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

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 and Frederick W. Alt ()
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Shan Zha: Howard Hughes Medical Institute, The Children’s Hospital, the Immune Disease Institute and the Harvard Medical School
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

Nature, 2011, vol. 469, issue 7329, 250-254

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.

Date: 2011
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DOI: 10.1038/nature09604

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