Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions
Identifieur interne : 002360 ( Istex/Corpus ); précédent : 002359; suivant : 002361Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions
Auteurs : Shengfang Jin ; David T. WeaverSource :
- The EMBO Journal [ 0261-4189 ] ; 1997-11-15.
English descriptors
- Teeft :
- Amino, Amino acid residues, Assay, Autoantigen, Bamhi, Binding, Binding activity, Binding properties, Biochemical features, Biol, Boubnov, Cdna, Cell extracts, Cell line, Cell lines, Cell lysates, Cells reconstituted, Chimera, Chimeric, Complementation, Core region, Derivative, Edta, Epitope, Expression vector, Hdf1, Heterodimerization, Higher mobility, Immunoprecipitation, Kinase, Kinase buffer, Lieber, Lysates, Lysis, Lysis buffer, Monoclonal, Monoclonal antibody, Mutagenesis, Mutant, Mutation, Mutational analysis, Nacl, Natl acad, Noti, Nucleic acids, Pefpuro, Peptide, Phosphoamino acid analysis, Phosphorylated, Phosphorylation, Primer, Protein kinase, Recombination, Reconstituted, Repair, Repair defects, Saccharomyces cerevisiae, Serine, Stably, Stably transfected, Subunit, Truncation, Truncation mutants, Yeast, Yeast expression vector.
Abstract
Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair in vivo. These studies reveal Ku70 features required for double‐strand break repair.
Url:
DOI: 10.1093/emboj/16.22.6874
Links to Exploration step
ISTEX:3EDB64B83F4CCB81DE70FEDF12BC270DEAAF83D7Le document en format XML
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Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair in vivo. 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(1997)</json:string><json:string>Blunt et al., 1995</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-38NNM99N-1</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - cell biology</json:string><json:string>2 - biochemistry & molecular biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - developmental biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - General Immunology and Microbiology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - General Biochemistry, Genetics and Molecular Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main"><p>Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair <hi rend="italic">in vivo</hi>. These studies reveal Ku70 features required for double‐strand break repair.</p></abstract><textClass><keywords><term xml:id="embj7590657-kwd-0001">double‐strand break repair</term><term xml:id="embj7590657-kwd-0002">DNA‐dependent protein kinase</term><term xml:id="embj7590657-kwd-0003">heterodimerization</term><term xml:id="embj7590657-kwd-0004">ionizing radiation</term><term xml:id="embj7590657-kwd-0005">Ku</term></keywords><keywords rend="articleCategory"><term>Article</term></keywords><keywords rend="tocHeading1"><term>Article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-38NNM99N-1/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:lang="en" xml:id="embj7590657"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi>10.1002/(ISSN)1460-2075</doi><issn type="print">0261-4189</issn><issn type="electronic">1460-2075</issn><idGroup><id type="product" value="EMBJ"></id></idGroup><titleGroup><title type="main" sort="THE EMBO JOURNAL">The EMBO Journal</title></titleGroup></publicationMeta><publicationMeta level="part" position="220"><doi>10.1002/emboj.v16.22</doi><copyright ownership="publisher">Copyright © 2013 Wiley Periodicals, Inc</copyright><numberingGroup><numbering type="journalVolume" number="16">16</numbering><numbering type="journalIssue">22</numbering></numberingGroup><coverDate startDate="1997-11-15">November 15, 1997</coverDate></publicationMeta><publicationMeta level="unit" position="250" type="article" status="forIssue"><doi>10.1093/emboj/16.22.6874</doi><idGroup><id type="unit" value="EMBJ7590657"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup>
