XLF and APLF bind Ku80 at two remote sites to ensure DNA repair by non-homologous end joining

The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ) repair pathway through molecular interactions that remain unclear. We have determined crystal structures of the Ku-binding motifs (KBM) of th...

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Veröffentlicht in:Nature structural & molecular biology Jg. 25; H. 10; S. 971 - 980
Hauptverfasser: Nemoz, Clement, Ropars, Virginie, Frit, Philippe, Gontier, Amandine, Drevet, Pascal, Yu, Jinchao, Guerois, Raphaël, Pitois, Aurelien, Comte, Audrey, Delteil, Christine, Barboule, Nadia, Legrand, Pierre, Baconnais, Sonia, Yin, Yandong, Tadi, Satish, Barbet-Massin, Emeline, Berger, Imre, Le Cam, Eric, Modesti, Mauro, Rothenberg, Eli, Calsou, Patrick, Charbonnier, Jean Baptiste
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Nature Publishing Group 01.10.2018
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ISSN:1545-9993, 1545-9985, 1545-9985
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Abstract The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ) repair pathway through molecular interactions that remain unclear. We have determined crystal structures of the Ku-binding motifs (KBM) of the NHEJ proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex. The two KBM motifs bind remote sites of the Ku80 α/β domain. The X-KBM occupies an internal pocket formed by an unprecedented large outward rotation of the Ku80 α/β domain. We observe independent recruitment of the APLF-interacting protein XRCC4 and of XLF to laser-irradiated sites via binding of A- and X-KBMs, respectively, to Ku80. Finally, we show that mutation of the X-KBM and A-KBM binding sites in Ku80 compromises both the efficiency and accuracy of end joining and cellular radiosensitivity. A- and X-KBMs may represent two initial anchor points to build the intricate interaction network required for NHEJ.
AbstractList The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ) repair pathway through molecular interactions that remain unclear. We have determined crystal structures of the Ku-binding motifs (KBM) of the NHEJ proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex. The two KBM motifs bind remote sites of the Ku80 α/β domain. The X-KBM occupies an internal pocket formed by an unprecedented large outward rotation of the Ku80 α/β domain. We observe independent recruitment of the APLF-interacting protein XRCC4 and of XLF to laser-irradiated sites via binding of A- and X-KBMs, respectively, to Ku80. Finally, we show that mutation of the X-KBM and A-KBM binding sites in Ku80 compromises both the efficiency and accuracy of end joining and cellular radiosensitivity. A- and X-KBMs may represent two initial anchor points to build the intricate interaction network required for NHEJ.
The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ) repair pathway through molecular interactions that remain unclear. We have determined crystal structures of the Ku-binding motifs (KBM) of the NHEJ proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex. The two KBM motifs bind remote sites of the Ku80 α/β domain. The X-KBM occupies an internal pocket formed by an unprecedented large outward rotation of the Ku80 α/β domain. We observe independent recruitment of the APLF-interacting protein XRCC4 and of XLF to laser-irradiated sites via binding of A- and X-KBMs, respectively, to Ku80. Finally, we show that mutation of the X-KBM and A-KBM binding sites in Ku80 compromises both the efficiency and accuracy of end joining and cellular radiosensitivity. A- and X-KBMs may represent two initial anchor points to build the intricate interaction network required for NHEJ.The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ) repair pathway through molecular interactions that remain unclear. We have determined crystal structures of the Ku-binding motifs (KBM) of the NHEJ proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex. The two KBM motifs bind remote sites of the Ku80 α/β domain. The X-KBM occupies an internal pocket formed by an unprecedented large outward rotation of the Ku80 α/β domain. We observe independent recruitment of the APLF-interacting protein XRCC4 and of XLF to laser-irradiated sites via binding of A- and X-KBMs, respectively, to Ku80. Finally, we show that mutation of the X-KBM and A-KBM binding sites in Ku80 compromises both the efficiency and accuracy of end joining and cellular radiosensitivity. A- and X-KBMs may represent two initial anchor points to build the intricate interaction network required for NHEJ.
