recA‐dependent DNA repair processes

Abstract

UV-radiation-induced lesions in DNA result in the formation of: (1) excision gaps (i.e. a lesion is excised, leaving a gap), (2) daughter-strand gaps (i.e. a lesion can be skipped during replication, leaving a gap), and (3) double-strand breaks (i.e. the DNA strand opposite a gap can be cut). In Escherichia coli, the recA gene product is involved in repairs of all three types of lesions--repair of daughter-strand gaps (2) and double-strand breaks (3) constitutes post-replication repair. The evidence suggests, furthermore, that recA-dependent repair of excision gaps (1) produced in DNA replicated prior to UV irradiation (pre-replication repair) appears to occur by similar mechanisms.

Treatment of Pea (Pisum sativum L.) Protoplasts with DNA-Damaging Agents Induces a 39-Kilodalton Chloroplast Protein Immunologically Related to Escherichia coli RecA

“…and Wang, 1989;Roca and Cox, 1990;Sassanfarand Roberts, 1990). According to the serial endosymbiosis theory, chloroplasts arose by symbiotic association between ancestral eukaryotes and free-living cyanobacterial progenitors (Gray, 1989).…”

“…DNA repair has been postulated as the primary role of enzymic system(s) involving RecA in E. coli (Walker, 1984;Smith and Wang, 1989;Roca and Cox, 1990). Activated RecA promotes the autocatalytic cleavage of the LexA represser, resulting in increased expression of genes involved in DNA repair (including recA itself).…”

“…Activated RecA promotes the autocatalytic cleavage of the LexA represser, resulting in increased expression of genes involved in DNA repair (including recA itself). In addition, genetic recombination is essential for the repair of certain DNA lesions, like double-strand breaks, where an intact complementary strand does not exist and the information required for repair must come from a separate DNA molecule (Sancar and Sancar, 1988;Resnick et al, 1989;Smith and Wang, 1989). …”

“…DNA repair has been considered the primary function of homologous recombination in maintaining cell viability, and this would be the most essential role of RecA in E. coli (Walker, 1984;Resnick et al, 1989;Smith and Wang, 1989;Roca and Cox, 1990). Therefore, we tested the effect of MMS, MMC, and NA on the steady-state level of the chloroplast cross-reacting protein.…”

“…Therefore, we tested the effect of MMS, MMC, and NA on the steady-state level of the chloroplast cross-reacting protein. The chemicals were used at concentrations causing DNA lesions that, presumably, could be repaired by a recombinational pathway (Tomasz et al, 1987;Drlica and Franco, 1988;Mirzayans et al, 1988;Dusre et al, 1989;Resnick et al, 1989;Smith and Wang, 1989). The amount of the 39-kD protein increased in response to these agents, reaching a maximum approximately 12 to 15 h after the onset of treatments.…”