<title type="articleCategory">Article</title><title type="tocHeading1">Article</title></titleGroup><copyright ownership="thirdParty">Copyright © 1997 European Molecular Biology Organization</copyright><eventGroup><event type="manuscriptReceived" date="1997-04-21"></event><event type="manuscriptRevised" date="1997-08-27"></event><event type="publishedOnlineFinalForm" date="1997-11-15"></event><event type="xmlConverted" agent="SPi Global Converter_TO_WileyML3Gv2.0 version:1.0; WileyML 3G Packaging Tool v1.0" date="2013-10-08"></event><event type="firstOnline" date="1997-11-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">6874</numbering><numbering type="pageLast">6885</numbering></numberingGroup><linkGroup><link type="toTypesetVersion" href="file:EMBJ.EMBJ7590657.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions</title></titleGroup><creators><creator creatorRole="author" xml:id="embj7590657-cr-0001" affiliationRef="#embj7590657-aff-0001"><personName><givenNames>Shengfang</givenNames><familyName>Jin</familyName></personName></creator><creator creatorRole="author" xml:id="embj7590657-cr-0002" affiliationRef="#embj7590657-aff-0001" corresponding="yes"><personName><givenNames>David T.</givenNames><familyName>Weaver</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="US" type="organization" xml:id="embj7590657-aff-0001"><orgDiv>Division of Tumor Immunology, Dana‐Farber Cancer Institute</orgDiv><orgName>Department of Microbiology and Molecular Genetics, Harvard Medical School</orgName><address><street>44 Binney Street</street><city>Boston</city><countryPart>MA</countryPart><postCode>02115</postCode><street>200 Longwood Avenue</street><city>Boston</city><countryPart>MA</countryPart><postCode>02115</postCode><country>USA</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="embj7590657-kwd-0001">double‐strand break repair</keyword><keyword xml:id="embj7590657-kwd-0002">DNA‐dependent protein kinase</keyword><keyword xml:id="embj7590657-kwd-0003">heterodimerization</keyword><keyword xml:id="embj7590657-kwd-0004">ionizing radiation</keyword><keyword xml:id="embj7590657-kwd-0005">Ku</keyword></keywordGroup><abstractGroup><abstract type="main"><p>Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair <i>in vivo</i>. These studies reveal Ku70 features required for double‐strand break repair.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions</title></titleInfo><name type="personal"><namePart type="given">Shengfang</namePart><namePart type="family">Jin</namePart><affiliation>Division of Tumor Immunology, Dana‐Farber Cancer Institute, Department of Microbiology and Molecular Genetics, Harvard Medical School, 44 Binney Street200 Longwood Avenue, MAMA, 0211502115, BostonBoston, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David T.</namePart><namePart type="family">Weaver</namePart><affiliation>Division of Tumor Immunology, Dana‐Farber Cancer Institute, Department of Microbiology and Molecular Genetics, Harvard Medical School, 44 Binney Street200 Longwood Avenue, MAMA, 0211502115, BostonBoston, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>John Wiley & Sons, Ltd</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">1997-11-15</dateIssued><dateCaptured encoding="w3cdtf">1997-04-21</dateCaptured><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair in vivo. These studies reveal Ku70 features required for double‐strand break repair.</abstract><subject><genre>keywords</genre><topic>double‐strand break repair</topic><topic>DNA‐dependent protein kinase</topic><topic>heterodimerization</topic><topic>ionizing radiation</topic><topic>Ku</topic></subject><relatedItem type="host"><titleInfo><title>The EMBO Journal</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Article</topic><topic>Article</topic></subject><identifier type="ISSN">0261-4189</identifier><identifier type="eISSN">1460-2075</identifier><identifier type="DOI">10.1002/(ISSN)1460-2075</identifier><identifier type="PublisherID">EMBJ</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>22</number></detail><extent unit="pages"><start>6874</start><end>6885</end><total>12</total></extent></part></relatedItem><relatedItem type="references" displayLabel="embj7590657-citation-0001"><titleInfo><title>The nuclear serine/threonine protein kinase DNA‐PK</title></titleInfo><name type="personal"><namePart type="given">CW</namePart><namePart type="family">Anderson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SP</namePart><namePart type="family">Lees‐Miller</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Anderson CW and Lees‐Miller SP (1992) The nuclear serine/threonine protein kinase DNA‐PK. 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