Radiation-resistant mutants of Salmonella typhimurium LT2: development and characterization.

TitleRadiation-resistant mutants of Salmonella typhimurium LT2: development and characterization.
Publication TypeJournal Article
Year of Publication1973
AuthorsDavies, R, Sinskey, AJ
JournalJ Bacteriol
Date Published1973 Jan
KeywordsBacterial Proteins, Bacteriophage Typing, Carbohydrate Metabolism, Cell Survival, Culture Media, DNA Nucleotidyltransferases, Hydrogen Sulfide, Ligases, Lysogeny, Mutation, Phenotype, Polynucleotides, Radiation Effects, RNA, Bacterial, Salmonella Phages, Salmonella typhimurium, Ultraviolet Rays

A series of repeated exposures to gamma irradiation with intervening outgrowth of survivors was used to develop radioresistant cultures of Salmonella typhimuium LT2. Stepwise increases in resistance to both ionizing and ultraviolet irradiation were obtained independently of the presence or absence of integrated P22 prophage. Single clonal isolates, representing parent and radioresistant populations, retained the general characteristics of the LT2 parent, including serological properties, phage typing, antibiotic sensitivities, mouse virulence, and most biochemical test reactions. Resistant cells were generally larger and contained 1.8 to 2.1 times more ribonucleic acid and protein than parent cells, but deoxyribonucleic acid (DNA) contents were similar. Heterogeneity in the populations with respect to release of H(2)S, utilization of carbon sources, and growth on minimal medium is considered to be ancillary, rather than causally related, to increased radioresistance. The resistant isolates displayed an increased ability to reactivate gamma-irradiated P22 phage. DNA polymerase I and polynucleotide-joining enzyme activities were elevated in extracts of radioresistant cells relative to parent cells. It is suggested that the observed increases in radioresistance result from a selection of mutations leading to an increased capacity to repair DNA.

Alternate JournalJ Bacteriol
Citation Key258
PubMed ID4567137
PubMed Central IDPMC251611