DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells |
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| Authors: | Fei Zhao Wootae Kim Jake A. Kloeber Zhenkun Lou |
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| Affiliation: | 1.Department of Oncology, Mayo Clinic, Rochester, MN 55905 USA ;2.Mayo Clinic Medical Scientist Training Program, Mayo Clinic, Rochester, MN 55905 USA ;3.Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905 USA |
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| Abstract: | DNA end resection has a key role in double-strand break repair and DNA replication. Defective DNA end resection can cause malfunctions in DNA repair and replication, leading to greater genomic instability. DNA end resection is initiated by MRN-CtIP generating short, 3′-single-stranded DNA (ssDNA). This newly generated ssDNA is further elongated by multiple nucleases and DNA helicases, such as EXO1, DNA2, and BLM. Effective DNA end resection is essential for error-free homologous recombination DNA repair, the degradation of incorrectly replicated DNA and double-strand break repair choice. Because of its importance in DNA repair, DNA end resection is strictly regulated. Numerous mechanisms have been reported to regulate the initiation, extension, and termination of DNA end resection. Here, we review the general process of DNA end resection and its role in DNA replication and repair pathway choice.Subject terms: Double-strand DNA breaks, Cell signalling |
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