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Rag mutations reveal robust alternative end joining

Author

Listed:
  • Barbara Corneo

    (New York University School of Medicine, New York, New York 10016, USA
    The Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, New York 10029, USA)

  • Rebecca L. Wendland

    (New York University School of Medicine, New York, New York 10016, USA)

  • Ludovic Deriano

    (New York University School of Medicine, New York, New York 10016, USA)

  • Xiaoping Cui

    (College of Veterinary Medicine, Pathobiology & Diagnostic Investigation, Michigan State University, East Lansing, Michigan 48824, USA)

  • Isaac A. Klein

    (New York University School of Medicine, New York, New York 10016, USA)

  • Serre-Yu Wong

    (New York University School of Medicine, New York, New York 10016, USA)

  • Suzzette Arnal

    (New York University School of Medicine, New York, New York 10016, USA)

  • Abigail J. Holub

    (New York University School of Medicine, New York, New York 10016, USA)

  • Geoffrey R. Weller

    (New York University School of Medicine, New York, New York 10016, USA)

  • Bette A. Pancake

    (New York University School of Medicine, New York, New York 10016, USA)

  • Sundeep Shah

    (Baylor College of Medicine, Houston, Texas 77030, USA
    Present address: Vertex Pharmaceuticals, 11010 Torreyana Road, San Diego, California 92121, USA.)

  • Vicky L. Brandt

    (New York University School of Medicine, New York, New York 10016, USA)

  • Katheryn Meek

    (College of Veterinary Medicine, Pathobiology & Diagnostic Investigation, Michigan State University, East Lansing, Michigan 48824, USA)

  • David B. Roth

    (New York University School of Medicine, New York, New York 10016, USA)

Abstract

In the process of generating antibody diversity, DNA in the V(D)J locus undergoes programmed double-strand breaks that are made by the Rag1–Rag 2 complex. These breaks are repaired by the non-homologous end-joining (NHEJ) pathway. Cells deficient in NHEJ factors show very low levels of recombinants, so it was believed there might be another repair pathway. But this paper shows that an alternative NHEJ pathway exists, and that it functions at low levels even in wild-type cells.

Suggested Citation

  • Barbara Corneo & Rebecca L. Wendland & Ludovic Deriano & Xiaoping Cui & Isaac A. Klein & Serre-Yu Wong & Suzzette Arnal & Abigail J. Holub & Geoffrey R. Weller & Bette A. Pancake & Sundeep Shah & Vick, 2007. "Rag mutations reveal robust alternative end joining," Nature, Nature, vol. 449(7161), pages 483-486, September.
    • Handle: RePEc:nat:nature:v:449:y:2007:i:7161:d:10.1038_nature06168
    DOI: 10.1038/nature06168
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    Cited by:

    1. Metztli Cisneros-Aguirre & Felicia Wednesday Lopezcolorado & Linda Jillianne Tsai & Ragini Bhargava & Jeremy M. Stark, 2022. "The importance of DNAPKcs for blunt DNA end joining is magnified when XLF is weakened," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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