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SUMO-1 modification of FEN1 facilitates its interaction with Rad9-Radl-Husl to counteract DNA replication stress

Journal of Molecular Cell Biology 2018年第5期10卷 460-474页

作者： Xiaoli Xu Rongyi Shi Li Zheng Zhigang Guo Liangyan Wang Mian Zhou Ye Zhao Bing Tian Khue Truong Yuan Chen Binghui Shen Yuejin Hua Hong Xu Institute of Nuclear-Agricultural Sciences Zhejiang University Hangzhou 310029 China Department of Cancer Genetics and Epigenetics City of Hope National Medical Center and Beckman Research Institute Duarte CA 91010 USA Jiangsu Key Laboratory for Molecular and Medical Biotechnology and College of Life Sciences Nanjing Normal University Nanjing 210046 China Department of Molecular Medicine City of Hope National Medical Center and Beckman Research Institute Duarte CA 91010 USA

Human flap endonuclease 1 （FEN1） is a structure-specific, multi-functional endonuclease essential for DNA replication and repair. We and others have shown that during DNA replication, FEN1 processes Okazaki fragments via its interaction with the proliferating cell nuclear antigen （PCNA）. Alternatively, in response to DNA damage, FEN1 interacts with the PCNA-like Radg-Radl-Husl complex instead of PCNA to engage in DNA repair activities, such as homology-directed repair of stalled DNA replication forks. However, it is unclear how FEN1 is able to switch between these interactions and its roles in DNA replication and DNA repair. Here, we report that FEN1 undergoes SUMOylation by SUMO-1 in response to DNA replication fork-staUing agents, such as UV irradiation, hydroxyurea, and mitomycin C. This DNA damage-induced SUMO-1 modification promotes the interaction of FEN1 with the Radg-Rad1-Husl complex. Furthermore, we found that FEN1 mutations that prevent its SUMO-1 modification also impair its ability to interact with HUS1 and to rescue stalled replication forks. These impairments lead to the accumulation of DNA damage and heightened sensitivity to fork-staUing agents. Altogether, our findings suggest an important role of the SUMO-1 modification of FEN1 in regulating its roles in DNA replication and repair.

关键词： flap endonuclease 1 Rad9-Rad1-Hus1 complex replication stress SUMOylation

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