Abstract
Two enzymatic mechanisms, DNA end-joining and homologous recombination, operate in eukaryotic cells to repair DNA double-strand breaks (DSB) induced by ionizing radiation and by other agents. The recombinational repair pathway relies on an intact DNA homolog to direct the healing of the DNA break, and is designed to restore the original configuration of the injured chromosome. In contrast, the DNA end joining process has no requirement for a DNA homolog and often results in gain or loss of genetic information, and at times chromosomal rearrangements and translocations. There is emerging evidence that DNA end-joining and homologous recombination are differentially required at specific stages of the cell cycle, with the former appearing to be the more critical mechanism in the G1 phase and the latter taking on a prominent role in late S and G2 when a sister chromatid becomes available to direct the repair process (113). In this article, we will provide an account of what is currently known about homologous recombination and its DNA repair role.
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Petukhova, G., Lee, E.YH.P., Sung, P. (2001). DNA End-Processing and Heteroduplex DNA Formation During Recombinational Repair of DNA Double-Strand Breaks. In: Nickoloff, J.A., Hoekstra, M.F. (eds) DNA Damage and Repair. Contemporary Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-095-7_6
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