Author Yu, Jinchao
Tadi, Satish
Comte, Audrey
Le Cam, Eric
Gontier, Amandine
Drevet, Pascal
Pitois, Aurelien
Rothenberg, Eli
Charbonnier, Jean Baptiste
Ropars, Virginie
Nemoz, Clement
Berger, Imre
Barboule, Nadia
Yin, Yandong
Delteil, Christine
Guerois, Raphaël
Baconnais, Sonia
Frit, Philippe
Modesti, Mauro
Barbet-Massin, Emeline
Calsou, Patrick
Legrand, Pierre
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  organization: Institute for Integrative Biology of the Cell, Institute Joliot, CEA, CNRS, Université Paris-Sud, Université Paris-Saclay, Gif-sur-Yvette, France
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  organization: Synchrotron Soleil, L'Orme des Merisiers, Saint-Aubin, Gif-sur-Yvette, France
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  organization: Signalisations, Noyaux et Innovations en Cancérologie, UMR 8126, CNRS, Université Paris-Sud, Gustave Roussy, Université Paris-Saclay, Villejuif, France
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  organization: New York University School of Medicine, Perlmutter Cancer Center, New York, USA
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  organization: Cancer Research Center of Marseille, CNRS UMR 7258, Inserm U1068, Institut Paoli-Calmettes, Aix-Marseille Université UM105, Marseille, France
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  organization: Dynamic Biosensors GmbH, Martinsried, Germany
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  organization: BrisSynBio Centre, School of Biochemistry, Faculty of Biomedical Sciences, University of Bristol, Bristol, UK
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  organization: Institute for Integrative Biology of the Cell, Institute Joliot, CEA, CNRS, Université Paris-Sud, Université Paris-Saclay, Gif-sur-Yvette, France. jb.charbonnier@cea.fr
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30291363$$D View this record in MEDLINE/PubMed
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Copyright Copyright Nature Publishing Group Oct 2018
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OpenAccessLink https://research-information.bris.ac.uk/ws/files/170642240/NSMB_revised_def.pdf
PMID 30291363
PQID 2188970604
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PublicationDate 2018-10-01
PublicationDateYYYYMMDD 2018-10-01
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  year: 2018
  text: 2018-10-01
  day: 01
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PublicationPlace United States
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PublicationTitle Nature structural & molecular biology
PublicationTitleAlternate Nat Struct Mol Biol
PublicationYear 2018
Publisher Nature Publishing Group
Publisher_xml – name: Nature Publishing Group
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Snippet The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ)...
The Ku70–Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ)...
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StartPage 971
SubjectTerms Binding sites
Conserved Sequence
Crystal structure
Crystallography, X-Ray
Deoxyribonucleic acid
DNA
DNA damage
DNA End-Joining Repair
DNA repair
DNA Repair Enzymes - chemistry
DNA Repair Enzymes - metabolism
DNA Repair Enzymes - physiology
DNA-(Apurinic or Apyrimidinic Site) Lyase - chemistry
DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism
DNA-(Apurinic or Apyrimidinic Site) Lyase - physiology
DNA-Binding Proteins - chemistry
DNA-Binding Proteins - metabolism
DNA-Binding Proteins - physiology
Homology
Humans
Ku Autoantigen - chemistry
Ku Autoantigen - metabolism
Ku Autoantigen - physiology
Models, Molecular
Molecular interactions
Mutation
Non-homologous end joining
Poly-ADP-Ribose Binding Proteins - chemistry
Poly-ADP-Ribose Binding Proteins - metabolism
Poly-ADP-Ribose Binding Proteins - physiology
Protein Domains
Proteins
Radiosensitivity
Repair
Title XLF and APLF bind Ku80 at two remote sites to ensure DNA repair by non-homologous end joining
URI https://www.ncbi.nlm.nih.gov/pubmed/30291363
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Volume 25
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