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A H Kung

Publications and source records attributed to A H Kung.

4 recordsLinked to original sources

R plasmids which alter ultraviolet light-sensitivity and enhance ultraviolet light-induced mutability in Pseudomonas aeruginosa.

R plasmids pMG1, R2, R931 and pMG15 increased the survival of Pseudomonas aeruginosa exposed to ultraviolet radiation (u.v.) in the wild type, and uvr and polA mutants but did not alter the u.v.-response of a recA mutant. The R plasmid RPL11 reduced u.v.-survival in the wild type, and uvr and polA mutants but did not alter the u.v.-response of a recA host. All the plasmids enhanced the level of spontaneous and u.v.-induced back mutation (Trp+) in a trpB1 strain. The effect of sublethal concentration of sodium arsenite following u.v.-irradiation was examined. It was concluded that in strains trpB1(pMG1) and trpB1(R931), u.v.-protection is determined by a recA+-dependent, arsenite-sensitive repair pathway, whereas in strains trpB1(R2) and trpB1(pMG15), u.v.-protection is determined by a recA+-dependent, arsenite-insensitive step in DNA repair.

Arsenic

Plasmid modification of radiation and chemical-mutagen sensitivity in Pseudomonas aeruginosa.

The R factor pMG2 protects Pseudomonas aeruginosa against the lethal effects of ultraviolet (u.v.) and gamma irradiation, and methyl methanesulphonate and N-methyl-N'-nitro-N-nitrosoguanidine treatment. Enhanced survival occurs in strains of uvr+ rec+ (wild-type) genotype and a variety of uvr rec+ type mutants. No protection occurs in a rec A-type mutant. The plasmid also enhances u.v.-induced mutagenesis. These effects appear to be due to host-cell controlled plasmid-determined DNA repair function(s). Studies on P. aeruginosa strains deficient in DNA polymerase I (polyA) suggest that a plasmid-determined repair resynthesis function may be responsible for increased u.v.-survival and enhanced u.v.-mutability in pMG2-containing bacteria.

DNA Polymerase I