The uvrA6 mutation blocks nucleotide excision repair, and the recA13 mutation blocks recombinational DNA repair. UV radiation survival curves for DNA repair deficient mutants of E. These studies led to the discovery of postreplication repair (see below).įigure 1. From the most fundamental principles of radiation biology and genetics, these data argue that, (a) these two systems, i.e., coded by the uvrA and the recA genes, function largely independently of each other, and (b) they are of about equal importance to the survival of UV-irradiated cells of E.
A double mutant ( uvrA recA), however, is much more sensitive to UV irradiation than either of the single mutants (Figure 1). The first indication that nucleotide excision repair ("cut and patch") is NOT the only mechanism by which cells repair damage to their DNA, was the observation that bacterial cells deficient in nucleotide excision repair (i.e., uvrA) or in genetic recombination (i.e., recA) are very sensitive to UV radiation, and show a similar level of survival after UV irradiation. It is a very complicated process that requires two DNA duplexes, and the exchange of a strand of DNA from one DNA duplex to the other (Rupp et al., 1971 Howard-Flanders and Rupp, 1972 Ganesan, 1974 Wang and Smith, 1984), and it produces mutations. It accounts for about 50% of the survival of UV irradiated Escherichia coli (see below). Quite to the contrary, recombinational DNA repair is critical for the survival of UV radiation-damaged cells. The sheer volume of publications on "cut and patch" nucleotide excision repair (e.g., Petit and Sancar, 1999) has generated the impression that cells possess only this simple repair system. This process is very accurate, and does not produce mutations.
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The patch is then joined to the main strand by DNA ligase. In nucleotide excision repair, damaged nucleotides (i.e., pyrimidine dimers) are recognized and cut out, and the resulting hole is patched by DNA polymerase l, using the DNA strand opposite the gap as the template. Emeritus Professor, Radiation Oncology (Radiation Biology)Ĩ00 Blossom Hill Road, Unit R169, Los Gatos, CA two major systems for the repair of ultraviolet (UV) radiation-induced DNA damage in cells are nucleotide excision repair (Petit and Sancar, 1999), and recombinational DNA repair (Kuzminov, 1999 Smith, 2004).
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