2007 ASBMB. 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However, cells sometimes deliberately cleave their own DNA to facilitate certain chromosomal processes, and there is much interest in how such self-inflicted breaks are effectively managed. Eukaryotic DSBs occur in the context of chromatin and the RSC chromatin-remodeling ATPase complex has been shown to promote DSB repair at the budding yeast MAT locus DSB, created by the HO endonuclease during mating type switching. We show that the role of RSC at MAT is highly specialized. The Rsc1p subunit of RSC directs nucleosome sliding immediately after DSB creation at both MAT and generally and is required for efficient DNA damage-induced histone H2A phosphorylation and strand resection during repair by homologous recombination. However, the Rsc2p and Rsc7p subunits are additionally required to set up a basal MAT locus structure. This RSC-dependent chromatin structure at MAT ensures accessibility to the HO endonuclease. The RSC complex therefore has chromatin remodeling roles both before and after DSB induction at MAT, promoting both DNA cleavage and subsequent repair.</description><subject>Chromatin - metabolism</subject><subject>Chromosomal Proteins, Non-Histone - metabolism</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>Fungal Proteins</subject><subject>Gene Expression Regulation, Fungal</subject><subject>Histones - chemistry</subject><subject>Models, Biological</subject><subject>Models, Genetic</subject><subject>Nucleosomes - metabolism</subject><subject>Phosphorylation</subject><subject>Protein Structure, Tertiary</subject><subject>Recombination, Genetic</subject><subject>Saccharomyces cerevisiae</subject><subject>Saccharomyces cerevisiae - metabolism</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS1ERZfClSPyAXHLduLEcXJcdvmotG2lbZHgZNnOpHFJ4sV2QPz3eLUr9YSYw4w0-r3R6D1C3uSwzEGUl4_aLK8FlAIEA3hGFjnURVbw_NtzsgBgedYwXp-TlyE8QqqyyV-Q81xUnIEQC-I3sxrouvduVNFOdIeja3Gw0wPduQED7Zynu7s1bWd_WG5uVnTjZj0gvYteTS394FH9oFdTO5to3UQPux3ulfVURRp7pN9RhUivV_d068wcXpGzTg0BX5_mBfn66eP9-ku2vf18tV5tM8N5ETOlmagLJXTTVJ2odKV50xjgTVsC4yy1rtOgGS8UN0XZMNYKZBWwKu_KhBcX5P3x7t67nzOGKEcbDA6DmtDNQVY1E8CT_n8gAyaSwZDA5RE03oXgsZN7b0fl_8gc5CEOmeKQT3EkwdvT5VmP2D7hJ_8T8O4I9Pah_209Sm2d6XGUrGayqCUTVVMkrD5imPz6ZdHLYCxOBtskMVG2zv7rhb9kjaIN</recordid><startdate>20070921</startdate><enddate>20070921</enddate><creator>Kent, Nicholas A.</creator><creator>Chambers, Anna L.</creator><creator>Downs, Jessica A.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20070921</creationdate><title>Dual Chromatin Remodeling Roles for RSC during DNA Double Strand Break Induction and Repair at the Yeast MAT Locus</title><author>Kent, Nicholas A. ; 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However, cells sometimes deliberately cleave their own DNA to facilitate certain chromosomal processes, and there is much interest in how such self-inflicted breaks are effectively managed. Eukaryotic DSBs occur in the context of chromatin and the RSC chromatin-remodeling ATPase complex has been shown to promote DSB repair at the budding yeast MAT locus DSB, created by the HO endonuclease during mating type switching. We show that the role of RSC at MAT is highly specialized. The Rsc1p subunit of RSC directs nucleosome sliding immediately after DSB creation at both MAT and generally and is required for efficient DNA damage-induced histone H2A phosphorylation and strand resection during repair by homologous recombination. However, the Rsc2p and Rsc7p subunits are additionally required to set up a basal MAT locus structure. This RSC-dependent chromatin structure at MAT ensures accessibility to the HO endonuclease. 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subjects | Chromatin - metabolism Chromosomal Proteins, Non-Histone - metabolism DNA Damage DNA Repair Fungal Proteins Gene Expression Regulation, Fungal Histones - chemistry Models, Biological Models, Genetic Nucleosomes - metabolism Phosphorylation Protein Structure, Tertiary Recombination, Genetic Saccharomyces cerevisiae Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - metabolism |
title | Dual Chromatin Remodeling Roles for RSC during DNA Double Strand Break Induction and Repair at the Yeast MAT Locus |
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