R Factor-mediated Resistance to Ultraviolet Light in Strains of Escherichia coli Deficient in Known Repair Functions

Abstract

U.V. irradiation mediated by R factor R46 has been studied in strains deficient in excision repair and recombination repair. The R factor protected wild-type bacteria and also wild-type cells in which repair had been inhibited by the substitution of bromouracil for chromosomal thymine. It increased the survival of strains defective in the endonucleolytic (uvr), repolymerizing (pol) and joining (lig) stages of the excision repair process. Recombination deficient bacteria mutant at the recB or recC loci were protected by R46, but the R factor had little effect on the survival of a recA strain or a recA recB double mutant. R46 increased the survival of cells that had been treated with chloramphenicol before U.V. irradiation, but did not protect cultures treated with chloramphenicol after irradiation. It is concluded that R46 confers resistance to the lethal effects of U.V. irradiation by a mechanism that is independent of excision repair. Resistance appears to be mediated by an inducible gene product, which is possibly a nuclease and dependent on a functional host recA gene for expression.

Plasmid R46-mediated Protection Against Bleomycin is polA+-dependent

“…This indicates that plasmid-mediated protection against BLM is independent of the uvrA+ or lig+ genotypes, which again agrees with results for R46 protection against U.V. irradiation (Tweats et al, 1976).…”

“…These results are comparable to those observed for R46 when protecting against U.V. light (Tweats et al, 1976).…”

“…This suggests that R46-mediated protection against BLM is polA +-dependent, which is in contrast to plasmid-mediated protection against U.V. light (Tweats et al, 1976).…”

“…This protective effect has been shown to be completely dependent upon the recA+ genotype in Salmonella typhimurium, but independent of the uvrB or polA gene functions (Mortelmans & Stocker, 1976). In Escherichia coli, R46 does not protect recA mutants but does protect recB, r e d , uvrA, polA or lig mutants (Tweats et al, 1976). It is therefore thought that u.v.-protecting plasmids function by interacting with recA+-dependent, error-prone (SOS) repair processes (Walker, 1977).…”

Suppression of Pathogenicity by P and V Plasmids in Vibrio cholerae

“…The gene controlling synthesis of enterotoxin in Escherichia coli has been shown to be located on a plasmid (Williams Smith & Halls, 1968;Skerman, Formal & Falkow, 1972). Recently, R and ColI plasmids have been found to increase the resistance of E. coli, Salmonella typhimurium and Pseudomonas aeruginosa to radiation and chemical treatments (Howarth, 1965;Marsh & Smith, 1969;Tweats et al, 1976;MacPhee, 1972;Mortelmans & Stocker, 1976;Lehrbach et al, 1977). We report here that the presence of P and/or V plasmids of V. cholerae renders the bacteria less pathogenic in experimental models of cholera and that this effect is due to decreased toxin production.…”