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JNK Phosphorylates SIRT6 to Stimulate DNA Double-Strand Break Repair in Response to Oxidative Stress by Recruiting PARP1 to DNA Breaks.

Abstract：

:The accumulation of damage caused by oxidative stress has been linked to aging and to the etiology of numerous age-related diseases. The longevity gene, sirtuin 6 (SIRT6), promotes genome stability by facilitating DNA repair, especially under oxidative stress conditions. Here we uncover the mechanism by which SIRT6 is activated by oxidative stress to promote DNA double-strand break (DSB) repair. We show that the stress-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphorylates SIRT6 on serine 10 in response to oxidative stress. This post-translational modification facilitates the mobilization of SIRT6 to DNA damage sites and is required for efficient recruitment of poly (ADP-ribose) polymerase 1 (PARP1) to DNA break sites and for efficient repair of DSBs. Our results demonstrate a post-translational mechanism regulating SIRT6, and they provide the link between oxidative stress signaling and DNA repair pathways that may be critical for hormetic response and longevity assurance.

journal_name

Cell Rep

journal_title

Cell reports

authors

Van Meter M,Simon M,Tombline G,May A,Morello TD,Hubbard BP,Bredbenner K,Park R,Sinclair DA,Bohr VA,Gorbunova V,Seluanov A

doi

10.1016/j.celrep.2016.08.006

subject

Has Abstract

pub_date

2016-09-06 00:00:00

pages

2641-2650

issue

10

issn

2211-1247

pii

S2211-1247(16)31052-X

journal_volume

16

pub_type

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