Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair
We developed a novel system to create DNA double-strand breaks (DSBs) at defined endogenous sites in the human genome, and used this system to detect protein recruitment and loss at and around these breaks by chromatin immunoprecipitation (ChIP). The detection of human ATM protein at site-specific D...
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| Veröffentlicht in: | Nature cell biology 2007-06, Vol.9 (6), p.683-690 |
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| creator | Kastan, Michael B Berkovich, Elijahu Monnat, Raymond J |
| description | We developed a novel system to create DNA double-strand breaks (DSBs) at defined endogenous sites in the human genome, and used this system to detect protein recruitment and loss at and around these breaks by chromatin immunoprecipitation (ChIP). The detection of human ATM protein at site-specific DSBs required functional NBS1 protein, ATM kinase activity and ATM autophosphorylation on Ser 1981. DSB formation led to the localized disruption of nucleosomes, a process that depended on both functional NBS1 and ATM. These two proteins were also required for efficient recruitment of the repair cofactor XRCC4 to DSBs, and for efficient DSB repair. These results demonstrate the functional importance of ATM kinase activity and phosphorylation in the response to DSBs, and support a model in which ordered chromatin structure changes that occur after DNA breakage depend on functional NBS1 and ATM, and facilitate DNA DSB repair. |
| doi_str_mv | 10.1038/ncb1599 |
| format | Article |
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The detection of human ATM protein at site-specific DSBs required functional NBS1 protein, ATM kinase activity and ATM autophosphorylation on Ser 1981. DSB formation led to the localized disruption of nucleosomes, a process that depended on both functional NBS1 and ATM. These two proteins were also required for efficient recruitment of the repair cofactor XRCC4 to DSBs, and for efficient DSB repair. These results demonstrate the functional importance of ATM kinase activity and phosphorylation in the response to DSBs, and support a model in which ordered chromatin structure changes that occur after DNA breakage depend on functional NBS1 and ATM, and facilitate DNA DSB repair.</description><identifier>ISSN: 1465-7392</identifier><identifier>EISSN: 1476-4679</identifier><identifier>DOI: 10.1038/ncb1599</identifier><identifier>PMID: 17486112</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - physiology ; Cell Line, Tumor ; Cellular proteins ; Chromatin ; Chromatin - genetics ; Chromatin - metabolism ; Deoxyribonucleic acid ; DNA ; DNA - genetics ; DNA Breaks, Double-Stranded ; DNA repair ; DNA Repair - genetics ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; DNA-Binding Proteins - physiology ; Genetic aspects ; Genomes ; Humans ; Infections ; Kinases ; Methods ; Microscopy ; Nuclear Proteins - genetics ; Nuclear Proteins - physiology ; Nucleosomes - genetics ; Nucleosomes - metabolism ; Phosphorylation ; Physiological aspects ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - physiology ; Proteins ; Structure ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - physiology ; Yeast</subject><ispartof>Nature cell biology, 2007-06, Vol.9 (6), p.683-690</ispartof><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-1b5f1745ad94b04ed1817cfba3e068e1d028c839b41b3b75b51ad1e630ab33a83</citedby><cites>FETCH-LOGICAL-c558t-1b5f1745ad94b04ed1817cfba3e068e1d028c839b41b3b75b51ad1e630ab33a83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,2728,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17486112$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kastan, Michael B</creatorcontrib><creatorcontrib>Berkovich, Elijahu</creatorcontrib><creatorcontrib>Monnat, Raymond J</creatorcontrib><title>Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair</title><title>Nature cell biology</title><addtitle>Nat Cell Biol</addtitle><description>We developed a novel system to create DNA double-strand breaks (DSBs) at defined endogenous sites in the human genome, and used this system to detect protein recruitment and loss at and around these breaks by chromatin immunoprecipitation (ChIP). The detection of human ATM protein at site-specific DSBs required functional NBS1 protein, ATM kinase activity and ATM autophosphorylation on Ser 1981. DSB formation led to the localized disruption of nucleosomes, a process that depended on both functional NBS1 and ATM. These two proteins were also required for efficient recruitment of the repair cofactor XRCC4 to DSBs, and for efficient DSB repair. These results demonstrate the functional importance of ATM kinase activity and phosphorylation in the response to DSBs, and support a model in which ordered chromatin structure changes that occur after DNA breakage depend on functional NBS1 and ATM, and facilitate DNA DSB repair.</description><subject>Ataxia Telangiectasia Mutated Proteins</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - physiology</subject><subject>Cell Line, Tumor</subject><subject>Cellular proteins</subject><subject>Chromatin</subject><subject>Chromatin - genetics</subject><subject>Chromatin - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA - genetics</subject><subject>DNA Breaks, Double-Stranded</subject><subject>DNA repair</subject><subject>DNA Repair - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Humans</subject><subject>Infections</subject><subject>Kinases</subject><subject>Methods</subject><subject>Microscopy</subject><subject>Nuclear Proteins - 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Academic</collection><jtitle>Nature cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kastan, Michael B</au><au>Berkovich, Elijahu</au><au>Monnat, Raymond J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair</atitle><jtitle>Nature cell biology</jtitle><addtitle>Nat Cell Biol</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>9</volume><issue>6</issue><spage>683</spage><epage>690</epage><pages>683-690</pages><issn>1465-7392</issn><eissn>1476-4679</eissn><abstract>We developed a novel system to create DNA double-strand breaks (DSBs) at defined endogenous sites in the human genome, and used this system to detect protein recruitment and loss at and around these breaks by chromatin immunoprecipitation (ChIP). The detection of human ATM protein at site-specific DSBs required functional NBS1 protein, ATM kinase activity and ATM autophosphorylation on Ser 1981. DSB formation led to the localized disruption of nucleosomes, a process that depended on both functional NBS1 and ATM. These two proteins were also required for efficient recruitment of the repair cofactor XRCC4 to DSBs, and for efficient DSB repair. These results demonstrate the functional importance of ATM kinase activity and phosphorylation in the response to DSBs, and support a model in which ordered chromatin structure changes that occur after DNA breakage depend on functional NBS1 and ATM, and facilitate DNA DSB repair.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>17486112</pmid><doi>10.1038/ncb1599</doi><tpages>8</tpages></addata></record> |
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| ispartof | Nature cell biology, 2007-06, Vol.9 (6), p.683-690 |
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| subjects | Ataxia Telangiectasia Mutated Proteins Cell Cycle Proteins - genetics Cell Cycle Proteins - physiology Cell Line, Tumor Cellular proteins Chromatin Chromatin - genetics Chromatin - metabolism Deoxyribonucleic acid DNA DNA - genetics DNA Breaks, Double-Stranded DNA repair DNA Repair - genetics DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism DNA-Binding Proteins - physiology Genetic aspects Genomes Humans Infections Kinases Methods Microscopy Nuclear Proteins - genetics Nuclear Proteins - physiology Nucleosomes - genetics Nucleosomes - metabolism Phosphorylation Physiological aspects Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - physiology Proteins Structure Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - physiology Yeast |
| title | Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair |
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