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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hwang, Patty Yi-hwa Truong, Lan N. Sun, Emily Ang, Katrina Wu, Xiaohua Li, Yongjiang |
| Description | Author Affiliation: Truong LN ( From the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La, Jolla, California 92037.); Li Y ( From the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La, Jolla, California 92037.); Sun E ( From the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La, Jolla, California 92037.); Ang K ( From the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La, Jolla, California 92037.); Hwang PY ( From the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La, Jolla, California 92037.); Wu X ( From the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La, Jolla, California 92037 xiaohwu@scripps.edu.) |
| Abstract | Re-initiation of DNA replication at origins within a given cell cycle would result in DNA rereplication, which can lead to genome instability and tumorigenesis. DNA rereplication can be induced by loss of licensing control at cellular replication origins, or by viral protein-driven multiple rounds of replication initiation at viral origins. DNA double-strand breaks (DSBs) are generated during rereplication, but the mechanisms of how these DSBs are repaired to maintain genome stability and cell viability are poorly understood in mammalian cells. We generated novel EGFP-based DSB repair substrates, which specifically monitor the repair of rereplication-associated DSBs. We demonstrated that homologous recombination (HR) is an important mechanism to repair rereplication-associated DSBs, and sister chromatids are used as templates for such HR-mediated DSB repair. Micro-homology-mediated non-homologous end joining (MMEJ) can also be used but to a lesser extent compared to HR, whereas Ku-dependent classical non-homologous end joining (C-NHEJ) has a minimal role to repair rereplication-associated DSBs. In addition, loss of HR activity leads to severe cell death when rereplication is induced. Therefore, our studies identify HR, the most conservative repair pathway, as the primary mechanism to repair DSBs upon rereplication. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 42 |
| Volume Number | 289 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2014-10-17 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | DNA Breaks, Double-Stranded DNA End-Joining Repair DNA Repair Homologous Recombination Recombination, Genetic Carcinogenesis Cell Death Cell Line, Tumor Cell Separation Cell Survival Flow Cytometry Green Fluorescent Proteins Metabolism HEK293 Cells Neoplasms Genetics Open Reading Frames Phosphorylation Plasmids RNA, Small Interfering Beta-Globins Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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