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

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, David A. Sinclair, Kenneth J. O’Byrne and Derek J. Richard ()
Additional contact information
Emma Bolderson: Queensland University of Technology (QUT)
Joshua T. Burgess: Queensland University of Technology (QUT)
Jun Li: Harvard Medical School
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)
Shu-Dong Zhang: University of Ulster
David A. Sinclair: Harvard Medical School
Kenneth J. O’Byrne: Queensland University of Technology (QUT)
Derek J. Richard: Queensland University of Technology (QUT)

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: 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.

Date: 2019
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-019-13167-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13167-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-019-13167-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().