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ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks

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  • Shan Zha

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School
    Present address: Department of Pathology and Cell Biology, Department of Pediatrics, Institute for Cancer Genetics, Columbia University, New York City, New York 10032, USA.)

  • Chunguang Guo

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Cristian Boboila

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Valentyn Oksenych

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Hwei-Ling Cheng

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Yu Zhang

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Duane R. Wesemann

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Grace Yuen

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Harin Patel

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Peter H. Goff

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

  • Richard L. Dubois

    (Institute for Cancer Genetics, Columbia University)

  • Frederick W. Alt

    (Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School)

Abstract

XLF, ATM and H2AX share role in joining DNA breaks The loss of a classical non-homologous end-joining (NHEJ) repair factor, XLF, shows strong effects in non-lymphoid cells, but in lymphoid cells its absence surprisingly has only modest effects on V(D)J recombination. Frederick Alt and colleagues show that in lymphoid cells, two other repair factors — ATM kinase and histone protein H2AX — have functional redundancy with XLF. Thus, mice that are deficient in both ATM and XLF have compromised conventional NHEJ, although alternative end-joining is retained. The results hint that the redundant function in end-joining that XLF has with both ATM and H2AX may be related to a role for ATM in chromatin accessibility.

Suggested Citation

  • Shan Zha & Chunguang Guo & Cristian Boboila & Valentyn Oksenych & Hwei-Ling Cheng & Yu Zhang & Duane R. Wesemann & Grace Yuen & Harin Patel & Peter H. Goff & Richard L. Dubois & Frederick W. Alt, 2011. "ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks," Nature, Nature, vol. 469(7329), pages 250-254, January.
    • Handle: RePEc:nat:nature:v:469:y:2011:i:7329:d:10.1038_nature09604
    DOI: 10.1038/nature09604
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    Cited by:

    1. Estelle Vincendeau & Wenming Wei & Xuefei Zhang & Cyril Planchais & Wei Yu & Hélène Lenden-Hasse & Thomas Cokelaer & Juliana Pipoli da Fonseca & Hugo Mouquet & David J. Adams & Frederick W. Alt & Step, 2022. "SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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