OGT Mediated Histone H2B S112 GlcNAcylation Regulates DNA Damage Response

Panfei Wang; Changmin Peng; Xia Liu; Hailong Liu; Yali Chen; Li Zheng; Baolin Han; Huadong Pei

doi:10.1016/j.jgg.2015.07.002

Volume 42 Issue 9

Sep. 2015

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OGT Mediated Histone H2B S112 GlcNAcylation Regulates DNA Damage Response

doi: 10.1016/j.jgg.2015.07.002

Panfei Wang^{a, b, d, #},
Changmin Peng^{a, b, d, #},
Xia Liu^{c, d, #},
Hailong Liu^b,
Yali Chen^b,
Li Zheng^d,
Baolin Han^c,
Huadong Pei^{a, b}

a
Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin Industrial Microbiology Key Lab, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China
b
State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China
c
Department of Radiotherapy, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin 301800, China
d
School of Nursing and Medical Technology, Jianghan University, Wuhan 430056, China

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Corresponding author: E-mail address: tjhanbaolin@163.com (Baolin Han); E-mail address: peihuadong@hotmail.com (Huadong Pei)
Received Date: 2015-04-06
Accepted Date: 2015-07-14
Rev Recd Date: 2015-07-01

Available Online: 2015-07-23

Publish Date: 2015-09-20

Abstract

Abstract

O-GlcNAcylation is an important post-translational modification and has been implicated in many fundamental cellular processes. Recent studies showed that O-linked N-acetylglucosamine (GlcNAc) transferase (OGT) mediated O-GlcNAcylation of histone H2B Ser 112 (H2B S112 GlcNAcylation) plays an important role in gene transcription. However, the role of this histone modification in DNA damage response has not been studied yet. In this study, we found that OGT and OGT mediated H2B S112 GlcNAcylation are involved in DNA damage response for maintaining genomic stability and are required for resistance to many DNA-damaging and replication stress-inducing agents. OGT mediated H2B S112 GlcNAcylation increased locally upon the induction of double-strand breaks (DSBs), and depletion of OGT or overexpression of H2B S112A mutant impaired homologous recombination (HR) and nonhomologous end-joining (NHEJ). Mechanistically, H2B S112 GlcNAcylation could bind Nijmegen breakage syndrome 1 (NBS1) and regulate NBS1 foci formation. Taken together, our results demonstrate a new function of histone O-GlcNAcylation in DNA damage response (DDR).
- OGT,
- H2B S112 GlcNAcylation,
- DNA damage response,
- NBS1

These authors contributed equally to this work.

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References(46)

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