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Interactome analysis identifies a new paralogue of XRCC4 in non-homologous end joining DNA repair pathway

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  • Mengtan Xing

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Mingrui Yang

    (State Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences
    State Key Laboratory of Virology, School of Basic Medicine, Wuhan University)

  • Wei Huo

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Feng Feng

    (State Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences)

  • Leizhen Wei

    (University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine)

  • Wenxia Jiang

    (Institute for Cancer Genetics, Columbia University Medical Center)

  • Shaokai Ning

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Zhenxin Yan

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Wen Li

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Qingsong Wang

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Mei Hou

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Chunxia Dong

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Rong Guo

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Ge Gao

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Jianguo Ji

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

  • Shan Zha

    (Institute for Cancer Genetics, Columbia University Medical Center)

  • Li Lan

    (University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine)

  • Huanhuan Liang

    (State Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences)

  • Dongyi Xu

    (State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University)

Abstract

Non-homologous end joining (NHEJ) is a major pathway to repair DNA double-strand breaks (DSBs), which can display different types of broken ends. However, it is unclear how NHEJ factors organize to repair diverse types of DNA breaks. Here, through systematic analysis of the human NHEJ factor interactome, we identify PAXX as a direct interactor of Ku. The crystal structure of PAXX is similar to those of XRCC4 and XLF. Importantly, PAXX-deficient cells are sensitive to DSB-causing agents. Moreover, epistasis analysis demonstrates that PAXX functions together with XLF in response to ionizing radiation-induced complex DSBs, whereas they function redundantly in response to Topo2 inhibitor-induced simple DSBs. Consistently, PAXX and XLF coordinately promote the ligation of complex but not simple DNA ends in vitro. Altogether, our data identify PAXX as a new NHEJ factor and provide insight regarding the organization of NHEJ factors responding to diverse types of DSB ends.

Suggested Citation

  • Mengtan Xing & Mingrui Yang & Wei Huo & Feng Feng & Leizhen Wei & Wenxia Jiang & Shaokai Ning & Zhenxin Yan & Wen Li & Qingsong Wang & Mei Hou & Chunxia Dong & Rong Guo & Ge Gao & Jianguo Ji & Shan Zh, 2015. "Interactome analysis identifies a new paralogue of XRCC4 in non-homologous end joining DNA repair pathway," Nature Communications, Nature, vol. 6(1), pages 1-12, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7233
    DOI: 10.1038/ncomms7233
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    Cited by:

    1. Sumin Feng & Sai Ma & Kejiao Li & Shengxian Gao & Shaokai Ning & Jinfeng Shang & Ruiyuan Guo & Yingying Chen & Britny Blumenfeld & Itamar Simon & Qing Li & Rong Guo & Dongyi Xu, 2022. "RIF1-ASF1-mediated high-order chromatin structure safeguards genome integrity," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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