SIRT7 is a histone desuccinylase that functionally links to chromatin compaction and genome stability

Lei Li(Peking University), Lan Shi(Peking University), Shangda Yang(Tianjin Medical University), Ruorong Yan(Peking University), Di Zhang(Peking University), Jianguo Yang(Peking University), Lin He(Peking University), Wanjin Li(Peking University), Xia Yi(Peking University), Luyang Sun(Peking University), Jing Liang(Peking University), Zhongyi Cheng(New England Biolabs (China)), Lei Shi(Peking University), Yongfeng Shang(Peking University), Wenhua Yu(Peking University)
Nature Communications
July 20, 2016
Cited by 390Open Access
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Abstract

Although SIRT7 is a member of sirtuin family proteins that are described as NAD(+)-dependent class III histone deacetylases, the intrinsic enzymatic activity of this sirtuin protein remains to be investigated and the cellular function of SIRT7 remains to be explored. Here we report that SIRT7 is an NAD(+)-dependent histone desuccinylase. We show that SIRT7 is recruited to DNA double-strand breaks (DSBs) in a PARP1-dependent manner and catalyses desuccinylation of H3K122 therein, thereby promoting chromatin condensation and DSB repair. We demonstrate that depletion of SIRT7 impairs chromatin compaction during DNA-damage response and sensitizes cells to genotoxic stresses. Our study indicates SIRT7 is a histone desuccinylase, providing a molecular basis for the understanding of epigenetic regulation by this sirtuin protein. Our experiments reveal that SIRT7-catalysed H3K122 desuccinylation is critically implemented in DNA-damage response and cell survival, providing a mechanistic insight into the cellular function of SIRT7.


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