Recruitment of DNA methyltransferase I to DNA repair sites

DOI Web Site 被引用文献10件
  • Oliver Mortusewicz
    Department of Biology II, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany; and Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany
  • Lothar Schermelleh
    Department of Biology II, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany; and Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany
  • Joachim Walter
    Department of Biology II, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany; and Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany
  • M. Cristina Cardoso
    Department of Biology II, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany; and Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany
  • Heinrich Leonhardt
    Department of Biology II, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany; and Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany

書誌事項

公開日
2005-06-13
DOI
  • 10.1073/pnas.0501034102
公開者
Proceedings of the National Academy of Sciences

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説明

<jats:p> In mammalian cells, the replication of genetic and epigenetic information is directly coupled; however, little is known about the maintenance of epigenetic information in DNA repair. Using a laser microirradiation system to introduce DNA lesions at defined subnuclear sites, we tested whether the major DNA methyltransferase (Dnmt1) or one of the two <jats:italic>de novo</jats:italic> methyltransferases (Dnmt3a, Dnmt3b) are recruited to sites of DNA repair <jats:italic>in vivo</jats:italic> . Time lapse microscopy of microirradiated mammalian cells expressing GFP-tagged Dnmt1, Dnmt3a, or Dnmt3b1 together with red fluorescent protein-tagged proliferating cell nuclear antigen (PCNA) revealed that Dnmt1 and PCNA accumulate at DNA damage sites as early as 1 min after irradiation in S and non-S phase cells, whereas recruitment of Dnmt3a and Dnmt3b was not observed. Deletion analysis showed that Dnmt1 recruitment was mediated by the PCNA-binding domain. These data point to a direct role of Dnmt1 in the restoration of epigenetic information during DNA repair. </jats:p>

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