SUMOylation of XRCC1 activated by poly (ADP-ribosyl)ation regulates DNA repair

被引：8

作者：

Hu, Ling-Yueh ^{[1
]}

Chang, Che-Chang ^{[2
]}

Huang, Yen-Sung ^{[1
]}

Ghou, Wen-Cheng ^{[1
]}

Lin, Ying-Mei ^{[1
]}

Ho, Chun-Chen ^{[1
]}

Chen, Wei-Ting ^{[1
]}

Shih, Hsiu-Ming ^{[1
,2
]}

Hsiung, Chia-Ni ^{[1
]}

Wu, Pei-Ei ^{[3
]}

Shen, Chen-Yang ^{[1
,4
]}

机构：

[1] Acad Sinica, Inst Biomed Sci, 128,Sec 2,Acad Rd, Taipei 115, Taiwan

[2] Taipei Med Univ, Coll Med Sci & Technol, Grad Inst Translat Med, Taipei 110, Taiwan

[3] Acad Sinica, Taiwan Biobank, Taipei 110, Taiwan

[4] China Med Univ, Coll Publ Hlth, Taichung 404, Taiwan

来源：

HUMAN MOLECULAR GENETICS | 2018年 / 27卷 / 13期

关键词：

BASE EXCISION-REPAIR; POLYMERASE-BETA INTERACTION; STRAND BREAK REPAIR; DAMAGE RESPONSE; POLY(ADP-RIBOSE) POLYMERASE; MAMMALIAN-CELLS; BRCT DOMAINS; LIGASE-III; PROTEIN; SUMO;

D O I：

10.1093/hmg/ddy135

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

XRCC1 is an essential scaffold protein for base excision repair (BER) and helps to maintain genomic stability. XRCC1 has been indicated as a substrate for small ubiquitin-like modifier modification (SUMOylation); however, how XRCC1 SUMOylation is regulated in cells and how SUMOylated XRCC1 regulates BER activity are not well understood. Here, we show that SUMOylation of XRCC1 is regulated in cells under methyl-methanesulfonate (MMS) treatment and facilitates BER. Poly(ADPribose) polymerase 1 (PARP1) is activated by MMS immediately and synthesizes poly(ADP-ribose) (PAR), which in turn promotes recruitment of SUMO E3 TOPORS to XRCC1 and facilitates XRCC1 SUMOylation. A SUMOylation-defective mutant of XRCC1 had lower binding activity for DNA polymerase beta (POLB) and was linked to a lower capacity for repair of MMS-induced DNA damages. Our study therefore identified a pathway in which DNA damage-induced poly(ADP-ribosyl)ation (PARylation) promotes SUMOylation of XRCC1, which leads to more efficient recruitment of POLB to complete BER.

引用

页码：2306 / 2317

页数：12

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