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Barrier-to-autointegration factor 1 (Banf1) regulates poly [ADP-ribose] polymerase 1 (PARP1) activity following oxidative DNA damage

Author

Listed:
  • Emma Bolderson

    (Queensland University of Technology (QUT)
    Ipswich Road, Woolloongabba)

  • Joshua T. Burgess

    (Queensland University of Technology (QUT))

  • Jun Li

    (Harvard Medical School
    Chinese Academy of Medical Sciences, Peking Union Medical College)

  • Neha S. Gandhi

    (Queensland University of Technology)

  • Didier Boucher

    (Queensland University of Technology (QUT))

  • Laura V. Croft

    (Queensland University of Technology (QUT))

  • Samuel Beard

    (Queensland University of Technology (QUT))

  • Jennifer J. Plowman

    (Queensland University of Technology (QUT))

  • Amila Suraweera

    (Queensland University of Technology (QUT))

  • Mark N. Adams

    (Queensland University of Technology (QUT))

  • Ali Naqi

    (Queensland University of Technology (QUT)
    Pennsylvania State University)

  • Shu-Dong Zhang

    (University of Ulster)

  • David A. Sinclair

    (Harvard Medical School
    The University of New South Wales)

  • Kenneth J. O’Byrne

    (Queensland University of Technology (QUT)
    Ipswich Road, Woolloongabba)

  • Derek J. Richard

    (Queensland University of Technology (QUT)
    Ipswich Road, Woolloongabba)

Abstract

The DNA repair capacity of human cells declines with age, in a process that is not clearly understood. Mutation of the nuclear envelope protein barrier-to-autointegration factor 1 (Banf1) has previously been shown to cause a human progeroid disorder, Néstor–Guillermo progeria syndrome (NGPS). The underlying links between Banf1, DNA repair and the ageing process are unknown. Here, we report that Banf1 controls the DNA damage response to oxidative stress via regulation of poly [ADP-ribose] polymerase 1 (PARP1). Specifically, oxidative lesions promote direct binding of Banf1 to PARP1, a critical NAD+-dependent DNA repair protein, leading to inhibition of PARP1 auto-ADP-ribosylation and defective repair of oxidative lesions, in cells with increased Banf1. Consistent with this, cells from patients with NGPS have defective PARP1 activity and impaired repair of oxidative lesions. These data support a model whereby Banf1 is crucial to reset oxidative-stress-induced PARP1 activity. Together, these data offer insight into Banf1-regulated, PARP1-directed repair of oxidative lesions.

Suggested Citation

  • Emma Bolderson & Joshua T. Burgess & Jun Li & Neha S. Gandhi & Didier Boucher & Laura V. Croft & Samuel Beard & Jennifer J. Plowman & Amila Suraweera & Mark N. Adams & Ali Naqi & Shu-Dong Zhang & Davi, 2019. "Barrier-to-autointegration factor 1 (Banf1) regulates poly [ADP-ribose] polymerase 1 (PARP1) activity following oxidative DNA damage," Nature Communications, Nature, vol. 10(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13167-5
    DOI: 10.1038/s41467-019-13167-5
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    Cited by:

    1. Souren Paul & Mark H. Kaplan & Dinesh Khanna & Preston M. McCourt & Anjan K. Saha & Pei-Suen Tsou & Mahek Anand & Alexander Radecki & Mohamad Mourad & Amr H. Sawalha & David M. Markovitz & Rafael Cont, 2022. "Centromere defects, chromosome instability, and cGAS-STING activation in systemic sclerosis," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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