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RMI1 contributes to DNA repair and to the tolerance to camptothecin
Author(s) -
Fang Lianying,
Sun Xiaohui,
Wang Yan,
Du Liqing,
Ji Kaihua,
Wang Jinhan,
He Ningning,
Liu Yang,
Wang Qin,
Zhai Hezheng,
Hao Jianxiu,
Xu Chang,
Liu Qiang
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201802014r
Subject(s) - genome instability , dna damage , rad51 , biology , dna repair , homologous recombination , mutagenesis , dna , genetics , camptothecin , genome , sulfolobus acidocaldarius , mutation , microbiology and biotechnology , gene , biochemistry , archaea
Maintenance of genome integrity is critical for faithful propagation of genetic information and the prevention of the mutagenesis induced by various DNA damage events. RecQ‐mediated genome instability protein 1 (RMI1), together with Bloom syndrome protein and topoisomerase IIIα, form an evolutionarily conserved complex that is critical for the maintenance of genomic stability. Herein, we report that RMI1 depletion increases cell sensitivity to camptothecin treatment, as shown by an elevation of genotoxic stress‐induced DNA double‐strand breaks, a stronger activation of the DNA damage response, and a greater G2/M cell cycle delay. Our findings support that, upon DNA damage, RMI1 forms nuclear foci at the damaged regions, interacts with RAD51, and facilitates the recruitment of RAD51 to initiate homologous recombination. Our data reveal the importance of RMI1 in response to DNA double‐strand breaks and shed light on the molecular mechanisms by which RMI1 contributes to maintain genome stability.—Fang, L., Sun, X., Wang, Y., Du, L., Ji, K., Wang, J., He, N., Liu, Y., Wang, Q., Zhai, H., Hao, J., Xu, C., Liu, Q. RMI1 contributes to DNA repair and to the tolerance to camptothecin. FASEB J. 33, 5561–5570 (2019). www.fasebj.org